[New pathophysiologic aspects of nephrolithiasis]

Abstract

Urinary supersaturation with stone-forming ions is the driving force of crystallization in renal tubules. Based on concentration measurements of the majority of ions, supersaturation can be calculated by means of a computer program. Assessments of 24-hour urine excretions of lithogenic substances do not necessarily detect intermittent supersaturation which may induce crystallization processes. Even the most elaborate metabolic evaluations fail to detect metabolic abnormalities in 10-30% of unselected patients with nephrolithiasis ("idiopathic" nephrolithiasis). Apart from supersaturation, crystal aggregation seems to be a most important factor in kidney stone formation whose pathophysiologic relevance has so far been underestimated. New studies demonstrate excellent inhibition of calcium oxalate monohydrate crystal aggregation by nephrocalcin and Tamm-Horsfall glycoprotein, 2 glycoproteins produced by the kidneys. In recurrent "idiopathic" calcium oxalate stone formers both proteins are structurally and functionally defective crystal aggregation inhibitors.