Kidney stones form when the urine contains too much crystal-forming substances such as calcium oxalate, calcium phosphate, or uric acid, and the urine volume is too low to dilute these substances. The process begins with supersaturation of the urine, leading to the nucleation (initial crystal formation), growth, and aggregation of crystals. These crystals can then develop into stones. Several factors contribute to stone formation, including genetics, diet, low fluid intake, certain medical conditions, urinary pH imbalances, and the presence or absence of natural inhibitors of crystal formation in the urine. Specifically, kidney stones often start forming when urine becomes supersaturated with calcium salts or uric acid. Crystals form either through homogeneous nucleation (in liquid) or faster heterogeneous nucleation (on solid surfaces like kidney tissue). Randall’s plaques, calcium phosphate deposits in the kidney, can serve as a nidus for stone growth. Urease- producing bacteria in infections can also raise urinary pH, promoting struvite stone formation. Normally, urine contains inhibitors like citrate that prevent crystals from sticking and growing, but when these are low, stones form more easily. Kidney stones tend to form when urine is either too acidic or too alkaline, depending on the stone type.
In summary, kidney stones form due to a complex interplay of high concentrations of stone-forming chemicals in urine, low urine volume, pH imbalances, and lack of natural inhibitors against crystal aggregation.
