Abstract

We have reviewed the general mechanisms involved in kidney stone formation, with reference to those composed of calcium oxalate or phosphate, uric acid, and cystine. These processes include nucleation of individual crystals, aggregation or secondary nucleation to produce small intrarenal multicrystalline aggregates, fixation within the kidney, and further aggregation and secondary nucleation to produce the clinical stone. The factors regulating these processes have been discussed as well as the effects of tubular fluid or urine pH and promoters or inhibitors, including urate or uric acid in the case of calcium oxalate stones, citrate, pyrophosphate, phytate, and urinary proteins. We also discuss the potential for macromolecular inhibitors to actually promote stone formation when they are fixed to some intrarenal structure or if they themselves become aggregated into protein–protein complexes.

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