Nephrology

PHILADELPHIA (EGMN) – Morbidly obese patients with a body mass index of 40 mg/m² or greater respond to kidney transplants as well as do ideal-weight patients, based on a review of 120,000 U.S. kidney transplant patients who received their organs during 1996-2009.

"The survival benefit of a kidney transplant is no different for morbidly obese and for ... ideal-weight patients," Dr. Roberto Kalil said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons. In both BMI categories, kidney transplants led to an average 45% reduction in the subsequent mortality risk, said Dr. Kalil, a nephrologist and kidney transplant physician at the University of Iowa in Iowa City.

"BMI is not a critical issue," agreed Dr. Lawrence G. Hunsicker, a professor of medicine at Iowa and a coauthor of the study. "You still need to evaluate each morbidly obese patient as a candidate for surgery and as a candidate for kidney transplant, as you would any patient. But should surgeons use BMI as a criterion for surgery? Probably not," Dr. Hunsicker said in an interview.

"BMI is a very imperfect parameter" for judging a patient’s suitability for transplant, added Dr. Kalil.

Despite this finding, many surgeons and transplant programs deny kidney transplants to morbidly obese patients, and many programs have a BMI ceiling for allowing transplants.

"Most centers do not accept patients for kidney transplant with a BMI of 35" or higher, noted Dr. Ignatius Y.S. Tang, a nephrologist and transplant physician at the University of Illinois in Chicago. Even the University of Iowa, where until recently Dr. Hunsicker served as medical director of organ transplantation, has a policy of not placing kidney transplants in patients with a BMI of 40 or higher. "I don’t think that’s right," Dr. Hunsicker said. Transplant centers apply BMI cutoffs individually, and the United Network for Organ Sharing (UNOS) has no blanket U.S. policy, he noted.

The findings reported by Dr. Kalil used data on 237,537 U.S. patients aged 18 years or older who were listed for a first kidney transplant with UNOS during 1996-2009. The group included 8,382 patients with a BMI of 40 or greater (4%). Among these morbidly obese patients, 2,581 actually received a transplant, which accounted for 2% of the more than 120,000 total U.S. patients who received a kidney transplant during the 14-year period examined.

In an analysis that controlled for age, sex, race and ethnicity, diabetes, blood type, listing priority, and type of health insurance, a kidney transplant improved the survival rate among morbidly obese patients by 48%, compared with the survival of morbidly obese patients who did not receive a transplant – similar to the 45% improvement seen in ideal-weight patients, and similar to the survival benefit seen in every other BMI subgroup. Dr. Kalil reported.

The finding carries one important caveat: The analysis could assess the outcomes of only the morbidly obese patients whose physicians decided to add them to the UNOS kidney waiting list. So the findings may represent exceptional, low-risk morbidly obese patients. "I think that’s unlikely, because generally the decision to list these patients or not depends on a center’s policy," said Dr. Hunsicker. "I think some centers listed these patients and others did not. I think the selection was by centers, not by patients," he said.

Additional, BMI-based analyses of the UNOS data showed that the listed morbidly obese patients had a statistically significant (26%) reduced chance of receiving a kidney transplant, compared with ideal-weight patients. Listed patients with a BMI of 40 or greater formed the only BMI subgroup with a significantly different transplantation rate.

The analysis also showed that patients who started with a BMI of 40 or more at the time they first appeared on the UNOS kidney transplant list lost an average index value of 4.7 in the period before they actually received a transplant. However, the change in BMI prior to transplantation had no relationship to the graft survival following transplantation, Dr. Kalil said. Waiting for patients to lose weight before proceeding with a transplant "was not associated with decreased mortality, and it wasted time," Dr. Hunsicker said. The better approach is to proceed with the transplant as soon as possible, he said.

Dr. Kalil, Dr. Hunsicker, and Dr. Tang all said that they had no disclosures.

PHILADELPHIA (EGMN) – Morbidly obese patients with a body mass index of 40 mg/m² or greater respond to kidney transplants as well as do ideal-weight patients, based on a review of 120,000 U.S. kidney transplant patients who received their organs during 1996-2009.

"The survival benefit of a kidney transplant is no different for morbidly obese and for ... ideal-weight patients," Dr. Roberto Kalil said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons. In both BMI categories, kidney transplants led to an average 45% reduction in the subsequent mortality risk, said Dr. Kalil, a nephrologist and kidney transplant physician at the University of Iowa in Iowa City.

"BMI is not a critical issue," agreed Dr. Lawrence G. Hunsicker, a professor of medicine at Iowa and a coauthor of the study. "You still need to evaluate each morbidly obese patient as a candidate for surgery and as a candidate for kidney transplant, as you would any patient. But should surgeons use BMI as a criterion for surgery? Probably not," Dr. Hunsicker said in an interview.

"BMI is a very imperfect parameter" for judging a patient’s suitability for transplant, added Dr. Kalil.

Despite this finding, many surgeons and transplant programs deny kidney transplants to morbidly obese patients, and many programs have a BMI ceiling for allowing transplants.

