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Guidelines on Hematuria: First-line Evaluation
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?
First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).1 The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.1
Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.
Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?
First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).1 The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.1
Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.
Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: I am studying for my boards and am deep into the renal/urology section. I graduated so long ago that IVPs were the evaluation of choice. What is the “expert opinion” now on managing the patient with hematuria? Do we go straight to cystoscopy or use a different test?
First-line evaluation for asymptomatic microscopic hematuria now requires CT urography instead of IV pyelography (IVP) or cystoscopy (see AUA guideline 10).1 The CT should be done with and without IV contrast and be multiphasic in nature. Specific high-resolution evaluation of the urothelium of the upper urinary tracts during the excretory phase must be included. This is the most sensitive and specific radiologic examination to adequately evaluate for a renal mass in the parenchyma as well as for abnormalities in the upper tracts simultaneously.1
Using contrast dye in a patient with decreased renal function is always problematic. Precautions to be taken include withholding ACE inhibitors and angiotensin receptor blockers before and after the procedure and hydrating the patient before, during, and after administration of contrast dye.
Sarah Sparks, NP, St. Luke’s Clinic–Nephrology, St. Luke’s Health System, Boise, ID
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
Guidelines on Hematuria: Best Approach to Microhematuria
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?
There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.2 Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.
What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).
A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.
The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.
When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,1 cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.3
For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.1
In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.
Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?
There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.2 Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.
What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).
A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.
The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.
When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,1 cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.3
For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.1
In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.
Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
The American Urological Association (AUA) published guidelines for asymptomatic microhematuria. The document includes 19 guidelines with recommendation levels ranging from A to C (high to low) and some expert opinion recommendations included. The full guidelines can be accessed at http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf.
Q: A 39-year-old woman came to my office for an annual physical, and there was blood in the urine when I sent her urine out for microscopy. She is having abnormal menses, so she could not be sure this was not contamination (and neither could I). I repeated the urine and it was positive for blood on micro. What do I do now? Where do I refer her?
There are numerous causes of microhematuria, and the answer can often be found by considering the possible differential diagnoses. The causes of hematuria include urinary tract infection (UTI), bladder or kidney stones, kidney disease, use of certain medications, strenuous exercise, and trauma.2 Health care professionals should follow a process to make logical assessments and decisions in the care of this 39-year-old woman with microhematuria.
What to do first? The first step is to obtain a complete history, including any associated symptoms, medication history, last menstrual period, family history, previous medical history, recent trauma, strenuous exercise, and easy bruising or bleeding. In this case, since the urinalysis was repeated and remained positive for hematuria, the next step is to consider a renal function panel and complete blood count (CBC).
A renal function panel (sodium, potassium, chloride, carbon dioxide, anion gap, glucose, urea reduction ratio, creatinine, albumin, calcium, and phosphorous) will help to rule out existing renal function dysfunction.
The CBC will help to rule out any blood loss or presence of systemic involvement. Also, look at other results noted on the urinalysis, such as protein, nitrates, and leukocytes. Looking for protein will help the clinician determine whether fever, diabetes, chronic kidney disease, or hypertension may be the cause. Nitrates will appear as a result of UTI, and leukocytes may suggest a UTI or possible contamination. Dysmorphic red blood cells (RBCs with irregular shapes) found on the microscopic exam of the urine indicate a glomerular etiology, in which case the patient should be referred to nephrology for possible renal biopsy. If the red blood cells are nonglomerular (ie, the glomerulus is not the source of the bleeding) and there is no other obvious cause, then the patient should be referred to urology.
When is it time to refer? If microhematuria is persistent, the patient will need to be referred to a urologist for further evaluation. According to AUA guidelines 7, 8, and 16 through 19,1 cystoscopy should be considered for patients 35 or older with asymptomatic hematuria. For younger patients, a cystoscopy may be considered at the discretion of the provider. Although blue light cystoscopy has FDA approval, in the opinion of the AUA, the risks of the technique outweigh its benefits. Blue light cystoscopy is reported to improve identification of bladder tumors.3
For patients with a history of persistent asymptomatic hematuria, no further urinalyses are needed after two consecutive yearly tests with negative results. Those with a negative urologic workup should have urinalyses performed annually. If a patient has persistent or recurrent asymptomatic microhematuria with an initially negative urologic workup, then patients should be considered for reevaluation by urology every 3 to 5 years.1
In conclusion, the best approach to microhematuria is to obtain a thorough history, check the necessary labs, and if microhematuria persists, make the necessary referral to the appropriate specialist, ensuring that the patient receives the best possible care.
Tia Austin Hayes, FNP-C, JMM Renal Clinic/Outpatient Dialysis, University of Mississippi Department of Nephrology; Donna Anderson, PA-C, CAQ, Nephrology Specialists of Oklahoma, Tulsa
References
1. Davis R, Jones JS, Barocas DA, et al; American Urological Association. Diagnosis, Evaluation, and Follow-up of Asymptomatic Microhematuria (AMH) in Adults: AUA Guideline. Linthicum, MD: American Urological Association Education and Research, Inc; 2012. http://www.auanet.org/common/pdf/education/clinical-guidance/Asymptomatic-Microhematuria.pdf. Accessed January 24, 2013.
