Kidney Stones (Renal Calculi) — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Kidney stones (nephrolithiasis/urolithiasis/renal calculi) are solid crystalline deposits that form within the kidney from supersaturated urine — when concentrations of stone-forming substances exceed their solubility in urine, crystals nucleate, aggregate, and grow into stones. Stones typically form in the renal collecting system (calyces and renal pelvis) and may remain there asymptomatically or pass down the ureter — the narrow muscular tube connecting the kidney to the bladder — causing the excruciating pain of ureteric colic. Kidney stones affect approximately 10-12% of people in high-income countries in their lifetime, with a 50% recurrence rate within 10 years if no preventive measures are taken. The global incidence is increasing, linked to obesity, dietary changes, dehydration, and climate change (increasing ambient temperature increases sweating and urine concentration). The majority (70-80%) of kidney stones are calcium oxalate; approximately 10% are uric acid stones; 5-15% struvite (infection-related); and 1-2% cystine (genetic). Most stones are detected when they obstruct the ureter causing the classic presentation of severe flank pain radiating to the groin (ureteric colic). Stones causing complete ureteric obstruction with infection (obstructed infected kidney) constitute a urological emergency requiring immediate drainage.

Stone formation requires supersaturation of urine with stone-forming ions, with reduced crystallisation inhibitors (citrate, magnesium, Tamm-Horsfall protein). Stone type-specific causes: Calcium oxalate stones (70-80%): hypercalciuria (excessive calcium in urine — from absorptive hypercalciuria from gut, primary hyperparathyroidism, vitamin D toxicity, or renal calcium wasting); hyperoxaluria (excess urine oxalate — from dietary excess, malabsorption in inflammatory bowel disease/short bowel syndrome causing increased gut oxalate absorption — enteric hyperoxaluria); and hypocitraturia (low urinary citrate — the most important crystallisation inhibitor — reduced by metabolic acidosis, diarrhoea, high protein diet, and thiazide use). Uric acid stones (10%): hyperuricosuria (gout, high purine diet); acidic urine pH below 5.5 (the most important risk factor for uric acid crystallisation — uric acid is insoluble in acidic urine; occurs in metabolic syndrome, diabetes, diarrhoea — all cause persistently acidic urine); and low urine volume. Struvite (magnesium ammonium phosphate) stones: urease-producing bacteria (Proteus, Klebsiella, Pseudomonas — split urea to ammonia, raising urine pH above 7 causing supersaturation) — always associated with urinary tract infection; form large 'staghorn' calculi in the renal pelvis. Cystine stones (1-2%): autosomal recessive cystinuria — defective renal tubular reabsorption of cystine, ornithine, lysine, arginine (COLA) — cystine is insoluble and crystallises. General risk factors: chronic dehydration (inadequate fluid intake — single most important risk factor); male sex (2-3x higher prevalence than women); White or South Asian ethnicity; family history; history of previous stones (50% recurrence rate); inflammatory bowel disease and malabsorption; obesity (reduces urinary citrate); type 2 diabetes; metabolic syndrome; urinary tract abnormalities (medullary sponge kidney, horseshoe kidney, ureteropelvic junction obstruction — all cause urine stasis); primary hyperparathyroidism (hypercalcaemia → hypercalciuria); vitamin D supplementation at pharmacological doses; and hot climates (dehydration).

Ureteric colic is classically described as one of the most severe pains experienced by humans. Loin (flank) pain: sudden onset, severe, colicky (waxes and wanes with ureteric peristalsis — not constant like renal abscess), originating in the flank and radiating to the ipsilateral iliac fossa and groin; the stone's position in the ureter determines radiation — upper ureteric stones cause loin and upper abdominal pain; lower ureteric stones cause pain radiating to the scrotum or labia majora and inner thigh (L1 dermatomal distribution); vesicoureteric junction (VUJ) stones cause bladder irritability (dysuria, frequency, urgency) mimicking cystitis. Restlessness: patients with ureteric colic typically cannot find a comfortable position (unlike peritonitis where any movement worsens pain). Nausea and vomiting (prominent — caused by visceral stimulation). Haematuria: macroscopic (visible blood in urine) in 70-90%; microscopic haematuria on dipstick in the remainder — absence does not exclude stones. Fever and rigors in combination with ureteric colic should prompt immediate imaging and treatment — infected obstructed kidney (pyonephrosis) requires emergency drainage. Asymptomatic stones: renal stones can be asymptomatic and discovered incidentally on ultrasound or CT for another indication — these 'silent' stones still require management planning. Staghorn calculi (struvite) may cause recurrent UTIs, haematuria, and gradual renal impairment rather than acute colic.

Non-contrast CT KUB (CT of kidneys, ureters, and bladder): the gold standard investigation for suspected ureteric colic — sensitivity 97%, specificity 96%; identifies stone composition (density in Hounsfield units — HU above 1000 = calcium stone; 500-1000 HU may be uric acid; below 500 = struvite), stone location, size (critical for management), degree of hydronephrosis (obstruction), and alternative diagnoses (appendicitis, AAA, ovarian pathology). Dose-reduction low-dose CT protocols are standard. Ultrasound (renal) with plain X-ray (KUB): ultrasound identifies hydronephrosis and radiopaque stones; KUB X-ray identifies calcium stones (radiopaque); uric acid and cystine stones are radiolucent (not visible on X-ray) — ultrasound + KUB combination has 74-84% sensitivity for stones above 5mm; suitable for pregnant women and children (avoiding radiation) as first-line, with CT if inconclusive. Urine dipstick: haematuria (present in 85-90%); positive nitrites and leucocytes (infection — urgent assessment for obstructed infected kidney). Urine microscopy, culture, and sensitivity: any UTI concurrent with stone requires urgent treatment. Blood tests: serum urea and electrolytes (AKI from obstruction); serum calcium (hypercalcaemia → hyperparathyroidism); uric acid; FBC (leucocytosis if infected); and parathyroid hormone (PTH — if hypercalcaemia). Stone analysis: when stones pass or are retrieved at surgery — infrared spectroscopy or X-ray diffraction identifies stone composition (essential for prevention guidance). Metabolic stone work-up (for recurrent or bilateral stones, or single kidney): 24-hour urine collection for stone risk factors — urine volume, pH, calcium, oxalate, citrate, uric acid, sodium, creatinine — guides targeted prevention.