"Most centers do not accept patients for kidney transplant with a BMI of 35" or higher, noted Dr. Ignatius Y.S. Tang, a nephrologist and transplant physician at the University of Illinois in Chicago. Even the University of Iowa, where until recently Dr. Hunsicker served as medical director of organ transplantation, has a policy of not placing kidney transplants in patients with a BMI of 40 or higher. "I don’t think that’s right," Dr. Hunsicker said. Transplant centers apply BMI cutoffs individually, and the United Network for Organ Sharing (UNOS) has no blanket U.S. policy, he noted.

The findings reported by Dr. Kalil used data on 237,537 U.S. patients aged 18 years or older who were listed for a first kidney transplant with UNOS during 1996-2009. The group included 8,382 patients with a BMI of 40 or greater (4%). Among these morbidly obese patients, 2,581 actually received a transplant, which accounted for 2% of the more than 120,000 total U.S. patients who received a kidney transplant during the 14-year period examined.

In an analysis that controlled for age, sex, race and ethnicity, diabetes, blood type, listing priority, and type of health insurance, a kidney transplant improved the survival rate among morbidly obese patients by 48%, compared with the survival of morbidly obese patients who did not receive a transplant – similar to the 45% improvement seen in ideal-weight patients, and similar to the survival benefit seen in every other BMI subgroup. Dr. Kalil reported.

The finding carries one important caveat: The analysis could assess the outcomes of only the morbidly obese patients whose physicians decided to add them to the UNOS kidney waiting list. So the findings may represent exceptional, low-risk morbidly obese patients. "I think that’s unlikely, because generally the decision to list these patients or not depends on a center’s policy," said Dr. Hunsicker. "I think some centers listed these patients and others did not. I think the selection was by centers, not by patients," he said.

Additional, BMI-based analyses of the UNOS data showed that the listed morbidly obese patients had a statistically significant (26%) reduced chance of receiving a kidney transplant, compared with ideal-weight patients. Listed patients with a BMI of 40 or greater formed the only BMI subgroup with a significantly different transplantation rate.

The analysis also showed that patients who started with a BMI of 40 or more at the time they first appeared on the UNOS kidney transplant list lost an average index value of 4.7 in the period before they actually received a transplant. However, the change in BMI prior to transplantation had no relationship to the graft survival following transplantation, Dr. Kalil said. Waiting for patients to lose weight before proceeding with a transplant "was not associated with decreased mortality, and it wasted time," Dr. Hunsicker said. The better approach is to proceed with the transplant as soon as possible, he said.

Dr. Kalil, Dr. Hunsicker, and Dr. Tang all said that they had no disclosures.

PHILADELPHIA (EGMN) – Morbidly obese patients with a body mass index of 40 mg/m² or greater respond to kidney transplants as well as do ideal-weight patients, based on a review of 120,000 U.S. kidney transplant patients who received their organs during 1996-2009.

"The survival benefit of a kidney transplant is no different for morbidly obese and for ... ideal-weight patients," Dr. Roberto Kalil said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons. In both BMI categories, kidney transplants led to an average 45% reduction in the subsequent mortality risk, said Dr. Kalil, a nephrologist and kidney transplant physician at the University of Iowa in Iowa City.

"BMI is not a critical issue," agreed Dr. Lawrence G. Hunsicker, a professor of medicine at Iowa and a coauthor of the study. "You still need to evaluate each morbidly obese patient as a candidate for surgery and as a candidate for kidney transplant, as you would any patient. But should surgeons use BMI as a criterion for surgery? Probably not," Dr. Hunsicker said in an interview.

"BMI is a very imperfect parameter" for judging a patient’s suitability for transplant, added Dr. Kalil.

Despite this finding, many surgeons and transplant programs deny kidney transplants to morbidly obese patients, and many programs have a BMI ceiling for allowing transplants.

"Most centers do not accept patients for kidney transplant with a BMI of 35" or higher, noted Dr. Ignatius Y.S. Tang, a nephrologist and transplant physician at the University of Illinois in Chicago. Even the University of Iowa, where until recently Dr. Hunsicker served as medical director of organ transplantation, has a policy of not placing kidney transplants in patients with a BMI of 40 or higher. "I don’t think that’s right," Dr. Hunsicker said. Transplant centers apply BMI cutoffs individually, and the United Network for Organ Sharing (UNOS) has no blanket U.S. policy, he noted.

The findings reported by Dr. Kalil used data on 237,537 U.S. patients aged 18 years or older who were listed for a first kidney transplant with UNOS during 1996-2009. The group included 8,382 patients with a BMI of 40 or greater (4%). Among these morbidly obese patients, 2,581 actually received a transplant, which accounted for 2% of the more than 120,000 total U.S. patients who received a kidney transplant during the 14-year period examined.

In an analysis that controlled for age, sex, race and ethnicity, diabetes, blood type, listing priority, and type of health insurance, a kidney transplant improved the survival rate among morbidly obese patients by 48%, compared with the survival of morbidly obese patients who did not receive a transplant – similar to the 45% improvement seen in ideal-weight patients, and similar to the survival benefit seen in every other BMI subgroup. Dr. Kalil reported.

The finding carries one important caveat: The analysis could assess the outcomes of only the morbidly obese patients whose physicians decided to add them to the UNOS kidney waiting list. So the findings may represent exceptional, low-risk morbidly obese patients. "I think that’s unlikely, because generally the decision to list these patients or not depends on a center’s policy," said Dr. Hunsicker. "I think some centers listed these patients and others did not. I think the selection was by centers, not by patients," he said.