2. National Kidney and Urologic Diseases Information Clearinghouse. Hematuria: blood in the urine (2012). http://kidney.niddk.nih.gov/kudiseases/pubs/hematuria. Accessed January 17, 2013.
3. Geavlete B, Jecu M, Multescu R, et al. HAL blue-light cystoscopy in high-risk nonmuscle-invasive bladder cancer: re-TURBT recurrence rates in a prospective, randomized study. Urology. 2010;76(3):664-669.
Suggested Reading
Feldman AS, Hsu C-Y, Kurtz M, Cho KC. Etiology and evaluation of hematuria in adults (2012). www.uptodate.com/contents/etiology-and-evaluation-of-hematuria-in-adults. Accessed January 17, 2013.
Jayne D. Hematuria and proteinuria. In: Greenberg A, ed; National Kidney Foundation. Primer on Kidney Diseases. 5th ed. Saunders; 2009:33-42.
Underlying Factors Influence Insulin's Effect
Q: Help! How do you proceed if, after you’ve continually increased a patient’s insulin dose, his/her blood glucose levels do not improve?
This is a common scenario in diabetes management. Here are nine things to consider when a patient’s situation just doesn’t make sense clinically:
1. Noncompliance with the prescribed dose. This is the most common scenario. Ask the patient, “How many injections do you miss in a typical week?” Assure that he or she is actually taking the currently prescribed amount of insulin before you further increase the dose.
2. Inaccurate insulin dosing. This problem can be due to impaired vision, poor technique, dexterity issues, or dementia. Ask the patient to demonstrate for you how he/she draws up and takes the insulin at home. You might just be surprised at what you see, even in patients who have been giving themselves insulin for years. Consider prescribing an insulin pen or having a family member or significant other dose the insulin if the patient is no longer reliable to accurately dose it for him- or herself.
3. “Bad insulin.” What this actually means is loss of potency. This can be caused by improper storage, exposure to heat or cold, or use of an insulin delivery device (ie, vial or pen) past the 28- to 45-day period recommended, depending on the type of insulin. Replace the vial or pen and re-assess for improvement in diabetes control.
4. Lipohypertrophy of injection sites due to overuse. Palpate and visually inspect injection sites to look for firm or hypertrophied tissue. Advise the patient to avoid these areas for future injection, as absorption from these sites can be poor and unpredictable.
5. Dietary issues. The patient may be increasing his/her food intake along with the increased insulin doses. One clue that should raise suspicion for this occurrence is rapidly increasing body weight. Consider referring the patient to a dietitian for nutrition counseling.
6. New medication. Sometimes a new treatment is added to a patient’s regimen by another provider, and the medication might have an adverse effect on blood glucose control. Common examples include steroids (typically a cortisone injection) or methylprednisolone dose-packs taken during an asthma flare.
7. Occult infection. Urinary tract infections, pneumonia, and the like can impact blood glucose control. Consider ordering a urinalysis and complete blood count if infection seems a likely cause.
8. Major life stressors. Inquire as to what is happening in the patient’s life that might impact his/her body’s response to insulin. They might be in the middle of a divorce or other family crisis or experiencing severe stress at work.
9. Technique and equipment issues. Inaccurate glucose monitoring technique or use of expired strips can lead to “false high” readings. Also, patients with a continuous glucose monitor may record false high results when they are taking acetaminophen. If this is the case, increasing the insulin dose will often result in hypoglycemia.
It may be helpful to keep this clinical checklist handy and add to it any other issues that you come across when the clinical picture doesn’t make sense. You may also want to consider referral to a diabetes educator; patients will often confide what is really going on to an educator in a longer visit, rather than in the typically shorter visits with their health care provider.
SUGGESTED READING
Sadler C, Einhorn D. Tailoring insulin regimens for type 2 diabetes mellitus. JAAPA. 1998;11(4):55-71.
Q: Help! How do you proceed if, after you’ve continually increased a patient’s insulin dose, his/her blood glucose levels do not improve?
This is a common scenario in diabetes management. Here are nine things to consider when a patient’s situation just doesn’t make sense clinically:
1. Noncompliance with the prescribed dose. This is the most common scenario. Ask the patient, “How many injections do you miss in a typical week?” Assure that he or she is actually taking the currently prescribed amount of insulin before you further increase the dose.
2. Inaccurate insulin dosing. This problem can be due to impaired vision, poor technique, dexterity issues, or dementia. Ask the patient to demonstrate for you how he/she draws up and takes the insulin at home. You might just be surprised at what you see, even in patients who have been giving themselves insulin for years. Consider prescribing an insulin pen or having a family member or significant other dose the insulin if the patient is no longer reliable to accurately dose it for him- or herself.
3. “Bad insulin.” What this actually means is loss of potency. This can be caused by improper storage, exposure to heat or cold, or use of an insulin delivery device (ie, vial or pen) past the 28- to 45-day period recommended, depending on the type of insulin. Replace the vial or pen and re-assess for improvement in diabetes control.
