acetylsalicylic acid × furosemide

Dual mechanism. First, aspirin competes with furosemide for tubular organic-anion secretion in the proximal tubule – delivery of furosemide to the luminal side of the loop of Henle falls. The effect is pronounced at high aspirin doses. Second, inhibition of renal prostaglandin synthesis reduces preglomerular vasodilation and natriuresis. At cardiovascular aspirin doses of 75–100 mg, both mechanisms are clinically minor. At analgesic and antipyretic doses of 500–1000 mg and above, the effect becomes clinically obvious – HF and ascites patients may lose diuretic efficacy and develop worsening edema.

Antiplatelet aspirin doses of 75–100 mg are compatible with furosemide. Avoid analgesic and antipyretic doses of 500–1000 mg in HF and ascites – replace with paracetamol. If an NSAID is essential, use the shortest possible course, monitor body weight daily, and check creatinine and potassium at 5–7 days. For worsening edema, temporarily increase the furosemide dose or add a thiazide (sequential nephron blockade).