Additional, BMI-based analyses of the UNOS data showed that the listed morbidly obese patients had a statistically significant (26%) reduced chance of receiving a kidney transplant, compared with ideal-weight patients. Listed patients with a BMI of 40 or greater formed the only BMI subgroup with a significantly different transplantation rate.

The analysis also showed that patients who started with a BMI of 40 or more at the time they first appeared on the UNOS kidney transplant list lost an average index value of 4.7 in the period before they actually received a transplant. However, the change in BMI prior to transplantation had no relationship to the graft survival following transplantation, Dr. Kalil said. Waiting for patients to lose weight before proceeding with a transplant "was not associated with decreased mortality, and it wasted time," Dr. Hunsicker said. The better approach is to proceed with the transplant as soon as possible, he said.

Dr. Kalil, Dr. Hunsicker, and Dr. Tang all said that they had no disclosures.

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

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

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

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

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: I was treating a patient for an uncomplicated urinary tract infection with trimethoprim–sulfamethoxazole (TMP-SMX). The pharmacist called and said the patient could not have any sulfa medications because she was going to donate a kidney to her brother. How do you explain this, and what should be my next step?

There is limited available evidence to support an answer to this question. Instead, I will provide a brief report of the available evidence, followed by the opinions of five experts in kidney transplantation.

TMP-SMX is a combination of two antimicrobial agents that act synergistically against a variety of bacteria.⁹ TMP decreases urinary excretion of potassium, leading to hyperkalemia—especially in persons with kidney disease or in those also taking other drugs that cause hyperkalemia.¹⁰ This scenario is unlikely, because the transplant team would have assessed the potential donor’s kidney function. When dosing the drug, clinicians should consider renal function and adjust the dose in those with a creatinine clearance less than or equal to 30 mL/min. Nephrotoxicity is uncommon in patients who take this drug; however, TMP is known to decrease tubular secretion of creatinine and may interfere with certain creatinine assays, leading to an artificial rise in serum creatinine. This is not reflective of a true reduction in the GFR and often is mild and reversible with discontinuation of the medication.

Querying experienced transplant professionals (two nephrologists, two transplant coordinators, and one doctoral-prepared pharmacist) yielded similar results. They all agreed that the only plausible reason to withhold TMP-SMX from this potential kidney donor was the risk of a transient rise in creatinine due to impaired secretion associated with TMP use. Many transplant teams recommend avoiding any medications that may affect the kidneys. So considering the lack of available evidence, I would recommend that you consult with the transplant team where your patient’s brother is receiving care before you prescribe TMP-SMX.

Debra Hain, PhD, APRN, GNP-BC
Florida Atlantic University, Boca Raton; Cleveland Clinic Florida; Department of Nephrology, Weston

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: I have a patient with CKD stage 4 (GFR, 30 mL/min/1.73m²). My supervising physician said to take him off his hydrochlorothiazide (50 mg qd) and start furosemide. Why do I do this, and at what dose do I start?

Thiazide diuretics work by blocking approximately 40% of sodium chloride reabsorption in the distal convoluting tubule of the nephron. This process increases the fractional excretion of sodium and provides a natriuresis with reduced blood pressure (BP). Thiazides also have a second mode of action in lowering BP by reducing peripheral vascular resistance.⁵

It is generally thought that thiazides are ineffective in patients with more advanced CKD because of more proximal sodium reabsorption in the nephron. This results in less sodium being delivered to the distal tubule and therefore less thiazide diuretic action in the distal tubule.⁵

The National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative (K/DOQI)⁶ recommends that hypertension in CKD be treated with combination therapy: renin-angiotensin system blockade (ACE inhibitor/angiotensin receptor blocker) and thiazide diuretics in patients with CKD stages 1 to 3; and loop diuretics in those with CKD stages 4 and 5. No large study has evaluated thiazide diuretic use in patients with CKD stages 4 and 5. In one small study (n = 7) in which thiazides were compared with loop diuretics, there was similar BP control between the groups, but patients in the thiazide group had superior urinary fractional sodium excretion.⁵

There is new concern that thiazides may partially contribute to the increased risk for metabolic syndrome or diabetes. Reungjui et al⁷ have used animal models to demonstrate that the hypokalemic and hyperuricemic effects of thiazides are the culprits for this risk. They recommend managing the potassium and uric acid levels to manage or prevent this risk.

When a change is made from thiazides to loop diuretics, K/DOQI recommends starting furosemide at 40 mg/d and titrating upward as needed for BP and edema control. In my experience, counseling patients to follow a low-sodium diet (the American Heart Association recommends restricting sodium intake to 1500 mg/d) allows for a lower dose of furosemide (20 mg) to be effective.⁸

Elizabeth Evans, DNP
Renal Medicine Associates, Albuquerque, NM

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Q: In my orthopedic practice, we have a woman we are treating conservatively for low back pain (NSAIDs, muscle relaxants, and physical therapy). Her primary care provider told her that she cannot take the NSAIDs because of her kidney disease (she has chronic kidney disease [CKD] stage 3). Is there a safe dose of NSAIDs that she can use, or do I need to start narcotics? I would rather not do that!