4. Lipohypertrophy of injection sites due to overuse. Palpate and visually inspect injection sites to look for firm or hypertrophied tissue. Advise the patient to avoid these areas for future injection, as absorption from these sites can be poor and unpredictable.
5. Dietary issues. The patient may be increasing his/her food intake along with the increased insulin doses. One clue that should raise suspicion for this occurrence is rapidly increasing body weight. Consider referring the patient to a dietitian for nutrition counseling.
6. New medication. Sometimes a new treatment is added to a patient’s regimen by another provider, and the medication might have an adverse effect on blood glucose control. Common examples include steroids (typically a cortisone injection) or methylprednisolone dose-packs taken during an asthma flare.
7. Occult infection. Urinary tract infections, pneumonia, and the like can impact blood glucose control. Consider ordering a urinalysis and complete blood count if infection seems a likely cause.
8. Major life stressors. Inquire as to what is happening in the patient’s life that might impact his/her body’s response to insulin. They might be in the middle of a divorce or other family crisis or experiencing severe stress at work.
9. Technique and equipment issues. Inaccurate glucose monitoring technique or use of expired strips can lead to “false high” readings. Also, patients with a continuous glucose monitor may record false high results when they are taking acetaminophen. If this is the case, increasing the insulin dose will often result in hypoglycemia.
It may be helpful to keep this clinical checklist handy and add to it any other issues that you come across when the clinical picture doesn’t make sense. You may also want to consider referral to a diabetes educator; patients will often confide what is really going on to an educator in a longer visit, rather than in the typically shorter visits with their health care provider.
SUGGESTED READING
Sadler C, Einhorn D. Tailoring insulin regimens for type 2 diabetes mellitus. JAAPA. 1998;11(4):55-71.
Q: Help! How do you proceed if, after you’ve continually increased a patient’s insulin dose, his/her blood glucose levels do not improve?
This is a common scenario in diabetes management. Here are nine things to consider when a patient’s situation just doesn’t make sense clinically:
1. Noncompliance with the prescribed dose. This is the most common scenario. Ask the patient, “How many injections do you miss in a typical week?” Assure that he or she is actually taking the currently prescribed amount of insulin before you further increase the dose.
2. Inaccurate insulin dosing. This problem can be due to impaired vision, poor technique, dexterity issues, or dementia. Ask the patient to demonstrate for you how he/she draws up and takes the insulin at home. You might just be surprised at what you see, even in patients who have been giving themselves insulin for years. Consider prescribing an insulin pen or having a family member or significant other dose the insulin if the patient is no longer reliable to accurately dose it for him- or herself.
3. “Bad insulin.” What this actually means is loss of potency. This can be caused by improper storage, exposure to heat or cold, or use of an insulin delivery device (ie, vial or pen) past the 28- to 45-day period recommended, depending on the type of insulin. Replace the vial or pen and re-assess for improvement in diabetes control.
4. Lipohypertrophy of injection sites due to overuse. Palpate and visually inspect injection sites to look for firm or hypertrophied tissue. Advise the patient to avoid these areas for future injection, as absorption from these sites can be poor and unpredictable.
5. Dietary issues. The patient may be increasing his/her food intake along with the increased insulin doses. One clue that should raise suspicion for this occurrence is rapidly increasing body weight. Consider referring the patient to a dietitian for nutrition counseling.
6. New medication. Sometimes a new treatment is added to a patient’s regimen by another provider, and the medication might have an adverse effect on blood glucose control. Common examples include steroids (typically a cortisone injection) or methylprednisolone dose-packs taken during an asthma flare.
7. Occult infection. Urinary tract infections, pneumonia, and the like can impact blood glucose control. Consider ordering a urinalysis and complete blood count if infection seems a likely cause.
8. Major life stressors. Inquire as to what is happening in the patient’s life that might impact his/her body’s response to insulin. They might be in the middle of a divorce or other family crisis or experiencing severe stress at work.
9. Technique and equipment issues. Inaccurate glucose monitoring technique or use of expired strips can lead to “false high” readings. Also, patients with a continuous glucose monitor may record false high results when they are taking acetaminophen. If this is the case, increasing the insulin dose will often result in hypoglycemia.
It may be helpful to keep this clinical checklist handy and add to it any other issues that you come across when the clinical picture doesn’t make sense. You may also want to consider referral to a diabetes educator; patients will often confide what is really going on to an educator in a longer visit, rather than in the typically shorter visits with their health care provider.
SUGGESTED READING
Sadler C, Einhorn D. Tailoring insulin regimens for type 2 diabetes mellitus. JAAPA. 1998;11(4):55-71.
Management Specifics in Kidney Disease: Rise in SCr
Q: How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?
ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.6 In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.8
Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.9 A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.9
Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.9 If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.8 Once SCr, K, and BP are stable, they should be rechecked annually.9
The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough.
Afix Kehinde, PharmD, 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 & Health Sciences System, Chicago
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: How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?
ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.6 In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.8
Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.9 A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.9
Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.9 If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.8 Once SCr, K, and BP are stable, they should be rechecked annually.9
The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough.
