In a patient with chronic kidney disease who requires an NSAID for osteoarthritis, sulindac is often considered relatively preferable among non-selective NSAIDs. The pharmacokinetic property responsible is that sulindac:

• A Is not protein bound, so it avoids competition with uremic toxins
• B Selectively inhibits COX-2 despite being chemically classified as a non-selective NSAID
• C Undergoes exclusively biliary excretion, so no dose adjustment is ever needed
• D Is a prodrug converted to the active sulfide metabolite mainly in the liver, and its inactive sulfone metabolite predominates in the kidney, causing less inhibition of renal prostaglandin synthesis ✓

Explanation

Sulindac is a sulfoxide prodrug reduced to the active sulfide in the liver. Within the kidney it is preferentially oxidised back to the inactive sulfone, so renal cyclooxygenase is largely spared and renal prostaglandin production falls less than with other NSAIDs. This makes it a traditional choice when an NSAID is unavoidable in renal impairment. It is not COX-2 selective and still needs caution and dose care in advanced kidney disease.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

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