Renal effects of nonselective NSAIDs and coxibs
Matthew R. Weir, MD
Division of Nephrology, University of Maryland School of Medicine, Baltimore
Correspondence: Matthew R. Weir, MD, Professor of Medicine and Director, Division of Nephrology, University of Maryland School of Medicine, 22 South Greene St., Baltimore, MD
21201; e-mail: firstname.lastname@example.org
The author has indicated that he has received grant or research support from Pharmacia, has been a consultant for Merck and Pharmacia, and is on the speaker’s bureau of Merck.
Despite the ubiquitous use of both over-the-counter and prescription nonsteroidal anti-inflammatory drugs (NSAIDs), clinical syndromes—NSAID-related hypertension, salt and water retention, edema, and hyperkalemia—are highly infrequent. Nevertheless, they remain a concern, and patient populations at risk for renal adverse effects from NSAIDs can be prospectively identified. Patients at risk include those with age-related declines in glomerular filtration rate; those with hypovolemia, particularly patients taking loop diuretics; and those with congestive heart failure, cirrhosis, or nephrosis. The following patient populations are at higher risk for increases in blood pressure with concomitant use of an NSAID and an antihypertensive: those with congestive heart failure, liver disease, or kidney disease, and those taking angiotensin-converting enzyme inhibitors or diuretics. Nonselective NSAIDs and COX (cyclooxygenase)-2-selective inhibitors (coxibs) appear to have similar effects on renal function if dosed equivalently, and standard precautions to avoid renal toxicity with use of nonselective NSAIDs apply to coxibs.