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Management Specifics in Kidney Disease: Fluid Prep for Cardiac Catheterizations
Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?
Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.10
A GFR below 60 mL/min/1.73m2, volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.11
Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.
In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial12 demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.13 There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.11
The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury14 recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.
Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al15 have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.11 The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury14 recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.15
Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.16 In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.10
In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and
Internal Medicine, Lawrence, MA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?
Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.10
A GFR below 60 mL/min/1.73m2, volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.11
Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.
In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial12 demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.13 There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.11
The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury14 recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.
Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al15 have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.11 The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury14 recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.15
Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.16 In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.10
In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and
Internal Medicine, Lawrence, MA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?
Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.10
A GFR below 60 mL/min/1.73m2, volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.11
Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.
In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial12 demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.13 There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.11
The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury14 recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.
Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al15 have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.11 The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury14 recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.15
Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.16 In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.10
In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and
Internal Medicine, Lawrence, MA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Management Specifics in Kidney Disease: Dietary Potassium
Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)?
Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring1 (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium.
Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)2 defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:
•Lowering the dose of the ACE inhibitor or ARB by 50%
•Stopping or reducing other medications that can cause hyperkalemia
•Starting or increasing the dosage of a loop diuretic; or
•Reinforcing dietary restriction.2
Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.
Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2. K/DOQI2 recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.3
Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.1
Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)?
Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring1 (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium.
Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)2 defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:
•Lowering the dose of the ACE inhibitor or ARB by 50%
•Stopping or reducing other medications that can cause hyperkalemia
•Starting or increasing the dosage of a loop diuretic; or
•Reinforcing dietary restriction.2
Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.
Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2. K/DOQI2 recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.3
Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.1
Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)?
Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring1 (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium.
Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)2 defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:
•Lowering the dose of the ACE inhibitor or ARB by 50%
•Stopping or reducing other medications that can cause hyperkalemia
•Starting or increasing the dosage of a loop diuretic; or
•Reinforcing dietary restriction.2
Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.
Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m2. K/DOQI2 recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.3
Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.1
Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA
REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.
2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.
3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.
4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.
5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.
6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy
.com/content.aspx?aid=9130075. Accessed November 21, 2012.
7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.
8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.
9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.
10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.
11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-
contrast-induced-nephropathy. Accessed November 21, 2012.
12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.
13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.
14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline
.pdf. Accessed November 21, 2012.
15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.
16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.
Developing Renal Education Classes
Q: We are trying to develop renal education classes in our hospital’s general medical clinic. Participating patients (pre-renal) will be those we hope can be managed by their primary care providers in coordination with our nephrology specialists before their initial renal clinic visits. Our team of educators will include an RN, an NP, a primary care physician, and a nephrologist. Any information, models, and/or links to educational resources would be much appreciated.
Everyone loses 1% of kidney function per year after age 40. If we lived long enough, all of us would need renal education!
As you try to develop classes, one of your first concerns will be whether you want to charge for them. If they are meant to be billed for, they will take a much different form than a free kidney disease education class would. Let’s explore both.
PAID CLASSES
Only Medicare pays for education classes, and patients must be at stage 4 kidney disease (ie, glomerular filtration rate [GFR], 15 to 30 mL/dL). The class can be taught in a group or an individualized format, and an RN, a dietician, or a social worker can assist—but the bulk of the class must be taught by a practitioner with a National Provider Identifier billing number (an NP, a PA, or a physician).
Medicare specifies the content of the classes and has set certain requirements regarding a class’s site and length. In addition, there must be preevaluation and postevaluation tools in place, and the number of classes over a patient’s lifetime is limited to six.
The best program available (one that contains all the needed tools, slide sets, and handouts) is Your Treatment, Your Choice8 from the National Kidney Foundation (www.kidney.org/profes sionals/KLS/YTYC.cfm). It is free, but you must be a PA, an NP, or an MD to request it.
NONPAID CLASSES AND PROGRAMS
These can be given by anybody, and the format is up to the teacher. Prevention always trumps a cure, and preventing advanced kidney disease (GFR < 60 mL/dL) fits in very well in general practice. Promoting good health habits is a common goal. To that end, instruction regarding diet, blood pressure control, blood sugar control, and smoking cessation all help slow kidney disease progression.
What’s best about offering classes like these is that you don’t have to reinvent the wheel. There are some fantastic free programs out there. Some of our favorites are available through the National Kidney Disease Education Program (NKDEP) Web site: http://nkdep.nih.gov/resources.shtml. This is a division of one of the National Institutes of Health, paid for by your tax dollars, and it offers free or very inexpensive handouts, videos, and slide sets, all written at an eighth-grade reading level.
