Kidney Stones — Causes, Renal Colic, ESWL & Prevention Guide — Symptoms, Causes & Treatment | MyMedicPlus

Kidney stones (nephrolithiasis) are hard crystalline deposits forming within the kidneys from supersaturated urine when mineral concentrations exceed solubility. They affect approximately 11% of men and 6% of women in their lifetime in Western populations, with incidence rising worldwide, likely driven by increasing obesity, diabetes, and dietary changes. Most stones (70-80%) are calcium oxalate; others include calcium phosphate (15%), uric acid (10%), struvite/infection stones (5%), and cystine (rare). Stone size ranges from a sand grain to several centimetres. Small stones (under 5 mm) pass spontaneously in approximately 68% of cases; larger stones require urological intervention. The classic presentation is renal colic — one of medicine's most severe acute pain syndromes, occurring as the stone passes from the kidney into the ureter and migrates towards the bladder. Without preventive measures, the lifetime recurrence rate is approximately 50% within 10 years of the first episode.

Dehydration — concentrated urine with low urine output (under 1.5 litres/day) — is the most important modifiable risk factor. Dietary: high sodium intake increases urinary calcium excretion; excessive animal protein raises urinary uric acid and oxalate; high oxalate foods (spinach, nuts, chocolate, rhubarb, tea) increase calcium oxalate supersaturation. Hypercalciuria (excess urinary calcium): primary hyperparathyroidism, vitamin D excess, immobilisation. Hyperoxaluria: inflammatory bowel disease, small bowel resection, fat malabsorption (fat binds calcium in the gut, leaving oxalate free to be absorbed). Hyperuricaemia: gout, metabolic syndrome, high purine diet — causes uric acid stones; urine pH below 5.5 promotes uric acid crystallisation. Infection with urease-producing organisms (Proteus, Klebsiella, Pseudomonas) raises urinary pH and produces struvite (magnesium ammonium phosphate) and staghorn calculi. Cystinuria (autosomal recessive): cystine stones — rare but recurrent. Hypocitraturia: low urinary citrate (which normally inhibits stone formation) — occurs with metabolic acidosis, thiazides, hypokalaemia. Family history, male sex, obesity, diabetes, and a hot climate are additional risk factors.

Renal colic is the classical presentation: sudden, severe pain originating in the loin/flank, radiating in a wave-like pattern to the groin, labia, or testicle (following the ureter), typically described as the most severe pain ever experienced; it comes in waves and does not resolve with positional changes (differentiating it from musculoskeletal pain). Associated features include nausea and vomiting (from ureteric-renal reflex); microscopic or visible haematuria in approximately 90% of cases; urinary frequency, urgency, and dysuria when the stone reaches the vesico-ureteric junction (VUJ); and lower abdominal or urethral pain. Large renal calculi may be completely silent — including staghorn calculi that can silently destroy renal function. Fever with renal colic is a medical emergency — it indicates infected obstructed kidney (pyonephrosis) requiring immediate drainage regardless of the patient's clinical appearance, as urosepsis can develop rapidly.

Non-contrast CT kidneys-ureters-bladder (CT KUB): the gold standard — detects all stone types (including uric acid and cystine, which are radiolucent on X-ray), with sensitivity 96% and specificity 99%; demonstrates stone size, location, hydronephrosis, and perinephric fat stranding (severity of obstruction). Renal ultrasound: avoids radiation — detects hydronephrosis and larger stones, but less sensitive for ureteric stones (particularly mid-ureter). Used first-line in pregnancy and children. Intravenous urography (IVU): largely superseded by CT KUB. Plain abdominal X-ray (KUB): detects radio-opaque (calcium-containing) stones — misses uric acid and cystine stones. Urinalysis: dipstick haematuria (90%); urine pH (acid: uric acid stones; alkaline: struvite); urine culture. Blood: creatinine, eGFR, calcium, urate, bicarbonate, FBC (leucocytosis suggests infection). 24-hour urine metabolic collection: the definitive test for stone prevention — measures calcium, oxalate, uric acid, citrate, sodium, and urine volume; performed after the second stone episode or in high-risk patients.

