Uric acid is the end product of enzymatic degradation of body purines, which arise from the endogenous biosynthesis of nucleoproteins and are ingested, in small part, in dietary foodstuffs. At physiologic pH (7.35-7.40) uric acid occurs as its soluble sodium salt, but at pH 5.0, approximately 75% of uric acid is free and insoluble. This physical-chemical characteristic favors uric acid precipitation and stone formation in a persistently acid urine. Renal excretion of uric acid drops sharply when urinary flow falls below 0.5 ml per minute, and if clearance remains impaired, hyperuricemia results. In addition, a low daily urine output increases urine uric acid concentration, enhancing solute precipitation and stone formation.
In a recent communication in the Archives of Surgery,1 Wilmore and Gots discuss the factors which predispose the patient to uric acid urolithiasis after ileostomy. Uric acid excretion was studied in ileostomy patients with proven uric acid calculi. Excessive