NSAIDs can precipitate acute kidney injury and accelerate the progression of chronic kidney disease by impairing renal prostaglandin‑mediated vasodilation, leading to reduced glomerular filtration and sodium‑water retention.
NSAIDs are contraindicated in moderate‑to‑severe CKD (eGFR < 60).
Even short‑term NSAID courses can cause a reversible rise in creatinine; repeated courses accelerate CKD.
Monitor serum creatinine and potassium 7–14 days after starting or changing NSAID therapy.
Use COX‑2 selective inhibitors (e.g., celecoxib) with caution; they still impair prostaglandin synthesis and carry similar renal risk.
Renal prostaglandins (especially PGE2 and PGI2) maintain afferent arteriolar vasodilation, especially in states of reduced renal perfusion. NSAIDs inhibit cyclo‑oxygenase (COX‑1/COX‑2), decreasing prostaglandin synthesis, causing afferent arteriole constriction, a drop in glomerular filtration rate (GFR), and potential ischemic injury. In CKD, the kidney already relies heavily on prostaglandin‑mediated flow, so NSAID‑induced inhibition has a disproportionate effect.
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