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NSAIDs may increase risk for nephrotic syndrome
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Use of NSAIDs was associated with a greater risk for nephrotic syndrome after at least 2 weeks of exposure, according to a recently published study.
“Several studies demonstrated that conventional NSAIDs were associated with a higher risk of acute kidney injury and glomerulonephritis,” Mohammad Bakhriansyah, MD, of the division of pharmacoepidemiology and clinical pharmacology at Utrecht Institute for Pharmaceutical Sciences, Utrecht University in the Netherlands, and colleagues wrote. “These adverse effects were not consistently seen for selective cyclooxygenase (COX)-2 inhibitors [and] occurred at a rate as low as 1% to 5% for NSAID users. However, because NSAIDs are one of the most prescribed drugs and some of them are available over the counter, these small increased risks may translate into high absolute numbers of patients being affected, especially in those with impaired kidney function. Several case reports indicate a potential causal relation between specific conventional NSAIDs or selective COX-2 inhibitors and nephrotic syndrome. The exact mechanism by which NSAIDs might cause nephrotic syndrome is largely unknown.”
Researchers conducted a systematic observational study matching 2,620 patients with a first diagnosis of nephrotic syndrome with 10,454 patients without nephrotic syndrome to serve as controls. NSAID exposure was classified as current (use at nephrotic syndrome diagnosis or corresponding date for controls), recent (discontinuation 1 month to 2 months before diagnosis date), past (discontinuation 2 months to 2 years before diagnosis date) or non-use. NSAIDs were also categorized by chemical group (eg, acetic acid derivatives, propionic acid derivatives, fenamates, oxicams, selective COX-2 inhibitors and other).
Comorbidities associated with nephrotic syndrome and factors associated with kidney toxicity were considered.
Researchers found that, compared with non-use, current use of NSAIDs for 15 to 28 days or for more than 28 days before diagnosis was associated with a higher relative risk of nephrotic syndrome (OR = 1.34 and OR = 1.42, respectively). Recent (OR = 1.55) or past (OR = 1.24) use of NSAIDs was also associated was a greater risk.
When use of NSAIDs was for fewer than 15 days, patients did not have a higher relative risk of nephrotic syndrome (OR = 0.78). Furthermore, no higher risk was observed when NSAIDs had been discontinued for more than 2 years.
When assessing chemical groups, researchers observed that acetic acid (eg, indomethacin, diclofenac and ketorolac) and propionic acid derivatives (eg, ibuprofen, naproxen and ketoprofen) were associated with a higher risk of nephrotic syndrome.
“A patient who develops nephrotic syndrome should be asked about the use of NSAIDs, including over the counter,” the researchers wrote. “Although our study indicated that current and past use (> 2 years) of selective COX-2 inhibitors were not associated with a higher risk, the number of participants was too small to draw definite conclusions.”
In a related editorial, Evangelina Merida, MD, and Manuel Praga, MD, wrote: “The study raises questions of great clinical importance for the clinician. Are we overlooking patients with NSAIDs-induced nephrotic syndrome? If so, are we prescribing long courses of immunosuppressive treatments to patients with minimal change disease or membranous nephropathy caused by NSAIDs that would have resolved with the discontinuation of the drug accompanied perhaps by a short course of corticosteroids? Considering that the existing literature on this topic is in general old and scarce, with only patient reports or short series of patients published, data from this study should encourage nephrologists to, on one hand, carefully review the current or recent intake of NSAIDs in any patient with nephrotic syndrome, particularly when minimal change disease or membranous nephropathy is found in kidney biopsies, and on the other hand, perform collaborative studies to collect large series of patients with unequivocal diagnosis of NSAIDs-induced nephrotic syndrome to identify their differential clinical and histopathologic characteristics and delineate their more efficient treatment.” – by Melissa J. Webb
Disclosures: Bakhriansyah reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
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