Among the materials offered is a phenomenal tear-off sheet, “Explaining Your Kidney Test Results,” which is available in English, Spanish, Chinese, and Vietnamese (with the first five copies free, then $1 each). It illustrates the stages of kidney function using the traffic light scenario: green, yellow, or red (stage 5 CKD is the red zone) and explains what patients can do to “stay out of the red.” We consider this one of the most effective tools we can use.
NKDEP also offers free handouts listing foods high in potassium, phosphorus, protein, and sodium. Nothing is as good as a renal dietician, but these forms are an excellent alternative.
NKDEP allows you to download and reprint almost all of their information free, or you can request 50 copies of just about any item at no cost. Put your best shopper on the Web site. The amount of materials offered is truly wonderful, and you can’t beat the price.
Another program is called Kidney School (http://kidneyschool
.org), a nonprofit organization set up by the kidney community that offers all kinds of videos and slide sets at no charge.
Last, but certainly not least, is Seymour Jones and the Temple of CKD, a five-minute video put out by the Renal Support Network (RSN; www.rsnhope.org). You can request the video from RSN or find it on YouTube (www.youtube.com/watch?v=lDJZHIVTNzo). Though hilarious, it makes excellent points about the symptoms of chronic kidney disease.
As you can see, there are many wonderful and varied (and free!) programs out there.
With the double-whammy of an aging population and increasing obesity, the number of people with kidney disease is growing exponentially; the past 20 years have seen a 67% increase in the number of patients with CKD, which now affects more than 20 million Americans. Yet in that same 20-year period, effective treatments have been developed for CKD that “can delay and, in some cases, prevent ESRD.”9 Patients with CKD need not assume there will be dialysis in their future.
Most importantly of all, we need to get out there and talk up prevention.
Kim Zuber, PA-C; Jane S. Davis, DNP, CRNP
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Q: We are trying to develop renal education classes in our hospital’s general medical clinic. Participating patients (pre-renal) will be those we hope can be managed by their primary care providers in coordination with our nephrology specialists before their initial renal clinic visits. Our team of educators will include an RN, an NP, a primary care physician, and a nephrologist. Any information, models, and/or links to educational resources would be much appreciated.
Everyone loses 1% of kidney function per year after age 40. If we lived long enough, all of us would need renal education!
As you try to develop classes, one of your first concerns will be whether you want to charge for them. If they are meant to be billed for, they will take a much different form than a free kidney disease education class would. Let’s explore both.
PAID CLASSES
Only Medicare pays for education classes, and patients must be at stage 4 kidney disease (ie, glomerular filtration rate [GFR], 15 to 30 mL/dL). The class can be taught in a group or an individualized format, and an RN, a dietician, or a social worker can assist—but the bulk of the class must be taught by a practitioner with a National Provider Identifier billing number (an NP, a PA, or a physician).
Medicare specifies the content of the classes and has set certain requirements regarding a class’s site and length. In addition, there must be preevaluation and postevaluation tools in place, and the number of classes over a patient’s lifetime is limited to six.
The best program available (one that contains all the needed tools, slide sets, and handouts) is Your Treatment, Your Choice8 from the National Kidney Foundation (www.kidney.org/profes sionals/KLS/YTYC.cfm). It is free, but you must be a PA, an NP, or an MD to request it.
NONPAID CLASSES AND PROGRAMS
These can be given by anybody, and the format is up to the teacher. Prevention always trumps a cure, and preventing advanced kidney disease (GFR < 60 mL/dL) fits in very well in general practice. Promoting good health habits is a common goal. To that end, instruction regarding diet, blood pressure control, blood sugar control, and smoking cessation all help slow kidney disease progression.
What’s best about offering classes like these is that you don’t have to reinvent the wheel. There are some fantastic free programs out there. Some of our favorites are available through the National Kidney Disease Education Program (NKDEP) Web site: http://nkdep.nih.gov/resources.shtml. This is a division of one of the National Institutes of Health, paid for by your tax dollars, and it offers free or very inexpensive handouts, videos, and slide sets, all written at an eighth-grade reading level.
Among the materials offered is a phenomenal tear-off sheet, “Explaining Your Kidney Test Results,” which is available in English, Spanish, Chinese, and Vietnamese (with the first five copies free, then $1 each). It illustrates the stages of kidney function using the traffic light scenario: green, yellow, or red (stage 5 CKD is the red zone) and explains what patients can do to “stay out of the red.” We consider this one of the most effective tools we can use.
