The formation of calcium (Ca) stones occurs in an initial phase by fixed growth on kidney calcifications consisting either of intratubular crystal accumulations protruding in renal calices (Randall’s plugs) or of interstitial hydroxyapatite deposits (Randall’s plaques) broken through the covering epithelial layers. Crystal aggregation (AGN) seems to be responsible for stone growth during crystalluria. This chapter reports on new aspects of the AGN of calcium oxalate being the most frequent stone compound and tries to explain why despite the widespread occurrence of kidney calcifications and crystalluria not everybody forms stones. Urinary crystals normally are protected from AGN by coats of urinary macromolecules (UMs) which by their identical electronegative charge create zones of electrostatic repulsion. At high urinary concentration or ionic strength respectively, these zones are compressed and can be bridged by self-aggregated UMs. Self-AGN occurs in concentrated urine by the adsorption of UMs on free surfaces like Randall’s plugs or plaques. High oxalate excretion and high urine concentration favoring intratubular crystal accumulation, breaking of epithelial layers on Randall’s plaques and self-AGN of UMs are most deleterious factors in Ca stone formation and have to be avoided by stone metaphylaxis.
Part of the book: Pathophysiology