Unfortunately, all NSAIDs increase the risk for acute kidney injury (AKI) and may exacerbate progression to chronic renal failure, particularly when large doses are taken chronically.^3,4 Increased incidence of renal injury with NSAIDs has been seen in patients with existing CKD, hypertension, diabetes, and frequent hospitalizations.³ Most renal damage associated with NSAIDs is related to inhibition of prostaglandin synthesis (discussed below), but NSAIDs can also cause other types of kidney injury, such as interstitial nephritis, analgesic nephropathy, and membranous nephropathy. NSAID use is also associated with hyperkalemia, hyponatremia, and edema (sodium retention).

The primary mechanism of NSAID nephrotoxicity is inhibition of prostaglandin synthesis in the setting of decreased renal perfusion.³ Prostaglandins induce vasodilation of the afferent arterioles to maintain renal perfusion (and consequently GFR). If renal perfusion or effective fluid volume decreases (as in dehydration, diuretic therapy, heart failure, and cirrhosis), renal perfusion is maintained by increasing prostaglandin synthesis. NSAIDs block prostaglandin synthesis, therefore blunting this protective mechanism. Blocking prostaglandin with NSAIDs when renal perfusion is decreased can cause an AKI.

AKI can occur in patients with or without CKD, and it is associated with increased morbidity and mortality. AKI due to NSAID use may progress to end-stage renal disease if the NSAID is not stopped promptly. When NSAIDs are discontinued, renal function most often stabilizes, but residual renal insufficiency is likely to be permanent. In some patients, even after discontinuing the NSAID, the AKI progresses to more advanced kidney disease.

All NSAIDs carry the same risk for acute and chronic kidney disease, with little evidence to suggest that some are safer than others. Higher doses are more likely to cause renal damage, but dosing to prevent renal damage has not been defined. Indomethacin and ketorolac have most frequently been associated with AKI. If appropriate for the patient, acetaminophen 650 mg taken three times daily (scheduled, not “as needed”) can provide pain relief with less risk for kidney injury.

Additionally, narcotic medications are often necessary when treating severe pain in patients with high risk for NSAID-associated kidney injury.

Catherine Wells, DNP, ACNP, CNN-NP
University of Mississippi Health Care, Division of Nephrology, Jackson

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Kristina Unterseher, CNN-NP
Idaho Nephrology Associates, Boise

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

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

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

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

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

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

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

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

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

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

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

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

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

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

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

PHILADELPHIA – Eliminating HLA-B matching from the U.S. priority-points formula that was used for allocating deceased-donor kidneys partially eliminated the allocation disparity against black recipients, but a residual disparity remained, based on an analysis of more than 57,000 U.S. kidney transplants during 2000-2009.

Removal of HLA-B matching from the allocation criteria cut the amount of disparity in organs received by black patients, compared with white patients, by a relative 23%, but during 2006-2009 blacks received deceased-donor kidneys at a rate that was 19% below the rate of kidneys that went to white patients, Dr. Erin C. Hall said at the American Transplant Congress, which was sponsored by the American Society of Transplant Surgeons.

In May 2003, the U.S. Organ Procurement and Transplantation Network – the deceased-donor organ distribution network established by the federal government and administered by the United Network for Organ Sharing (UNOS) – eliminated HLA-B matching as an allocation criterion.

Factors that may explain the residual disparity remain unidentified. Future studies could focus on an examination of center-by-center allocation differences by race in an effort to identify other sources for the disparity, said Dr. Hall, a researcher in the transplant surgery division at Johns Hopkins Hospital in Baltimore.

Before May 2003, U.S. kidney allocation procedures gave priority to recipients who matched for more of the six HLA loci, a policy that improved transplantation outcomes but decreased the number of nonwhite recipients who received organs (N. Engl. J. Med. 2004;350:545-51).

To investigate the impact of this change, Dr. Hall and her associated reviewed UNOS records for the 12,956 kidney transplants that were done during 2000–May 2003 using deceased-donor organs, and for the 44,704 transplants done during May 2003–2009. During the two periods, the level of black patients who were registered with UNOS to await kidney transplants held very steady, accounting for 44% all of listed patients before the criterion change, and for 45% after the change.

During 2000-2003, black patients received deceased-donor kidney transplants at 38% below the rate of white patients, according to a multivariate analysis that adjusted for patient differences in age, sex, primary renal disease cause, dialysis modality, use of preemptive transplant, insurance status, education, panel-reactive antibody level over time, and blood type. During 2003-2009, the transplantation rate among black patients was 23% less than it was in white patients. To allow for equilibration in transplant rates following the 2003 criterion change, Dr. Hall also analyzed transplantation rates during 2006-2009. During this period, the rate in black patients lagged 19% behind the rate in white patients, she reported. All three between-group differences were statistically significant. The amount of change between the 38% disparity rate during 2000-2003 and the 23% disparity rate during 2003-2009 constituted a 23% relative decline in the disparity rate.

Dr. Hall said that she had no relevant financial disclosures.

BOCA RATON, FLA. – A novel simulation-based training curriculum in laparoscopic totally extraperitoneal inguinal herniorrhaphy for general surgery residents led to shorter operating times, better trainee performance, and fewer patient complications in a randomized clinical trial.