Afix Kehinde, PharmD, 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 & Health Sciences System, Chicago
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: How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?
ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.6 In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.8
Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.9 A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.9
Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.9 If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.8 Once SCr, K, and BP are stable, they should be rechecked annually.9
The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough.
Afix Kehinde, PharmD, 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 & Health Sciences System, Chicago
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: 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.
How to Handle "Incidentalomas"
Maggie, 42, presents to the emergency department with chronic intermittent abdominal pain and bloating with constipation and occasional diarrhea. She denies fever, chills, nausea, vomiting, melana, bright red blood per rectum, or changes in stool caliper, and she says she otherwise feels well.
Relevant lab and study results include: a comprehensive metabolic panel, complete blood count with differential, beta hCG (human chorionic gonadotropin), urinalysis, and amylase and lipase, all within normal limits; pregnancy test, negative; abdominal x-ray, within normal limits except increased stool in distal colon; and abdominal CT, 2.3-cm right adrenal mass and a Hounsfield measurement of 4 units.
Maggie has a right adrenal incidentaloma (incidentally discovered adenoma that was not in the differential diagnosis). Such findings have become all too often the case, due to the immediate access to and overutilization of high-resolution CT, MRI, and ultrasound. We are now seeing a significantly increased number of incidental adrenal lesions/masses discovered on images not intended to look for adrenal-related diseases (eg, Cushing syndrome, pheochromocytomas, and aldosterone-producing adenomas).
Q: How common are adrenal adenomas, and what must I consider?
Incidental adrenal adenomas are found on 4.4% of abdominal CTs, and in one autopsy series were discovered in 8.7%. Prevalence increases with age, with occurrence of < 1% in patients younger than 30 and about 7% for patients 70 or older.
Evaluation is based on two concerns: First, is the adrenal mass benign or malignant? Second, is the mass secretory or nonsecretory (non-hormone secreting) in nature?
The fortunate news about adrenal incidentalomas is that 80% are benign and nonsecretory, which provides immediate reassuring news to the patient. Examples of benign adrenal masses are: adenoma, lipoma, cyst, ganglioneuroma, hematoma, and infection (eg, tuberculosis, fungal).
The other encouraging statistic is that only 1:4,000 adrenal incidentalomas are malignant. Examples of malignant adrenal masses are: adrenocortical carcinoma, metastatic neoplasm, lymphoma, and malignant pheochromocytoma.
Q: Does adrenal adenoma size matter?
Yes, the larger the size of the adenoma, the higher the association with malignancy. The guide below (based on CT findings) shows not only malignancy potential as it relates to size, but also the importance of Hounsfield units and when surgical intervention is recommended.
Imaging (CT scan)
< 4 cm: homogeneous mass with smooth borders and < 10 Hounsfield units; suggests benign mass (likelihood of malignancy, about 2%)
4 to 6 cm: follow closely, consider surgery (likelihood of malignancy, about 6%)
> 6 cm: surgery indicated (likelihood of malignancy, about 25%)
Some providers and patients inquire whether it is helpful or necessary to biopsy. It is generally not advisable to biopsy, especially if the findings are favorable for benign nonsecretory masses, since there is a high false-negative rate. An indication for biopsy is if the patient has a history of extra-adrenal malignancy; this will distinguish recurrence or metastatic disease from a benign mass. A final proviso: If biopsy is performed, make sure the adrenal mass is not a pheochromocytoma, as biopsy of a hormone-secreting neoplasm can lead to a hypertensive emergency.
Q: How do I determine whether the mass is hormone-secreting?
Although 80% are nonsecretory, you must still maintain a high index of suspicion so as not to miss a potentially problematic and fully treatable adenoma. A thorough history is essential in screening for hormonal excess arising from adrenal adenomas, since the signs and symptoms can be insidious. The three hormones secreted by adrenal adenomas are cortisol, aldosterone, and catecholamines (seen in Cushing syndrome, aldosterone-producing adenoma [APA], and pheochromocytoma, respectively).
It is important to note that Cushing syndrome has an insidious onset and can be easily missed. Hyperaldosteronism presents with hypertension (requiring several medications) and commonly hypokalemia. And pheochromocytoma can be “written off as” anxiety disorder, panic attack, or even hypoglycemia symptoms (especially if patients are treated for diabetes with agents that cause hypoglycemia). To help in your differential diagnosis of secretory adenomas, know that APA accounts for only 1%, and therefore the majority will secrete cortisol and (far less likely) catecholamines.
Q: What is the appropriate laboratory work-up?
The best simple screening test for hypercortisolemia is a 1-mg overnight dexamethasone suppression test. If this value is increased to ≥ 3 µg/dL, it should be followed up with a more sensitive test (a 24-hour urine for creatinine and free cortisol) to further assess for hypercortisolemia.
Patients thought to have a potential pheochromocytoma should undergo measurement of plasma fractionated metanephrines and normetanephrines or 24-hour urine for total metanephrines and fractionated catecholamines.