NKDEP also offers free handouts listing foods high in potassium, phosphorus, protein, and sodium. Nothing is as good as a renal dietician, but these forms are an excellent alternative.
NKDEP allows you to download and reprint almost all of their information free, or you can request 50 copies of just about any item at no cost. Put your best shopper on the Web site. The amount of materials offered is truly wonderful, and you can’t beat the price.
Another program is called Kidney School (http://kidneyschool
.org), a nonprofit organization set up by the kidney community that offers all kinds of videos and slide sets at no charge.
Last, but certainly not least, is Seymour Jones and the Temple of CKD, a five-minute video put out by the Renal Support Network (RSN; www.rsnhope.org). You can request the video from RSN or find it on YouTube (www.youtube.com/watch?v=lDJZHIVTNzo). Though hilarious, it makes excellent points about the symptoms of chronic kidney disease.
As you can see, there are many wonderful and varied (and free!) programs out there.
With the double-whammy of an aging population and increasing obesity, the number of people with kidney disease is growing exponentially; the past 20 years have seen a 67% increase in the number of patients with CKD, which now affects more than 20 million Americans. Yet in that same 20-year period, effective treatments have been developed for CKD that “can delay and, in some cases, prevent ESRD.”9 Patients with CKD need not assume there will be dialysis in their future.
Most importantly of all, we need to get out there and talk up prevention.
Kim Zuber, PA-C; Jane S. Davis, DNP, CRNP
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Q: We are trying to develop renal education classes in our hospital’s general medical clinic. Participating patients (pre-renal) will be those we hope can be managed by their primary care providers in coordination with our nephrology specialists before their initial renal clinic visits. Our team of educators will include an RN, an NP, a primary care physician, and a nephrologist. Any information, models, and/or links to educational resources would be much appreciated.
Everyone loses 1% of kidney function per year after age 40. If we lived long enough, all of us would need renal education!
As you try to develop classes, one of your first concerns will be whether you want to charge for them. If they are meant to be billed for, they will take a much different form than a free kidney disease education class would. Let’s explore both.
PAID CLASSES
Only Medicare pays for education classes, and patients must be at stage 4 kidney disease (ie, glomerular filtration rate [GFR], 15 to 30 mL/dL). The class can be taught in a group or an individualized format, and an RN, a dietician, or a social worker can assist—but the bulk of the class must be taught by a practitioner with a National Provider Identifier billing number (an NP, a PA, or a physician).
Medicare specifies the content of the classes and has set certain requirements regarding a class’s site and length. In addition, there must be preevaluation and postevaluation tools in place, and the number of classes over a patient’s lifetime is limited to six.
The best program available (one that contains all the needed tools, slide sets, and handouts) is Your Treatment, Your Choice8 from the National Kidney Foundation (www.kidney.org/profes sionals/KLS/YTYC.cfm). It is free, but you must be a PA, an NP, or an MD to request it.
NONPAID CLASSES AND PROGRAMS
These can be given by anybody, and the format is up to the teacher. Prevention always trumps a cure, and preventing advanced kidney disease (GFR < 60 mL/dL) fits in very well in general practice. Promoting good health habits is a common goal. To that end, instruction regarding diet, blood pressure control, blood sugar control, and smoking cessation all help slow kidney disease progression.
What’s best about offering classes like these is that you don’t have to reinvent the wheel. There are some fantastic free programs out there. Some of our favorites are available through the National Kidney Disease Education Program (NKDEP) Web site: http://nkdep.nih.gov/resources.shtml. This is a division of one of the National Institutes of Health, paid for by your tax dollars, and it offers free or very inexpensive handouts, videos, and slide sets, all written at an eighth-grade reading level.
Among the materials offered is a phenomenal tear-off sheet, “Explaining Your Kidney Test Results,” which is available in English, Spanish, Chinese, and Vietnamese (with the first five copies free, then $1 each). It illustrates the stages of kidney function using the traffic light scenario: green, yellow, or red (stage 5 CKD is the red zone) and explains what patients can do to “stay out of the red.” We consider this one of the most effective tools we can use.
NKDEP also offers free handouts listing foods high in potassium, phosphorus, protein, and sodium. Nothing is as good as a renal dietician, but these forms are an excellent alternative.
NKDEP allows you to download and reprint almost all of their information free, or you can request 50 copies of just about any item at no cost. Put your best shopper on the Web site. The amount of materials offered is truly wonderful, and you can’t beat the price.
