Nephrolithiasis

Nephrolithiasis is the formation of solid mineral calculi (stones) within the kidney. Stones develop when urine becomes supersaturated with stone-forming substances — most often because of low urine volume from inadequate fluid intake — allowing crystals to precipitate, aggregate, and grow.

Stone composition drives the clinical picture. Calcium oxalate stones are by far the most common and are radiopaque on imaging. Struvite (ammonium magnesium phosphate) stones form in alkaline urine infected with urease-producing bacteria such as Proteus and can grow into large staghorn calculi. Uric acid stones form in acidic urine, are radiolucent on plain X-ray, and associate with gout and high cell turnover. Cystine stones occur in the inherited disorder cystinuria, classically in young patients with hexagonal urinary crystals.

The classic presentation is renal colic: sudden, severe, crampy flank pain that waxes and wanes and radiates toward the groin as the stone moves down the ureter, accompanied by hematuria (visible or microscopic), nausea, and restlessness. Stones obstruct most often at narrow points such as the ureteropelvic junction, the pelvic brim, and the ureterovesical junction; persistent obstruction risks hydronephrosis and infection. Small stones usually pass with hydration and analgesia, while larger ones may require lithotripsy or urologic intervention, and prevention centers on high fluid intake.

The USMLE Step 1 tests nephrolithiasis in renal pathology: matching stone types to urine pH, radiographic appearance, crystal shape, and predisposing conditions. It also appears in pharmacology contexts, since drugs such as the protease inhibitor indinavir are classic causes of medication-induced stones.