Medications and the Renal Patient: Dialysis and BP

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.

When prescribing medications for patients, it is always advisable to know their estimated glomerular filtration rate (eGFR). The creatinine and blood urea nitrogen (BUN) by themselves are not always good indicators of renal function. If you have doubts, any reliable pharmacy source can guide you to dosing adjustments. Most medications do not require adjustments for eGFR greater than 60 mL/min/1.73m².

Patients with an eGFR of less than 60 should never be prescribed NSAIDs, and extreme caution is advised with use of aminoglycosides and contrast dyes.

With medications such as ACE inhibitors, which can affect renal function (particularly levels of creatinine and potassium), eGFR should be monitored initially and within two weeks of each dosing adjustment. Other commonly prescribed drugs requiring dosing adjustment in patients with eGFR below 60 include gabapentin, metoclopramide, and ­ranitidine.^1,2

As always, inquire about your patient’s use of complementary and alternative therapies, including herbal remedies, as these often are contraindicated in this population.
Jane S. Davis, CRNP, DNP

Q: I work in a cardiology practice. We received a note from the dialysis center telling us that one of our patients is hypotensive (systole < 100 mm Hg) during his dialysis treatment. His BP is usually 140/86 mm Hg in the office. Why the difference?

When considering BP values within this population, it is important to keep in mind that BP in dialysis patients can vary widely, with lower values in the period immediately following dialysis, then slowly increasing as patients’ fluid levels rise.

There are a few reasons why hypotension typically occurs during treatment. Taking sedating medication just before arriving for dialysis can dramatically lower BP during dialysis and should generally be avoided; advise the patient to take the medication after dialysis or at night instead.¹¹ Many antihypertensive drugs that are removed by dialysis are often prescribed to be taken at night.

Another common reason for hypotension during dialysis is large-volume fluid removal. Patients are advised to limit fluids between treatments to avoid fluid overload, thereby limiting the volume of removal needed. Incorrect dry weight calculations can also cause hypotension during dialysis; if a patient gains weight that is not fluid related and attempts are made to dialyze the patient to the dry weight, hypotension can occur.¹¹ The patient who sees another practitioner right before dialysis may appear volume-overloaded—or immediately after dialysis, may appear volume-depleted; neither impression is correct. Also, a 2- to 4-kg weight gain between dialysis treatments is acceptable.

It has been learned through observational research that hemodialysis patients tend to have higher mortality rates with a predialysis systolic BP (SBP) below 110 mm Hg, a postdialysis SBP greater than 180 mm Hg, or a postdialysis diastolic BP exceeding 110 mm Hg.¹² According to the National Kidney Foundation’s K/DOQI practice guidelines,¹³ a predialysis BP of 140/90 mm Hg and a postdialysis BP of 130/80 mm Hg are reasonable targets. However, as with all guidelines, goals must be individualized to fit the patient’s age, comorbidities, and symptoms.¹⁴ This is a delicate balance, and safe management requires ongoing communication between providers.

Of interest, researchers for the Dialysis Outcomes and Practice Patterns Study suggested that patients with a predialysis SBP of 110 to 130 mm Hg had a higher risk for mortality than those with an SBP of 130 to 140 mm Hg. The same study showed an increased risk for death in patients with predialysis SBP greater than 160 mm Hg.¹⁴

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

REFERENCES
1. Gabardi S, Abramson S. Drug dosing in chronic kidney disease. Med Clin North Am. 2005;89(3):649-687.

2. Munar MY, Singh H. Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician. 2007;75(10):1487-1496.

3. Huerta C, Castellsague J, Varas-Lorenzo C, Garcia Rodriguez LA. Nonsteroidal anti-inflammatory drugs and risk of ARF in the general population. Am J Kidney Dis. 2005;45(3): 531-539.

4. Schneider V, Lévesque LE, Zhang B, et al. Association of selective and conventional nonsteroidal antiinflammatory drugs with acute renal failure: a population-based, nested case-control analysis. Am J Epidemiol. 2006; 164(9):881-889.

5. Loyd J, Wright P. Are thiazide diuretics an effective treatment for hypertension in patients with chronic kidney disease? J Okla State Med Assoc. 2008;101(5):84-85.

6. Kidney Disease Outcomes Quality Initiative (K/DOQI). K/DOQI clinical practice guidelines on hypertension and antihypertensive agents in chronic kidney disease. Am J Kidney Dis. 2004;43(5 suppl 1):S1-S290.

7. Reungjui S, Pratipanawatr T, Johnson RJ, Nakagawa T. Do thiazides worsen metabolic syndrome and renal disease? The pivotal roles for hyperuricemia and hypokalemia. Curr Opin Nephrol Hypertens. 2008;17(5):470-476.

8. Lichtenstein AH, Appel LJ, Brands M, et al. Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee. Circulation. 2006;114(1):82-96.

9. Pharmacokinetics. In: Golan DE, Tashjian AH, Armstrong EJ, Armstrong AW, eds. Principles of Pharmacology: The Pathophysiologic Basis of Drug Therapy. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007:31-48.

10. Masters PA, O’Bryan TA, Zurlo J, et al. Trimethoprim-sulfamethoxazole revisited. Arch Intern Med. 2003;163(4):402-410.

11. Singapuri MS, Lea JP. Management of hypertension in the end-stage renal disease patient. J Clin Outcomes Manage. 2010;17(2):87-95.

12. Port FK, Hulbert-Shearon TE, Wolfe RA, et al. Predialysis blood pressure and mortality risk in a national sample of maintenance hemodialysis patients. Am J Kidney Dis. 1999;33(3): 507-517.

13. K/DOQI Workgroup. K/DOQI clinical practice guidelines for cardiovascular disease in dialysis patients. Am J Kidney Dis. 2005;45(4 suppl 3):S1–S153.

14. Schieszer J. BP guidelines may be inappropriate for HD patients. Renal Urol News. 2010 May 21. www.renalandurologynews.com/bp-guidelines-may-be-inappropriate-for-hd-patients/article/170707. Accessed May 19, 2011.