Abstract

Nearly 60% of patients with CKD suffer pain. Of those patients with CKD who have pain, most rate their pain as moderate or severe in intensity. Undermanaged pain is associated with higher rates of mood disorders, maladaptive coping, and decreased quality of life for patients with CKD (1). In general, nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended as first-line for analgesia and also act as antipyretics and anti-inflammatory medications. Estimates indicate that 98 million patients annually are prescribed NSAIDs (2), which likely represents only a fraction of total use given widespread nonprescription access. Epidemiologic studies suggest that 70%–80% of all NSAID users consume over-the-counter products like ibuprofen or naproxen (3,4). In the National Health and Nutrition Examination Survey, routine NSAID use was common in patients with CKD and use increased with increasing CKD severity (3). NSAIDs have well-known adverse effects in CKD patients. These risks can broadly be categorized into affecting the kidneys, gastrointestinal (GI) tract, or cardiovascular system. Among these risks, it is the direct and indirect nephrotoxicity that has primarily led to hesitation with the use of NSAIDs in patients with CKD. In one study, patients with CKD were more likely to receive an opioid than an NSAID or gabapentinoid across the entire spectrum of CKD (5). The highest rates of opioid prescribing were in patients with the lowest GFR. Indirect nephrotoxicity from NSAIDs is linked to altered intraglomerular hemodynamics. NSAIDs inhibit PG synthesis, which decreases afferent arteriolar vasodilation and can reduce glomerular pressure. This is especially prominent in patients with already jeopardized renal perfusion as in shock or intravascular volume depletion. For this reason, use of NSAIDs in acutely ill patients with AKI, acute kidney disease, or in the midst of renal recovery remains ill-advised. Patterns of direct nephrotoxicity include interstitial nephritis, papillary necrosis, and …

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