Pain management: NSAIDs (diclofenac 75 mg IM/IV or oral) are first-line — superior to opioids for renal colic (reduce ureteral smooth muscle spasm); combine with an antiemetic (metoclopramide or ondansetron). Opioids (morphine) for severe pain or NSAID contraindication. Medical expulsive therapy (MET): alpha-blockers (tamsulosin 0.4 mg daily) facilitate passage of stones 5-10 mm in the lower ureter by relaxing ureteral smooth muscle — reduces time to spontaneous passage and need for intervention. Stones under 5 mm: 68% pass spontaneously; MET recommended. Stones 5-10 mm: MET plus monitoring; ureteroscopy if not passed within 4 weeks. Indications for surgical intervention: stones over 10 mm; failure to pass after 4 weeks; obstructed infected kidney (pyonephrosis — emergency nephrostomy or ureteric stent); solitary kidney; intractable symptoms. Extracorporeal shock wave lithotripsy (ESWL): non-invasive fragmentation by focused ultrasonic energy — first-line for renal stones under 20 mm; requires stone-free follow-up. Ureteroscopy (URS) with holmium:YAG laser lithotripsy: the most effective single-treatment for ureteric stones — day-case procedure; stone-free rate over 90%. Percutaneous nephrolithotomy (PCNL): for large stones (over 20 mm) or staghorn calculi — higher stone-free rate but more invasive. Uric acid stone dissolution: oral alkalinisation with potassium citrate (target urinary pH 6.5-7.0) dissolves uric acid stones non-invasively.

Obstructive nephropathy: prolonged ureteral obstruction causes irreversible renal parenchymal damage and chronic kidney disease — complete bilateral obstruction causes acute kidney injury within hours requiring emergency decompression. Infected obstructed kidney (pyonephrosis): infected urine under pressure with systemic sepsis — a urological emergency requiring emergency drainage (nephrostomy or ureteric stent) regardless of antibiotic therapy alone; mortality without drainage is high. Urosepsis: gram-negative sepsis from obstructed infected kidney causing septic shock with 20-40% mortality if not treated urgently. Chronic kidney disease: from recurrent stone episodes, particularly bilateral, or obstructing the only functional kidney. Staghorn calculi (struvite): if untreated, can destroy the entire ipsilateral kidney, causing xanthogranulomatous pyelonephritis. Haematuria causing significant anaemia in rare cases of prolonged heavy haematuria.

High fluid intake: target urine output of 2-2.5 litres daily (urine should appear pale yellow); increase intake in hot weather, after exercise, and during illness. Dietary modification: reduce sodium below 2.3 g/day (reduces urinary calcium excretion); reduce animal protein below 80 g/day (reduces oxalate, calcium, and uric acid excretion); maintain adequate dietary calcium intake (1000-1200 mg/day from food sources — dietary calcium binds intestinal oxalate, reducing its absorption; calcium supplements, however, may increase risk if taken between meals). Reduce high-oxalate foods. Pharmacological prevention based on metabolic work-up: thiazide diuretics (hydrochlorothiazide or indapamide) for hypercalciuria; allopurinol for hyperuricaemia and uric acid stones; potassium citrate for hypocitraturia, calcium oxalate stones, and uric acid stones (raises urinary citrate and pH). Cystine stones: very high fluid intake (3-4 litres/day), alkalinisation, tiopronin or D-penicillamine. Annual ultrasound surveillance for established stone-formers to monitor for subclinical growth.

Attend A&E immediately for: fever with loin pain or renal colic (infected obstructed kidney — a urological emergency requiring urgent decompression; antibiotics alone are insufficient); uncontrolled pain despite analgesia; persistent vomiting causing dehydration; inability to void; renal colic in a patient with a solitary kidney; or any new obstruction in a transplant kidney. See a GP or attend urgent care for: first-ever episode of suspected renal colic; visible blood in urine; or urinary symptoms not resolving within 24-48 hours. All patients with a first kidney stone should be referred for metabolic workup (24-hour urine) and urged to hydrate adequately, as the 50% recurrence rate is substantially reducible with targeted prevention.