Finally, for patients with hypokalemia and hypertension or refractory hypertension requiring multiple (> 3) antihypertensive medications, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) should be obtained. A low PRA and a PAC > 15 ng/dL, along with a PAC/PRA ratio of > 20, is highly suggestive of an APA.
Q: What is the treatment and follow-up?
Here is a quick reference guide regarding surgical treatment and medical follow-up and surveillance:
• Adrenalectomy (pheochromocytoma, APA, Cushing syndrome): for masses 4 to 6 cm, consider surgery, especially if > 10 Hounsfield units; for masses > 6 cm, there is an increased risk for malignancy and surgery is required.
• Follow-up for low-suspicion, nonsecretory masses: abdominal CT 3 to 6 months after the initial scan, then annually for 1 to 2 years; hormonal evaluation and follow-up annually for 5 years, to evaluate for signs and symptoms of hormonal excess.
SUGGESTED READING
American Association of Clinical Endocrinologists/American Association of Endocrine Surgeons Medical Guidelines for the Management of Adrenal Incidentalomas. Endocr Pract. 2009;15(Suppl 1).
Management of the Clinically Inapparent Adrenal Mass (Incidentaloma). NIH State-of-the-Science Conference Statement; February 4-6, 2002.
Slawik M, Reincke M. Adrenal incidentalomas (Chapter 20). EndoText.com. www.endotext.org/adrenal/adrenal20/adrenal20.htm. Accessed October 12, 2012.
Fitzgerald PA, Goldfien A. Adrenal medulla. In: Greenspan F, Gardner D, eds. Basic and Clinical Endocrinology. 7th ed. McGraw-Hill: 2003;453-473.
The Washington Manual Endocrinology Specialty Consult. 2005;57-61, 71-84.
Endocrine Secrets. 4th ed. 2005;197-204, 241-252, 257-265.
Cleveland Clinic Endocrine & Metabolism Board Review. www.clevelandclinicmeded.com/live/courses/ann/endoreview/default.asp. Accessed October 12, 2012.
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Maggie, 42, presents to the emergency department with chronic intermittent abdominal pain and bloating with constipation and occasional diarrhea. She denies fever, chills, nausea, vomiting, melana, bright red blood per rectum, or changes in stool caliper, and she says she otherwise feels well.
Relevant lab and study results include: a comprehensive metabolic panel, complete blood count with differential, beta hCG (human chorionic gonadotropin), urinalysis, and amylase and lipase, all within normal limits; pregnancy test, negative; abdominal x-ray, within normal limits except increased stool in distal colon; and abdominal CT, 2.3-cm right adrenal mass and a Hounsfield measurement of 4 units.
Maggie has a right adrenal incidentaloma (incidentally discovered adenoma that was not in the differential diagnosis). Such findings have become all too often the case, due to the immediate access to and overutilization of high-resolution CT, MRI, and ultrasound. We are now seeing a significantly increased number of incidental adrenal lesions/masses discovered on images not intended to look for adrenal-related diseases (eg, Cushing syndrome, pheochromocytomas, and aldosterone-producing adenomas).
Q: How common are adrenal adenomas, and what must I consider?
Incidental adrenal adenomas are found on 4.4% of abdominal CTs, and in one autopsy series were discovered in 8.7%. Prevalence increases with age, with occurrence of < 1% in patients younger than 30 and about 7% for patients 70 or older.
Evaluation is based on two concerns: First, is the adrenal mass benign or malignant? Second, is the mass secretory or nonsecretory (non-hormone secreting) in nature?
The fortunate news about adrenal incidentalomas is that 80% are benign and nonsecretory, which provides immediate reassuring news to the patient. Examples of benign adrenal masses are: adenoma, lipoma, cyst, ganglioneuroma, hematoma, and infection (eg, tuberculosis, fungal).
The other encouraging statistic is that only 1:4,000 adrenal incidentalomas are malignant. Examples of malignant adrenal masses are: adrenocortical carcinoma, metastatic neoplasm, lymphoma, and malignant pheochromocytoma.
Q: Does adrenal adenoma size matter?
Yes, the larger the size of the adenoma, the higher the association with malignancy. The guide below (based on CT findings) shows not only malignancy potential as it relates to size, but also the importance of Hounsfield units and when surgical intervention is recommended.
Imaging (CT scan)
< 4 cm: homogeneous mass with smooth borders and < 10 Hounsfield units; suggests benign mass (likelihood of malignancy, about 2%)
4 to 6 cm: follow closely, consider surgery (likelihood of malignancy, about 6%)
> 6 cm: surgery indicated (likelihood of malignancy, about 25%)
Some providers and patients inquire whether it is helpful or necessary to biopsy. It is generally not advisable to biopsy, especially if the findings are favorable for benign nonsecretory masses, since there is a high false-negative rate. An indication for biopsy is if the patient has a history of extra-adrenal malignancy; this will distinguish recurrence or metastatic disease from a benign mass. A final proviso: If biopsy is performed, make sure the adrenal mass is not a pheochromocytoma, as biopsy of a hormone-secreting neoplasm can lead to a hypertensive emergency.
