Renal or ureteric colic - acute

Acute renal or ureteric colic is a clinical syndrome of sudden, severe unilateral loin/flank pain caused by a urinary stone moving into, or obstructing, the ureter. It is the painful presentation of urolithiasis and is typically colicky, may radiate to the groin/testicle or labia, and is frequently associated with nausea, vomiting, and haematuria.

Most stones form in the kidney when urine becomes supersaturated (commonly with calcium oxalate, less often calcium phosphate, uric acid, struvite, or cystine), allowing crystal nucleation, growth, and aggregation. Pain begins when a stone causes partial or complete ureteric obstruction: luminal pressure rises, ureteric wall tension increases, and prostaglandin-mediated vasodilation/diuresis further elevates intrarenal pressure. Ureteric smooth-muscle spasm, hyperperistalsis, mucosal oedema, and local irritation amplify nociception. Obstruction commonly occurs at three narrowing points (pelvi-ureteric junction, crossing of iliac vessels, vesico-ureteric junction). If obstruction persists, GFR in the affected unit falls; prolonged obstruction (beyond ~48 hours) risks permanent renal damage, and superadded infection can progress to pyonephrosis and sepsis. See Figure: anatomical ureteric narrowing points (PUJ, iliac crossing, VUJ).

• Male sex (historically ~2-3:1, though gap is narrowing)
• Peak incidence age 40-50 years
• Low fluid intake/chronic dehydration and hot ambient climates
• Diet high in sodium, animal protein, oxalate, or urate
• Obesity and metabolic syndrome associations (including low urine pH)
• Family history of stone disease
• Previous stone episode (high recurrence risk)
• Urinary tract anatomical abnormalities (e. g, UPJ obstruction, medullary sponge kidney, reflux)
• GI malabsorption states (e. g, Crohn disease, bowel resection, bariatric surgery, enteric hyperoxaluria)
• Metabolic/systemic disease (e. g, hyperparathyroidism, gout, renal tubular acidosis, diabetes, hypertension)
• Genetic disorders (e. g, cystinuria, primary hyperoxaluria)
• Drug exposures linked to stones (e. g, topiramate, acetazolamide, loop diuretics, high-dose vitamin C; crystallizing drugs such as indinavir, triamterene, sulfonamides)

• Persistent urinary obstruction causing reduced GFR and possible irreversible renal damage
• Obstructive pyelonephritis/pyonephrosis with risk of life-threatening urosepsis
• Acute kidney injury (especially with bilateral obstruction or solitary kidney)
• High recurrence burden of future stones
• Association with long-term CKD risk
• Rare spontaneous calyceal rupture and urinoma

Spontaneous passage is common but strongly size- and site-dependent: roughly two-thirds pass overall, with higher passage rates for distal and smaller stones (<5 mm). Mean passage time is around 2-3 weeks. Recurrence is frequent (about 50% by 5 years, up to 80% by 10 years), so secondary prevention and stone analysis are key after the acute episode.