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
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