Q: How do I determine whether the mass is hormone-secreting?
Although 80% are nonsecretory, you must still maintain a high index of suspicion so as not to miss a potentially problematic and fully treatable adenoma. A thorough history is essential in screening for hormonal excess arising from adrenal adenomas, since the signs and symptoms can be insidious. The three hormones secreted by adrenal adenomas are cortisol, aldosterone, and catecholamines (seen in Cushing syndrome, aldosterone-producing adenoma [APA], and pheochromocytoma, respectively).
It is important to note that Cushing syndrome has an insidious onset and can be easily missed. Hyperaldosteronism presents with hypertension (requiring several medications) and commonly hypokalemia. And pheochromocytoma can be “written off as” anxiety disorder, panic attack, or even hypoglycemia symptoms (especially if patients are treated for diabetes with agents that cause hypoglycemia). To help in your differential diagnosis of secretory adenomas, know that APA accounts for only 1%, and therefore the majority will secrete cortisol and (far less likely) catecholamines.
Q: What is the appropriate laboratory work-up?
The best simple screening test for hypercortisolemia is a 1-mg overnight dexamethasone suppression test. If this value is increased to ≥ 3 µg/dL, it should be followed up with a more sensitive test (a 24-hour urine for creatinine and free cortisol) to further assess for hypercortisolemia.
Patients thought to have a potential pheochromocytoma should undergo measurement of plasma fractionated metanephrines and normetanephrines or 24-hour urine for total metanephrines and fractionated catecholamines.
Finally, for patients with hypokalemia and hypertension or refractory hypertension requiring multiple (> 3) antihypertensive medications, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) should be obtained. A low PRA and a PAC > 15 ng/dL, along with a PAC/PRA ratio of > 20, is highly suggestive of an APA.
Q: What is the treatment and follow-up?
Here is a quick reference guide regarding surgical treatment and medical follow-up and surveillance:
• Adrenalectomy (pheochromocytoma, APA, Cushing syndrome): for masses 4 to 6 cm, consider surgery, especially if > 10 Hounsfield units; for masses > 6 cm, there is an increased risk for malignancy and surgery is required.
• Follow-up for low-suspicion, nonsecretory masses: abdominal CT 3 to 6 months after the initial scan, then annually for 1 to 2 years; hormonal evaluation and follow-up annually for 5 years, to evaluate for signs and symptoms of hormonal excess.
SUGGESTED READING
American Association of Clinical Endocrinologists/American Association of Endocrine Surgeons Medical Guidelines for the Management of Adrenal Incidentalomas. Endocr Pract. 2009;15(Suppl 1).
Management of the Clinically Inapparent Adrenal Mass (Incidentaloma). NIH State-of-the-Science Conference Statement; February 4-6, 2002.
Slawik M, Reincke M. Adrenal incidentalomas (Chapter 20). EndoText.com. www.endotext.org/adrenal/adrenal20/adrenal20.htm. Accessed October 12, 2012.
Fitzgerald PA, Goldfien A. Adrenal medulla. In: Greenspan F, Gardner D, eds. Basic and Clinical Endocrinology. 7th ed. McGraw-Hill: 2003;453-473.
The Washington Manual Endocrinology Specialty Consult. 2005;57-61, 71-84.
Endocrine Secrets. 4th ed. 2005;197-204, 241-252, 257-265.
Cleveland Clinic Endocrine & Metabolism Board Review. www.clevelandclinicmeded.com/live/courses/ann/endoreview/default.asp. Accessed October 12, 2012.
Maggie, 42, presents to the emergency department with chronic intermittent abdominal pain and bloating with constipation and occasional diarrhea. She denies fever, chills, nausea, vomiting, melana, bright red blood per rectum, or changes in stool caliper, and she says she otherwise feels well.
Relevant lab and study results include: a comprehensive metabolic panel, complete blood count with differential, beta hCG (human chorionic gonadotropin), urinalysis, and amylase and lipase, all within normal limits; pregnancy test, negative; abdominal x-ray, within normal limits except increased stool in distal colon; and abdominal CT, 2.3-cm right adrenal mass and a Hounsfield measurement of 4 units.
Maggie has a right adrenal incidentaloma (incidentally discovered adenoma that was not in the differential diagnosis). Such findings have become all too often the case, due to the immediate access to and overutilization of high-resolution CT, MRI, and ultrasound. We are now seeing a significantly increased number of incidental adrenal lesions/masses discovered on images not intended to look for adrenal-related diseases (eg, Cushing syndrome, pheochromocytomas, and aldosterone-producing adenomas).
Q: How common are adrenal adenomas, and what must I consider?
Incidental adrenal adenomas are found on 4.4% of abdominal CTs, and in one autopsy series were discovered in 8.7%. Prevalence increases with age, with occurrence of < 1% in patients younger than 30 and about 7% for patients 70 or older.
Evaluation is based on two concerns: First, is the adrenal mass benign or malignant? Second, is the mass secretory or nonsecretory (non-hormone secreting) in nature?
