The regulation of renal calcium excretion: an approach to hypercalciuria.

Abstract

Urinary calculi are a major cause of morbidity in the United States. It is estimated that one of every 1000 people in the US is hospitalized annually for urinary tract stones, and that 1 5 of every 1 00 episodes results in urologic surgery (1). Renal stones are classified into five major crystalline types: cystine, uric acid, struvite (magnesium ammonium phosphate, triple phosphate, and infection stones are synonyms), calcium phosphate (brushite), and calcium oxalate. Approximately half of calcium oxalate stones contain a component of calcium phosphate; the term calcium stone is used when the calcium phosphate content exceeds 15% of the crystalline mass of the stone. Calcium oxalate and mixed calcium stones constitute about 80% of the stones encountered in the US, and the remaining four crystalline types are individually uncommon. Many investigators stress the concepts of supersaturation chemistry in attempting to understand the pathogenesis of renal formation. These concepts are particularly useful when applied to the formation of the four minor types. For example, cystine is the least soluble of the natu­ rally occurring amino acids, with a maximum solubility of about 300 mglliter in aqueous solution. Patients with homozygous cystinuria com­ monly excrete 600-1400 mg of cystine per day so that their predisposition to cystine formation is self-evident. Further, there is a discrete causal relationship between cystinuria and the formation of cystine stones.