Published online Nov 6, 2014. doi: 10.5527/wjn.v3.i4.256
Revised: July 23, 2014
Accepted: September 6, 2014
Published online: November 6, 2014
Nephrolithiasis seems to be the result of crystal formation, aggregation and retention in the kidney during crystalluria. These processes have to occur within the short urinary transit time through the kidney being in the order of few minutes. Recently much work was done on rather qualitative aspects of nephrolithiasis like genetics, metabolism and morphology. In this review we try to provide some quantitative information on urinary supersaturation with respect to stone minerals, especially Ca oxalate (CaOx), on the formation and aggregation of CaOx crystals and on crystal retention in the kidney. The paper is centered on idiopathic Ca nephrolithiasis being the most frequent stone disease with only partially known pathogenesis. New aspects of the role of urinary macromolecules in stone formation and of the mechanism of crystal aggregation are provided.
Core tip: The state of urinary saturation with respect to Ca salts is governed by pH, Ca and Ox concentration. Growth of calcium oxalate (CaOx) in urine is too slow that single crystals could acquire a size to be trapped in nephron. The aggregation (AGN) of CaOx in urine was lacking or severely delayed due to inhibition by urinary macromolecules (UM’s). Albumin, after temporary adsorption on calcium phosphate, showed self aggregation and promoted AGN of CaOx. Self aggregated UM’s probably overwhelm the electrostatic repulsion of crystals coated by negatively charged UM’s. This mechanism may explain the effect of Randall’s plaques.