Acute renal failure from hemoglobinuric and interstitial nephritis secondary to iodine and mefenamic acid

Mefenamic acid ingestion, usually in excess and over prolonged period is kn own to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure. However, it is not dose-dependent for the induct ion of tubulointerstitial damage. Excess iodine ingestion is known to produ ce toxicity and possible death, but acute renal failure is rare. There is e vidence from clinical and experimental data that iodine has toxic effect on tubular epithelial cells. Iodine has not been documented to produce red ce ll hemolysis and hemoglobinuria. We present a unique case of acute renal fa ilure from hemoglobinuric and acute interstitial nephritis secondary to sui cidal ingestion of potassium iodide solution and also ingestion of a few me fenamic acid tablets. These agents led to potentiation of the renal injury from hemoglobinuric tubulopathy, probably from the iodine, and renal dysfun ction from alteration of renal perfusion by selective COX-1 inhibition of p rostaglandin production, and induction of acute interstitial nephritis from mefenamic acid, leading to acute renal failure which was reversible by hem odialysis and supportive therapy.