Effect of Urinary Macromolecules on Calcium Oxalate Dihydrate Crystal Growth and Nucleation Rates

Abstract

Two major theories of calcium oxalate urinary stone disease are the hyperexcretion-supersaturation theory and the inhibitor theory. Both are centrally related to the crystallization kinetics of calcium oxalate (CaOx). In the supersaturation theory oxalate stone is a result of persistent overconcentration of Ca²⁺ and/or Ox^2- ions in the urine brought about by dietary and metabolic irregularities or inadequate fluid intake. CaOx precipitation (mono or dihydrate form) occurs when the CaOx ion product exceeds the formation product. The supersaturation theory maintains that persistent overconcentration causes excessive crystalluria growth, nucleation, and/or aggregation which raises the probability of a particle eventually lodging in the kidney to become the nidus for a stone. High supersaturations aggravate further growth of the stone by molecular growth, surface nucleation of dendrites and/or aggregation with additional crystalluria. Finlayson¹ demonstrated convincingly using order-of-magnitude calculations that growth of 200μm particles (approximate dimensions of the ducts of Bellini) is virtually impossible solely by molecular accretion on single crystals; agglomeration/aggregation mechanisms are a likely part of the overall stone formation process. Nevertheless, the presence of small CaOx crystalluria sets up these mechanisms and therefore the hyperexcretion-supersaturation theory correctly focuses on the importance of crystallization kinetics.