The training program has two elements: a cognitive component featuring Web-based PowerPoint presentations and videos along with assigned readings, and psychomotor training on a totally extraperitoneal inguinal herniorrhaphy (TEP) simulator, Dr. Benjamin Zendejas said at the annual meeting of the American Surgical Association.

A key feature is that the skills training – with one instructor per resident – is performed until mastery is attained, however long that takes. Only then does the resident start performing TEPs in the operating room under supervision, explained Dr. Zendejas of the Mayo Clinic, Rochester, Minn.

He presented a study in which 50 general surgery residents performed a baseline TEP in the operating room, and then were randomized to the simulation-based training program or standard training.

The simulator was the Limbs & Things Ltd.’s TEP Guildford MATTU Hernia Trainer. Mastery was defined by the average 2 minutes required for five experienced instructors to perform a TEP on the simulator. An average of roughly eight attempts was required for fifth-year residents to achieve mastery on the simulator, compared with 26 for first-year residents.

In the operating room, the 50 residents performed 219 TEP repairs on 146 patients. Each repair was evaluated immediately afterward by two independent raters. The simulation-based training group outperformed residents who were trained in the standard fashion in all outcome measures, including the key end point of operative time adjusted for the impact of supervising surgeon takeover for poorly performing trainees. (See box.)

Intraoperative complications, such as peritoneal tears and procedure conversions, occurred in 7% of procedures performed by simulation-trained residents, and in 29% of controls. Urinary retention, seroma, and other postoperative complications resulted from 9% of the simulation-trained residents’ operations, compared with 26% of those performed by residents trained in TEP in standard fashion. In all, 7% of procedures carried out by simulation-trained residents led to an overnight hospital stay, compared with 21% for controls.

"This will become a seminal paper in simulation-based training education," said discussant Dr. Gary L. Dunnington, who called the study "outstanding."

This work suggests that, on an hour-by-hour basis, training in a psychomotor skills laboratory may be more efficient for residents than time spent in the operating room. These data, "if further substantiated, will be of great value with the increasing constraints of decreasing duty hours," noted Dr. Dunnington, professor and chairman of the department of surgery at Southern Illinois University, Springfield.

He was impressed with the investigators’ documentation of improved clinically relevant patient outcomes in the operating room after simulation-based training – the first study to do so. He also liked the investigators’ use of video recordings rather than crude recall to facilitate the study of operative errors.

"This study sets a new bar for simulation researchers," he concluded.

Dr. Zendejas reported having no financial conflicts.

BOCA RATON, FLA. – A novel simulation-based training curriculum in laparoscopic totally extraperitoneal inguinal herniorrhaphy for general surgery residents led to shorter operating times, better trainee performance, and fewer patient complications in a randomized clinical trial.

The training program has two elements: a cognitive component featuring Web-based PowerPoint presentations and videos along with assigned readings, and psychomotor training on a totally extraperitoneal inguinal herniorrhaphy (TEP) simulator, Dr. Benjamin Zendejas said at the annual meeting of the American Surgical Association.

A key feature is that the skills training – with one instructor per resident – is performed until mastery is attained, however long that takes. Only then does the resident start performing TEPs in the operating room under supervision, explained Dr. Zendejas of the Mayo Clinic, Rochester, Minn.

He presented a study in which 50 general surgery residents performed a baseline TEP in the operating room, and then were randomized to the simulation-based training program or standard training.

The simulator was the Limbs & Things Ltd.’s TEP Guildford MATTU Hernia Trainer. Mastery was defined by the average 2 minutes required for five experienced instructors to perform a TEP on the simulator. An average of roughly eight attempts was required for fifth-year residents to achieve mastery on the simulator, compared with 26 for first-year residents.

In the operating room, the 50 residents performed 219 TEP repairs on 146 patients. Each repair was evaluated immediately afterward by two independent raters. The simulation-based training group outperformed residents who were trained in the standard fashion in all outcome measures, including the key end point of operative time adjusted for the impact of supervising surgeon takeover for poorly performing trainees. (See box.)

Intraoperative complications, such as peritoneal tears and procedure conversions, occurred in 7% of procedures performed by simulation-trained residents, and in 29% of controls. Urinary retention, seroma, and other postoperative complications resulted from 9% of the simulation-trained residents’ operations, compared with 26% of those performed by residents trained in TEP in standard fashion. In all, 7% of procedures carried out by simulation-trained residents led to an overnight hospital stay, compared with 21% for controls.

"This will become a seminal paper in simulation-based training education," said discussant Dr. Gary L. Dunnington, who called the study "outstanding."

This work suggests that, on an hour-by-hour basis, training in a psychomotor skills laboratory may be more efficient for residents than time spent in the operating room. These data, "if further substantiated, will be of great value with the increasing constraints of decreasing duty hours," noted Dr. Dunnington, professor and chairman of the department of surgery at Southern Illinois University, Springfield.

He was impressed with the investigators’ documentation of improved clinically relevant patient outcomes in the operating room after simulation-based training – the first study to do so. He also liked the investigators’ use of video recordings rather than crude recall to facilitate the study of operative errors.

