Renal Calculi (Uric Acid, Hyperuricosuria, Gouty Diathesis)

Uric acid, a heterocyclic compound, is produced as a byproduct of purine metabolism. Uric acid can be generated from endogenous as well as exogenous sources. The human body makes about 300-400 mg of uric acid per day, with most of it being built in the liver. Purines degenerate into inosine and hypoxanthine. Hypoxanthine is further metabolized into xanthine and uric acid in the ubiquity of the xanthine oxidase enzyme. In most of the mammals, uric acid is transformed to allantoin in the bearing of the uricase enzyme. Allantoin being a very dissolvable commodity does not create any pathogenies. However, in humans, this enzyme is nonfunctional due to nonsense and frameshift mutations, so the end product of the metabolism is uric acid, a comparatively insoluble outcome. Thus high levels of uric acid in serum can lead to its deposition in joints and kidneys, leading to gout and nephrolithiasis. Exogenous sources include nondairy meat, fish, alcohol, sweet drinks, sweetbreads. The organs accountable for the elimination and excretion of uric acid are kidneys and intestines. In the intestines, uric acid is transformed into ammonia and carbon dioxide. Bacteria, moreover, utilize the ammonia in the intestine for metabolism. In Kidneys, almost 100% of uric acid is filtered in glomerulus. However, it is further reabsorbed, secreted, and reabsorbed in the proximal convoluted tubule (PCT), ultimately resulting in only 10% fractional elimination of urate. Uric acid stone was first secluded by a Swedish pharmacist Scheele in 1776. Fourcroy examined about 600 stones from 1736 to 1802 and also suggested the term uric acid.