Nephrolithiasis

Nephrolithiasis (kidney stones) results from supersaturation of urine with lithogenic solutes that exceeds the capacity of urinary inhibitors to prevent crystallization. Stone formation follows a sequence: nucleation (initial crystal formation when solute concentration exceeds the metastable supersaturation threshold), crystal growth (accretion of additional solute onto the crystal lattice), aggregation (crystals clump together), and retention (crystals anchor to the urothelium, particularly at Randall plaques — subepithelial hydroxyapatite deposits on renal papillae that serve as nidi for calcium oxalate stone formation). Calcium oxalate stones (70-80% of all stones) form when urinary calcium and oxalate concentrations exceed saturation, promoted by hypercalciuria (absorptive, resorptive from hyperparathyroidism, or renal leak), hyperoxaluria (dietary or enteric from fat malabsorption binding calcium in the gut, freeing oxalate for absorption), hypocitraturia (citrate is the primary endogenous inhibitor, chelating urinary calcium and inhibiting crystal growth), and low urine volume. Calcium phosphate stones (brushite, hydroxyapatite) form in alkaline urine (pH greater than 6.5), often associated with distal renal tubular acidosis or primary hyperparathyroidism. Uric acid stones (5-10%) form in persistently acidic urine (pH less than 5.5) because uric acid has a...