"This study sets a new bar for simulation researchers," he concluded.

Dr. Zendejas reported having no financial conflicts.

BOCA RATON, FLA. – A novel simulation-based training curriculum in laparoscopic totally extraperitoneal inguinal herniorrhaphy for general surgery residents led to shorter operating times, better trainee performance, and fewer patient complications in a randomized clinical trial.

The training program has two elements: a cognitive component featuring Web-based PowerPoint presentations and videos along with assigned readings, and psychomotor training on a totally extraperitoneal inguinal herniorrhaphy (TEP) simulator, Dr. Benjamin Zendejas said at the annual meeting of the American Surgical Association.

A key feature is that the skills training – with one instructor per resident – is performed until mastery is attained, however long that takes. Only then does the resident start performing TEPs in the operating room under supervision, explained Dr. Zendejas of the Mayo Clinic, Rochester, Minn.

He presented a study in which 50 general surgery residents performed a baseline TEP in the operating room, and then were randomized to the simulation-based training program or standard training.

The simulator was the Limbs & Things Ltd.’s TEP Guildford MATTU Hernia Trainer. Mastery was defined by the average 2 minutes required for five experienced instructors to perform a TEP on the simulator. An average of roughly eight attempts was required for fifth-year residents to achieve mastery on the simulator, compared with 26 for first-year residents.

In the operating room, the 50 residents performed 219 TEP repairs on 146 patients. Each repair was evaluated immediately afterward by two independent raters. The simulation-based training group outperformed residents who were trained in the standard fashion in all outcome measures, including the key end point of operative time adjusted for the impact of supervising surgeon takeover for poorly performing trainees. (See box.)

Intraoperative complications, such as peritoneal tears and procedure conversions, occurred in 7% of procedures performed by simulation-trained residents, and in 29% of controls. Urinary retention, seroma, and other postoperative complications resulted from 9% of the simulation-trained residents’ operations, compared with 26% of those performed by residents trained in TEP in standard fashion. In all, 7% of procedures carried out by simulation-trained residents led to an overnight hospital stay, compared with 21% for controls.

"This will become a seminal paper in simulation-based training education," said discussant Dr. Gary L. Dunnington, who called the study "outstanding."

This work suggests that, on an hour-by-hour basis, training in a psychomotor skills laboratory may be more efficient for residents than time spent in the operating room. These data, "if further substantiated, will be of great value with the increasing constraints of decreasing duty hours," noted Dr. Dunnington, professor and chairman of the department of surgery at Southern Illinois University, Springfield.

He was impressed with the investigators’ documentation of improved clinically relevant patient outcomes in the operating room after simulation-based training – the first study to do so. He also liked the investigators’ use of video recordings rather than crude recall to facilitate the study of operative errors.

"This study sets a new bar for simulation researchers," he concluded.

Dr. Zendejas reported having no financial conflicts.

PHILADELPHIA – At least five live-kidney donors died worldwide since 2005 from catastrophic hemorrhages attributable to insecure ligation of their renal artery by a locking clip rather than by transfixion.

The most recent of these deaths occurred earlier this year, despite concerns raised during 2004-2006 about the safety of clip ligations and a Food and Drug Administration temporary ban in 2006 on the U.S. sale of polymer locking clips, Dr. Amy L. Friedman said at the American Transplant Congress. Following reintroduction of the polymer locking clips in late 2006, two other deaths attributable to severe renal artery hemorrhages in live kidney donors occurred in 2008, said Dr. Friedman, professor of surgery and director of transplants at Upstate Medical University Hospital in Syracuse, N.Y.

"It’s clear that this is not a frequent event, but even though it’s infrequent it is catastrophic," Dr. Friedman said in an interview. The relative infrequency "does not justify it. We ask surgeons to please respect the privilege of operating on a living kidney donor and not use" a polymer clip to close off the donor’s severed renal artery. Dr. Friedman also noted several other cases since 2003 where patients did not die but had severe hemorrhages because of unreliable artery ligations that produced near-death events.

Dr, Friedman admitted that alternative closure techniques that use transfixion are "challenging." The options are suture ligature, oversewing, or stapling. The most commonly used, safe closure is stapling, which has the drawback of using more of an artery’s length. "If the patient has early branching" of their renal artery, this closure may produce two small arteries instead of one larger one" on the removed kidney, "forcing you to sew them together and making the kidney harder to transplant." But any added inconvenience in transplanting the donated kidney does not outweigh safely closing the donor’s artery, she said. "The stapler is the best alternative to the clip," she said.

The surgeons performing nephrectomies for transplantable kidneys from living donors most commonly are transplant surgeons, urologists, and minimally-invasive surgeons. "There has been extensive pushback" arguing in favor of continued clip use in the urology literature, Dr. Friedman said at the meeting cosponsored by the American Society of Transplant Surgeons.

"The urology community uses clips more frequently, especially for nephrectomies done for other purposes," she said. "In those cases, the length of renal artery that they leave is much longer," experience that seems to have convinced urologists that clipping is safe even when the renal artery is shorter. "What we clearly know is that when the artery stump is left very short to allow a long length of artery to remain with the kidney, clips cannot be used." Some clip proponents also note that clips are less expensive than staples are, and many surgeons also cite personal experience performing hundreds of uneventful renal-artery closures with clips. Dr. Friedman contends that this is not surprising since the severe adverse event rate from clips is very low, but even a handful of deaths is too many.

