Clinical meaning
Kidney stones (nephrolithiasis or renal calculi) form when dissolved minerals and salts in the urine crystallise and aggregate into solid masses within the urinary tract. The process begins with supersaturation - when the concentration of stone-forming substances exceeds the capacity of urine to keep them dissolved. Normal urine contains inhibitors of crystallisation (citrate, magnesium, pyrophosphate, glycosaminoglycans), and stones form when the balance between promoters and inhibitors tips toward crystallisation. Four main types of kidney stones exist, each with distinct pathophysiology. Calcium stones (calcium oxalate and calcium phosphate) account for 70-80% of all stones. Calcium oxalate stones are the most common subtype, forming when urinary calcium and oxalate concentrations are elevated. Hypercalciuria can result from increased intestinal absorption, decreased renal reabsorption, or increased bone resorption. Hyperoxaluria occurs with high dietary oxalate intake, inflammatory bowel disease (increased colonic oxalate absorption), or rarely primary hyperoxaluria (genetic enzyme deficiency). Struvite stones (magnesium ammonium phosphate) account for 10-15% and form exclusively in the setting of urinary tract infections with urease-producing organisms (Proteus, Klebsiella, Pseudomonas). Urease splits urea into ammonia and carbon dioxide, alkalinising the urine...