PATHOGENESIS AND MANAGEMENT OF HYPERCALCIURIC NEPHROLITHIASIS

Hypercalciuria has long been recognized as an important metabolic dera ngement associated with the formation of calcareous renal stones. Hype rcalciuria increases the saturation of the urine with respect to stone -forming salts and reduces inhibitor activity. There is now ample evid ence that 'idiopathic hypercalciuria' is a heterogeneous disorder, com prising several entities including absorptive, renal and resorptive fo rms of hypercalciuria. Absorptive hypercalciuria is the most common va riety, and recent studies suggest that in a large subset of these pati ents, increased intestinal calcium absorption is caused by increased p roduction of calcitriol or greater sensitivity to calcitriol (e.g. upr egulation of vitamin D receptors). Reduced spinal bone density found i n these patients may relate to increased action of calcitriol on bone or to other factors. Since patients with vitamin D-dependent absorptiv e hypercalciuria may develop negative calcium balance when placed on d iets restricted in calcium, therapy is shifting from severe dietary ca lcium restriction and sodium cellulose phosphate (calcium-binding resi n) to thiazides and orthophosphates, which promote calcium retention. For each form of hypercalciuria, selective therapy should provide the best results.