The fortunate news about adrenal incidentalomas is that 80% are benign and nonsecretory, which provides immediate reassuring news to the patient. Examples of benign adrenal masses are: adenoma, lipoma, cyst, ganglioneuroma, hematoma, and infection (eg, tuberculosis, fungal).
The other encouraging statistic is that only 1:4,000 adrenal incidentalomas are malignant. Examples of malignant adrenal masses are: adrenocortical carcinoma, metastatic neoplasm, lymphoma, and malignant pheochromocytoma.
Q: Does adrenal adenoma size matter?
Yes, the larger the size of the adenoma, the higher the association with malignancy. The guide below (based on CT findings) shows not only malignancy potential as it relates to size, but also the importance of Hounsfield units and when surgical intervention is recommended.
Imaging (CT scan)
< 4 cm: homogeneous mass with smooth borders and < 10 Hounsfield units; suggests benign mass (likelihood of malignancy, about 2%)
4 to 6 cm: follow closely, consider surgery (likelihood of malignancy, about 6%)
> 6 cm: surgery indicated (likelihood of malignancy, about 25%)
Some providers and patients inquire whether it is helpful or necessary to biopsy. It is generally not advisable to biopsy, especially if the findings are favorable for benign nonsecretory masses, since there is a high false-negative rate. An indication for biopsy is if the patient has a history of extra-adrenal malignancy; this will distinguish recurrence or metastatic disease from a benign mass. A final proviso: If biopsy is performed, make sure the adrenal mass is not a pheochromocytoma, as biopsy of a hormone-secreting neoplasm can lead to a hypertensive emergency.
Q: How do I determine whether the mass is hormone-secreting?
Although 80% are nonsecretory, you must still maintain a high index of suspicion so as not to miss a potentially problematic and fully treatable adenoma. A thorough history is essential in screening for hormonal excess arising from adrenal adenomas, since the signs and symptoms can be insidious. The three hormones secreted by adrenal adenomas are cortisol, aldosterone, and catecholamines (seen in Cushing syndrome, aldosterone-producing adenoma [APA], and pheochromocytoma, respectively).
It is important to note that Cushing syndrome has an insidious onset and can be easily missed. Hyperaldosteronism presents with hypertension (requiring several medications) and commonly hypokalemia. And pheochromocytoma can be “written off as” anxiety disorder, panic attack, or even hypoglycemia symptoms (especially if patients are treated for diabetes with agents that cause hypoglycemia). To help in your differential diagnosis of secretory adenomas, know that APA accounts for only 1%, and therefore the majority will secrete cortisol and (far less likely) catecholamines.
Q: What is the appropriate laboratory work-up?
The best simple screening test for hypercortisolemia is a 1-mg overnight dexamethasone suppression test. If this value is increased to ≥ 3 µg/dL, it should be followed up with a more sensitive test (a 24-hour urine for creatinine and free cortisol) to further assess for hypercortisolemia.
Patients thought to have a potential pheochromocytoma should undergo measurement of plasma fractionated metanephrines and normetanephrines or 24-hour urine for total metanephrines and fractionated catecholamines.
Finally, for patients with hypokalemia and hypertension or refractory hypertension requiring multiple (> 3) antihypertensive medications, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) should be obtained. A low PRA and a PAC > 15 ng/dL, along with a PAC/PRA ratio of > 20, is highly suggestive of an APA.
Q: What is the treatment and follow-up?
Here is a quick reference guide regarding surgical treatment and medical follow-up and surveillance:
• Adrenalectomy (pheochromocytoma, APA, Cushing syndrome): for masses 4 to 6 cm, consider surgery, especially if > 10 Hounsfield units; for masses > 6 cm, there is an increased risk for malignancy and surgery is required.
• Follow-up for low-suspicion, nonsecretory masses: abdominal CT 3 to 6 months after the initial scan, then annually for 1 to 2 years; hormonal evaluation and follow-up annually for 5 years, to evaluate for signs and symptoms of hormonal excess.
SUGGESTED READING
American Association of Clinical Endocrinologists/American Association of Endocrine Surgeons Medical Guidelines for the Management of Adrenal Incidentalomas. Endocr Pract. 2009;15(Suppl 1).
Management of the Clinically Inapparent Adrenal Mass (Incidentaloma). NIH State-of-the-Science Conference Statement; February 4-6, 2002.
Slawik M, Reincke M. Adrenal incidentalomas (Chapter 20). EndoText.com. www.endotext.org/adrenal/adrenal20/adrenal20.htm. Accessed October 12, 2012.
Fitzgerald PA, Goldfien A. Adrenal medulla. In: Greenspan F, Gardner D, eds. Basic and Clinical Endocrinology. 7th ed. McGraw-Hill: 2003;453-473.
The Washington Manual Endocrinology Specialty Consult. 2005;57-61, 71-84.
Endocrine Secrets. 4th ed. 2005;197-204, 241-252, 257-265.
Cleveland Clinic Endocrine & Metabolism Board Review. www.clevelandclinicmeded.com/live/courses/ann/endoreview/default.asp. Accessed October 12, 2012.
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.