Another program is called Kidney School (http://kidneyschool
.org), a nonprofit organization set up by the kidney community that offers all kinds of videos and slide sets at no charge.
Last, but certainly not least, is Seymour Jones and the Temple of CKD, a five-minute video put out by the Renal Support Network (RSN; www.rsnhope.org). You can request the video from RSN or find it on YouTube (www.youtube.com/watch?v=lDJZHIVTNzo). Though hilarious, it makes excellent points about the symptoms of chronic kidney disease.
As you can see, there are many wonderful and varied (and free!) programs out there.
With the double-whammy of an aging population and increasing obesity, the number of people with kidney disease is growing exponentially; the past 20 years have seen a 67% increase in the number of patients with CKD, which now affects more than 20 million Americans. Yet in that same 20-year period, effective treatments have been developed for CKD that “can delay and, in some cases, prevent ESRD.”9 Patients with CKD need not assume there will be dialysis in their future.
Most importantly of all, we need to get out there and talk up prevention.
Kim Zuber, PA-C; Jane S. Davis, DNP, CRNP
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Loop Diuretics
Q: When (at what GFR) do you change over from hydrochlorothiazide (HCTZ) to loop diuretics? And what should be the starting dose?
The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for hypertension and antihypertensive agents in chronic kidney disease1 (CKD) recommend replacing thiazide diuretics with loop diuretics once a patient’s glomerular filtration rate (GFR) falls below 30 mL/min/1.73 m2.
The mechanism of action for thiazide and loop diuretics differs by site of action in the kidney. Thiazide diuretics work in the distal convoluted tubules by inhibiting sodium (Na+)/chloride (Cl-) channels while the action of loop diuretics is exerted by inhibiting Na+/potassium (K+)/2Cl- channels in the thick ascending limb of the loop of Henle.2 Thiazide diuretics, with exception of metolazone, are ineffective in CKD stages 4 and 5 due to thiazide’s inability to reach the site of action.1,3
The initial furosemide dose should be 40 to 80 mg/d by mouth, preferably divided into two doses to minimize rebound sodium reabsorption.1,4 Weekly dose titrations by 25% to 50% may be made based on fluid status, blood pressure, and potassium level.1 Bumetanide and torsemide are loop diuretics that may also be used to therapeutically replace HCTZ when the GFR falls below 30 mL/min/1.73 m2. The relative potency of bumetanide: furosemide: torsemide is 1:40:20, respectively.5 The relative initiating dose equivalency of furosemide 40 mg would be bumetanide 1 mg or torsemide 20 mg.5,6
Finally, metolazone is a thiazide-related diuretic that retains its effectiveness even at GFR below 30 mL/min/1.73 m2.1,6 Metolazone can be initiated at oral doses of 2.5 to 5.0 mg/d and titrated up to 10 to 20 mg/d. Patients with residual renal function, defined as daily urine output exceeding 100 mL, may continue to use metolazone and loop diuretics even after dialysis is initated.5,7 Upon the loss of residual renal function, all diuretics should be discontinued.
Min Sik Shin
PharmD candidate, 2012, College of Pharmacy, University of Illinois at Chicago
Cheryl L. Gilmartin, PharmD
Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago;
Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital and Health Sciences System, Chicago
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Q: When (at what GFR) do you change over from hydrochlorothiazide (HCTZ) to loop diuretics? And what should be the starting dose?
The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for hypertension and antihypertensive agents in chronic kidney disease1 (CKD) recommend replacing thiazide diuretics with loop diuretics once a patient’s glomerular filtration rate (GFR) falls below 30 mL/min/1.73 m2.
The mechanism of action for thiazide and loop diuretics differs by site of action in the kidney. Thiazide diuretics work in the distal convoluted tubules by inhibiting sodium (Na+)/chloride (Cl-) channels while the action of loop diuretics is exerted by inhibiting Na+/potassium (K+)/2Cl- channels in the thick ascending limb of the loop of Henle.2 Thiazide diuretics, with exception of metolazone, are ineffective in CKD stages 4 and 5 due to thiazide’s inability to reach the site of action.1,3
The initial furosemide dose should be 40 to 80 mg/d by mouth, preferably divided into two doses to minimize rebound sodium reabsorption.1,4 Weekly dose titrations by 25% to 50% may be made based on fluid status, blood pressure, and potassium level.1 Bumetanide and torsemide are loop diuretics that may also be used to therapeutically replace HCTZ when the GFR falls below 30 mL/min/1.73 m2. The relative potency of bumetanide: furosemide: torsemide is 1:40:20, respectively.5 The relative initiating dose equivalency of furosemide 40 mg would be bumetanide 1 mg or torsemide 20 mg.5,6
Finally, metolazone is a thiazide-related diuretic that retains its effectiveness even at GFR below 30 mL/min/1.73 m2.1,6 Metolazone can be initiated at oral doses of 2.5 to 5.0 mg/d and titrated up to 10 to 20 mg/d. Patients with residual renal function, defined as daily urine output exceeding 100 mL, may continue to use metolazone and loop diuretics even after dialysis is initated.5,7 Upon the loss of residual renal function, all diuretics should be discontinued.