Many transplant surgeons remain skeptical of the risk because they want to see case reports from deaths and other severe sequelae, data that the FDA, the Centers for Medicare & Medicaid Services, and the United Network for Organ Sharing (UNOS) have generally not shared.

Dr. Friedman contended that these regulatory agencies have balked at releasing case details out of medicolegal concerns about discoverability and confidentiality.

These agencies "make it hard, but these data should be easily available. If surgeons knew that there have been at least five deaths since 2005, it’s hard to imagine that they would not be convinced. I’m doing my best to get the information out," she said.

The five deaths from unstable renal artery closures in kidney donors using locking polymer clips comprised two cases in 2005, two in 2008, and the most recent case reported by UNOS earlier this year. Dr. Friedman said that she had also reviewed a report of a possible sixth death in February 2005, but it remains unclear whether this was the same case as one of the other 2005 deaths she cited. In addition, Dr. Friedman said she was aware of five additional cases of severe hemorrhage complications in living kidney donors treated with polymer clips since 2005.

Following notification by UNOS of the most recent death in February of this year, and a reminder to transplant surgeons not to use polymer clips for artery ligations, Dr. Friedman sent out an electronic survey in March to the members of the American Society of Transplant Surgeons (ASTS). From the 1,095 members she received 217 replies (20%). In reply to a question whether the ASTS members had received the UNOS notification, about two-thirds said they had not. She also asked the ASTS members whether their institutions continued to use hemostatic clips to ligate the renal arteries of live kidney donors. About 20% of all 201 respondents to this question, and more than 10% of the U.S.-based surgeons who responded said that their institutions used clips at least sometimes for these ligations.

Dr. Friedman said that she and her associates have no relevant financial disclosures.

PHILADELPHIA – At least five live-kidney donors died worldwide since 2005 from catastrophic hemorrhages attributable to insecure ligation of their renal artery by a locking clip rather than by transfixion.

The most recent of these deaths occurred earlier this year, despite concerns raised during 2004-2006 about the safety of clip ligations and a Food and Drug Administration temporary ban in 2006 on the U.S. sale of polymer locking clips, Dr. Amy L. Friedman said at the American Transplant Congress. Following reintroduction of the polymer locking clips in late 2006, two other deaths attributable to severe renal artery hemorrhages in live kidney donors occurred in 2008, said Dr. Friedman, professor of surgery and director of transplants at Upstate Medical University Hospital in Syracuse, N.Y.

"It’s clear that this is not a frequent event, but even though it’s infrequent it is catastrophic," Dr. Friedman said in an interview. The relative infrequency "does not justify it. We ask surgeons to please respect the privilege of operating on a living kidney donor and not use" a polymer clip to close off the donor’s severed renal artery. Dr. Friedman also noted several other cases since 2003 where patients did not die but had severe hemorrhages because of unreliable artery ligations that produced near-death events.

Dr, Friedman admitted that alternative closure techniques that use transfixion are "challenging." The options are suture ligature, oversewing, or stapling. The most commonly used, safe closure is stapling, which has the drawback of using more of an artery’s length. "If the patient has early branching" of their renal artery, this closure may produce two small arteries instead of one larger one" on the removed kidney, "forcing you to sew them together and making the kidney harder to transplant." But any added inconvenience in transplanting the donated kidney does not outweigh safely closing the donor’s artery, she said. "The stapler is the best alternative to the clip," she said.

The surgeons performing nephrectomies for transplantable kidneys from living donors most commonly are transplant surgeons, urologists, and minimally-invasive surgeons. "There has been extensive pushback" arguing in favor of continued clip use in the urology literature, Dr. Friedman said at the meeting cosponsored by the American Society of Transplant Surgeons.

"The urology community uses clips more frequently, especially for nephrectomies done for other purposes," she said. "In those cases, the length of renal artery that they leave is much longer," experience that seems to have convinced urologists that clipping is safe even when the renal artery is shorter. "What we clearly know is that when the artery stump is left very short to allow a long length of artery to remain with the kidney, clips cannot be used." Some clip proponents also note that clips are less expensive than staples are, and many surgeons also cite personal experience performing hundreds of uneventful renal-artery closures with clips. Dr. Friedman contends that this is not surprising since the severe adverse event rate from clips is very low, but even a handful of deaths is too many.

Many transplant surgeons remain skeptical of the risk because they want to see case reports from deaths and other severe sequelae, data that the FDA, the Centers for Medicare & Medicaid Services, and the United Network for Organ Sharing (UNOS) have generally not shared.

Dr. Friedman contended that these regulatory agencies have balked at releasing case details out of medicolegal concerns about discoverability and confidentiality.

These agencies "make it hard, but these data should be easily available. If surgeons knew that there have been at least five deaths since 2005, it’s hard to imagine that they would not be convinced. I’m doing my best to get the information out," she said.