Glucose Control and Avoidance of Hypoglycemia
Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |
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Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |
Q: I am frustrated by the “always bring the blood sugars down slowly” philosophy, which I know is intended to avoid hypoglycemic symptoms. However, it often seems to be done at the expense of prolonged hyperglycemia, which is dangerous for patients’ long-term health and may cause more rapid beta-cell destruction. What’s the deal? There is evidence that rapid achievement of tight glucose control using intensive insulin therapy with multiple daily injections or insulin pumps in patients with newly diagnosed type 2 diabetes has favorable outcomes on recovery and maintenance of beta-cell function and prolonged glycemic remission, compared with treatment with oral hypoglycemic agents.1 However, this approach is time consuming and not practical in most primary care settings. Overcoming “clinical inertia” (the failure to initiate or intensify therapy when indicated) has been identified as a major barrier to achieving rapid glycemic control, to the detriment of the patient’s health. One recent study showed that more frequent follow-up with a multidisciplinary team and regular use of a computer-analyzed 7-point glucose profile resulted in more rapid and significantly better glycemic control with a lower A1C, compared to standard care.2 This approach is much more practical in a primary care setting. Additionally, we always treat our patients as individuals. There are very few maxims that are correct in all situations. Almost every answer to a clinical question begins with the qualifier “It depends….” The specifics of the individual case will clarify the appropriate answer. In regard to this particular question, the answer will vary by the clinical history of the patient. For example, for a pregnant patient with poor glycemic control, potential hospitalization and rapid titration of insulin would be the most judicious plan. In this case, quickly bringing glucose into tight control helps minimize risks to the developing fetus. However, if the patient is a frail 80-year-old with advanced cardiovascular disease, then slow and careful titration of medications would be the prudent course to meticulously avoid hypoglycemia. New guidelines from the American Diabetes Association and the European Association for the Study of Diabetes (ADA/EASD)3 are helpful in that they identify various clinical issues and give guidance on which medication regimens would be more appropriate for the specific clinical history. They categorize medications based on efficacy, weight gain, hypoglycemia, major side effects, and costs. Guidelines from the American Association of Clinical Endocrinologists/American College of Endocrinology (AACE/ACE)4 are also very useful, because they categorize treatment based on the A1C level, as well as potential for weight gain and hypoglycemia. For example, a patient with an A1C < 7.5% may be an appropriate candidate for monotherapy, while a symptomatic patient with an A1C > 9% would likely benefit from insulin therapy or triple oral agent therapy. First, it is helpful to set individual glycemic targets for your patient. The following factors can help you in determining A1C targets: • Psychosocial considerations (motivation, adherence to therapy, self-care capacity) • Resources or support systems (family support, community resources, living situation, etc) • Risk for hypoglycemia • Duration of diabetes • Life expectancy • Microvascular complications • Cardiovascular disease and coexisting conditions. For example, an older individual with poor motivation, lack of support systems, short life expectancy, and coexisting terminal cancer would have a less stringent A1C target of ≤ 8%, whereas a young, motivated individual with no complications or serious coexisting complications would have an A1C target of 6%. The new ADA/EASD guidelines list additional considerations for medication choices for various comorbidities, including coronary disease, heart failure, renal disease, liver dysfunction, and hypoglycemia. For each comorbidity listed, there are suggested medications that are preferred and those that should be avoided. If your goal is to avoid hypoglycemia, the ADA/EASD guidelines list medication choices that have low propensity to cause hypoglycemia (eg, metformin, pioglitazone, DPP-4 inhibitors, and GLP-1 receptor agonists). (Of note, special attention is given to medications that do not cause weight gain, such as GLP-1 receptor agonists, DPP-4 inhibitors, and metformin.) Finally, the consensus statement emphasizes the need for individualizing therapy. Many patients have multiple comorbidities and may have medication sensitivities, cost constraints, etc. All of these factors must be taken into consideration when making therapeutic choices. Keep in mind, “one size does not fit all” when it comes to diabetes therapy. The recent releases from both the ADA/EASD and AACE/ACE give us much more detailed guidance addressing medication choices in regard to efficacy, potential for hypoglycemia and weight gain, major side effects, and costs. As always, guidelines do not replace good clinical judgment, based on the patient sitting in front of you. REFERENCES 2. Pimazoni-Netto A, Rodbard D, Zanella MT; Diabetes Education and Control Group. Rapid improvement of glycemic control in type 2 diabetes using weekly intensive multifactorial interventions: structured glucose monitoring, patient education, and adjustment of therapy—a randomized controlled trial. Diabetes Technol Therapeutics. 2011;13(10):997-1004. 3. Inzucchi SE, Bergenstahl RM, Buse JB, et al. Management of hyperglycemia in type 2 diabetes: a patient centered approach. Diabetes Care. [Epub ahead of print; April 19, 2012]. 4. Rodbard HW, Jellinger PS, Davidson JA, et al. Statement by an American Association of Clinical Endocrinologists/American College of Endocrinology consensus panel on type 2 diabetes mellitus: an algorithm for glycemic control. Endocr Pract. 2009;15(6):540-559. |