Min Sik Shin
PharmD candidate, 2012, College of Pharmacy, University of Illinois at Chicago
Cheryl L. Gilmartin, PharmD
Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago;
Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital and Health Sciences System, Chicago
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Q: When (at what GFR) do you change over from hydrochlorothiazide (HCTZ) to loop diuretics? And what should be the starting dose?
The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for hypertension and antihypertensive agents in chronic kidney disease1 (CKD) recommend replacing thiazide diuretics with loop diuretics once a patient’s glomerular filtration rate (GFR) falls below 30 mL/min/1.73 m2.
The mechanism of action for thiazide and loop diuretics differs by site of action in the kidney. Thiazide diuretics work in the distal convoluted tubules by inhibiting sodium (Na+)/chloride (Cl-) channels while the action of loop diuretics is exerted by inhibiting Na+/potassium (K+)/2Cl- channels in the thick ascending limb of the loop of Henle.2 Thiazide diuretics, with exception of metolazone, are ineffective in CKD stages 4 and 5 due to thiazide’s inability to reach the site of action.1,3
The initial furosemide dose should be 40 to 80 mg/d by mouth, preferably divided into two doses to minimize rebound sodium reabsorption.1,4 Weekly dose titrations by 25% to 50% may be made based on fluid status, blood pressure, and potassium level.1 Bumetanide and torsemide are loop diuretics that may also be used to therapeutically replace HCTZ when the GFR falls below 30 mL/min/1.73 m2. The relative potency of bumetanide: furosemide: torsemide is 1:40:20, respectively.5 The relative initiating dose equivalency of furosemide 40 mg would be bumetanide 1 mg or torsemide 20 mg.5,6
Finally, metolazone is a thiazide-related diuretic that retains its effectiveness even at GFR below 30 mL/min/1.73 m2.1,6 Metolazone can be initiated at oral doses of 2.5 to 5.0 mg/d and titrated up to 10 to 20 mg/d. Patients with residual renal function, defined as daily urine output exceeding 100 mL, may continue to use metolazone and loop diuretics even after dialysis is initated.5,7 Upon the loss of residual renal function, all diuretics should be discontinued.
Min Sik Shin
PharmD candidate, 2012, College of Pharmacy, University of Illinois at Chicago
Cheryl L. Gilmartin, PharmD
Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago;
Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital and Health Sciences System, Chicago
REFERENCES
1. K/DOQI [Kidney Disease Outcome Quality Initiative] clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.
2. Reilly RF, Jackson EK. Ch 25. Regulation of renal function and vascular volume. In: Chabner BA, Brunton LL, Knollman BC, eds. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. New York: McGraw-Hill Professional; 2010.
3. Sica DA, Gehr TW. Diuretic use in stage 5 chronic kidney disease and end-stage renal disease. Curr Opin Nephrol Hypertens. 2003;12(5): 483-490.
4. Cohen DL, Townsend RR. Treatment of hypertension in patients with chronic kidney disease. US Cardiology. 2009;6(2):54-58.
5. Wickersham RM, ed. Drug Facts and Comparisons. St. Louis, MO: Wolters Kluwer Health; 2009.
6. Comparison of commonly used diuretics (Detail Document). Pharmacist’s Letter/Prescriber’s Letter. February 2012.
7. DRUGDEX® System [Internet database]. Greenwood Village, Colo: Thomson Reuters (Healthcare) Inc. Updated periodically.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed September 19, 2012.
9. Turner JM, Bauer C, Abramowitz MK, et al. Treatment of chronic kidney disease. Kidney Int. 2012;81(4):351-362.
Kidney Failure Risk
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Statin Use
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Dialysis: How, When, and at What Dose?
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Clinicians Are Asking: Renal Diet
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Clinicians Are Asking: Kidney Disease Education Classes
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Clinicians Are Asking: Dialysis Patients Requiring Surgery
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.