The five deaths from unstable renal artery closures in kidney donors using locking polymer clips comprised two cases in 2005, two in 2008, and the most recent case reported by UNOS earlier this year. Dr. Friedman said that she had also reviewed a report of a possible sixth death in February 2005, but it remains unclear whether this was the same case as one of the other 2005 deaths she cited. In addition, Dr. Friedman said she was aware of five additional cases of severe hemorrhage complications in living kidney donors treated with polymer clips since 2005.

Following notification by UNOS of the most recent death in February of this year, and a reminder to transplant surgeons not to use polymer clips for artery ligations, Dr. Friedman sent out an electronic survey in March to the members of the American Society of Transplant Surgeons (ASTS). From the 1,095 members she received 217 replies (20%). In reply to a question whether the ASTS members had received the UNOS notification, about two-thirds said they had not. She also asked the ASTS members whether their institutions continued to use hemostatic clips to ligate the renal arteries of live kidney donors. About 20% of all 201 respondents to this question, and more than 10% of the U.S.-based surgeons who responded said that their institutions used clips at least sometimes for these ligations.

Dr. Friedman said that she and her associates have no relevant financial disclosures.

PHILADELPHIA – At least five live-kidney donors died worldwide since 2005 from catastrophic hemorrhages attributable to insecure ligation of their renal artery by a locking clip rather than by transfixion.

The most recent of these deaths occurred earlier this year, despite concerns raised during 2004-2006 about the safety of clip ligations and a Food and Drug Administration temporary ban in 2006 on the U.S. sale of polymer locking clips, Dr. Amy L. Friedman said at the American Transplant Congress. Following reintroduction of the polymer locking clips in late 2006, two other deaths attributable to severe renal artery hemorrhages in live kidney donors occurred in 2008, said Dr. Friedman, professor of surgery and director of transplants at Upstate Medical University Hospital in Syracuse, N.Y.

"It’s clear that this is not a frequent event, but even though it’s infrequent it is catastrophic," Dr. Friedman said in an interview. The relative infrequency "does not justify it. We ask surgeons to please respect the privilege of operating on a living kidney donor and not use" a polymer clip to close off the donor’s severed renal artery. Dr. Friedman also noted several other cases since 2003 where patients did not die but had severe hemorrhages because of unreliable artery ligations that produced near-death events.

Dr, Friedman admitted that alternative closure techniques that use transfixion are "challenging." The options are suture ligature, oversewing, or stapling. The most commonly used, safe closure is stapling, which has the drawback of using more of an artery’s length. "If the patient has early branching" of their renal artery, this closure may produce two small arteries instead of one larger one" on the removed kidney, "forcing you to sew them together and making the kidney harder to transplant." But any added inconvenience in transplanting the donated kidney does not outweigh safely closing the donor’s artery, she said. "The stapler is the best alternative to the clip," she said.

The surgeons performing nephrectomies for transplantable kidneys from living donors most commonly are transplant surgeons, urologists, and minimally-invasive surgeons. "There has been extensive pushback" arguing in favor of continued clip use in the urology literature, Dr. Friedman said at the meeting cosponsored by the American Society of Transplant Surgeons.

"The urology community uses clips more frequently, especially for nephrectomies done for other purposes," she said. "In those cases, the length of renal artery that they leave is much longer," experience that seems to have convinced urologists that clipping is safe even when the renal artery is shorter. "What we clearly know is that when the artery stump is left very short to allow a long length of artery to remain with the kidney, clips cannot be used." Some clip proponents also note that clips are less expensive than staples are, and many surgeons also cite personal experience performing hundreds of uneventful renal-artery closures with clips. Dr. Friedman contends that this is not surprising since the severe adverse event rate from clips is very low, but even a handful of deaths is too many.

Many transplant surgeons remain skeptical of the risk because they want to see case reports from deaths and other severe sequelae, data that the FDA, the Centers for Medicare & Medicaid Services, and the United Network for Organ Sharing (UNOS) have generally not shared.

Dr. Friedman contended that these regulatory agencies have balked at releasing case details out of medicolegal concerns about discoverability and confidentiality.

These agencies "make it hard, but these data should be easily available. If surgeons knew that there have been at least five deaths since 2005, it’s hard to imagine that they would not be convinced. I’m doing my best to get the information out," she said.

The five deaths from unstable renal artery closures in kidney donors using locking polymer clips comprised two cases in 2005, two in 2008, and the most recent case reported by UNOS earlier this year. Dr. Friedman said that she had also reviewed a report of a possible sixth death in February 2005, but it remains unclear whether this was the same case as one of the other 2005 deaths she cited. In addition, Dr. Friedman said she was aware of five additional cases of severe hemorrhage complications in living kidney donors treated with polymer clips since 2005.

Following notification by UNOS of the most recent death in February of this year, and a reminder to transplant surgeons not to use polymer clips for artery ligations, Dr. Friedman sent out an electronic survey in March to the members of the American Society of Transplant Surgeons (ASTS). From the 1,095 members she received 217 replies (20%). In reply to a question whether the ASTS members had received the UNOS notification, about two-thirds said they had not. She also asked the ASTS members whether their institutions continued to use hemostatic clips to ligate the renal arteries of live kidney donors. About 20% of all 201 respondents to this question, and more than 10% of the U.S.-based surgeons who responded said that their institutions used clips at least sometimes for these ligations.

Dr. Friedman said that she and her associates have no relevant financial disclosures.