This update reviews salient progress in pathophysiology, diagnosis, and medical management. In absorptive hypercalciuria, bone loss accompanies stone formation in some patients. Potential putative gene (soluble adenylyl cyclase) has been identified. The invariant feature in hypocitraturia is low intracellular pH that alters renal tubular metabolism and reabsorption of citrate. In gouty diathesis, uric acid stones develop from low urinary pH, probably resulting from impaired renal ammonia genesis of acquired insulin resistance. The protection against stone formation, conferred by citrus fruits, depends on the potassium content that determines the amount of alkali load delivered. Animal protein excess such as with the Atkins diet confers an acid load that increases urinary calcium and lowers citrate. Dietary calcium restriction lowers urinary calcium and saturation of calcium oxalate among patients with hypercalciuria, but not in those with normocalciuria. A simplified diagnostic evaluation and management may be used among patients with uncomplicated stone disease in an office setting. A 24-hour urine on a random diet should be collected for a full stone risk analysis. Among patients with hypercalciuria, dietary restriction of calcium and oxalate with indapamide (or thiazide) and potassium citrate is recommended. Among normocalciuric patients, liberal calcium intake and potassium citrate should be beneficial.