Supersaturation is the driving force behind crystal formation in the kidneys. It can, however, result only in the formation of crystals that can often be harmlessly excreted. For stone formation, crystals must form, grow, and be retained in the kidneys, which is indeed a rare occurrence. Crystalluria is universal while stone formation is not. Only pathological changes in the kidneys and renal cell dysfunction and injury can accomplish crystal retention and formation of stone nidus. Cellular dysfunction can be intrinsic or provoked. Lethal epithelial cellular injury promotes crystal nucleation, aggregation, and retention. Sublethal injury or dysfunctional cells may produce ineffective crystallization modulators and localized areas of supersaturation in the interstitium. The former will affect crystallization in the urine while the latter may cause precipitation in the interstitium and development of Randall's plaques. In addition, dysfunctional cells affect supersaturation, by influencing the excretion of participating ions such as calcium, oxalate, and citrate, and modulating urinary pH and production and excretion of macromolecular promoters and inhibitors of crystallization.
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