Management depends on stone size, location, symptoms, obstruction, infection, and patient factors. Acute management of ureteric colic: diclofenac (75mg IM or 100mg PR — NSAID — reduces ureteric muscle spasm and prostaglandin-mediated inflammation; superior to opioids in most studies; contraindicated in AKI, elderly, renal impairment); morphine IV/IM (for breakthrough pain not controlled by NSAIDs); IV fluids for nausea/vomiting; anti-emetics (ondansetron, metoclopramide). Medical expulsive therapy (MET): tamsulosin 0.4mg once daily (alpha-1 blocker — relaxes ureteric smooth muscle — increases spontaneous passage rate for ureteric stones 5-10mm by approximately 44-65% at 4 weeks — particularly effective for distal ureteric stones; EAU guidelines support MET for stones 5-10mm — evidence for stones below 5mm is less certain as most pass spontaneously). Spontaneous stone passage: stones below 5mm: 90% pass spontaneously within 4 weeks; stones 5-10mm: 50% pass; stones above 10mm: rarely pass spontaneously. Surgical intervention (when indicated — persistent obstruction after 4 weeks, pain not controlled, infection, single kidney, bilateral obstruction, stones above 10mm): Ureteroscopy + laser lithotripsy (URS): rigid or flexible ureteroscope inserted through the urethra and bladder into the ureter — holmium laser fragmentation of the stone + extraction with basket — stone-free rate 90-95% for most ureteric stones; standard for ureteric stones; also used for 5-20mm renal stones. Extracorporeal shockwave lithotripsy (ESWL): focused acoustic shockwaves generated outside the body and focused on the stone — fragments stone into small pieces to pass spontaneously; stone-free rate 60-80% for renal stones below 20mm; non-invasive; multiple treatments may be required; contraindicated in pregnancy. Percutaneous nephrolithotomy (PCNL): percutaneous puncture into the kidney under radiological/ultrasound guidance + nephroscope + fragmentation — stone-free rate above 95% for large stones (above 20mm) and staghorn calculi; more invasive (puncture through kidney parenchyma — risk of haemorrhage, 1-5%); gold standard for complex stones. Stenting (JJ ureteric stent): a double-J plastic stent placed from the kidney to bladder (cystoscopically or radiologically) to relieve obstruction urgently (in infected or symptomatic obstruction) and allow elective definitive treatment. Emergency drainage for obstructed infected kidney: urgent percutaneous nephrostomy (PCN — radiological drainage of obstructed kidney — lifesaving in pyonephrosis) or retrograde JJ stent placement; IV broad-spectrum antibiotics immediately.

Acute kidney injury (AKI — complete ureteric obstruction stops glomerular filtration in the affected kidney; a single functioning kidney with a totally obstructing stone can lose significant renal function within 24-48 hours; urgent JJ stent or nephrostomy drainage is required to prevent permanent renal damage). Obstructed infected kidney or pyonephrosis (the most dangerous complication — concurrent ureteric obstruction and bacterial infection creates a rapidly fatal condition if not treated immediately; the infected kidney becomes a pus-filled sac under pressure; mortality without emergency drainage is extremely high; requires percutaneous nephrostomy or retrograde stenting within hours plus IV broad-spectrum antibiotics). Recurrent stone disease (50% recurrence rate within 10 years without prevention — progressive bilateral stone burden can cause bilateral obstruction, bilateral renal scarring, and chronic kidney disease). Ureteric stricture (stone impaction, infection, or surgical trauma during ureteroscopy can cause ureteric scarring and permanent narrowing — creating persistent obstruction after stone clearance requiring subsequent ureteric reconstruction). Sepsis (Gram-negative bacteraemia from urinary tract obstruction and infection — a life-threatening systemic inflammatory response requiring immediate source control by decompression).

Kidney stone recurrence rate is 50% within 10 years without prevention — targeted lifestyle and pharmacological prevention is highly effective. Universal recommendations for all stone types: increase fluid intake to produce urine output of at least 2-2.5 litres per day (the most important single preventive measure — increases urine volume, reducing crystallisation); aim for pale yellow urine throughout the day and night; dietary sodium restriction below 2g/day (reduces urinary calcium excretion); reduce animal protein intake (purine-rich meat increases urinary uric acid; red meat particularly high in purines); maintain healthy BMI; physical activity. Calcium oxalate stone prevention (most common): normal dietary calcium intake (1,000-1,200mg/day — calcium binds oxalate in the gut, reducing absorption; dietary calcium restriction paradoxically increases stone risk); reduce dietary oxalate (avoid excessive oxalate-rich foods — spinach, rhubarb, nuts, chocolate, tea — in patients with documented hyperoxaluria); potassium citrate (15-30 mEq twice daily) — the most important pharmacological intervention for calcium oxalate stones — alkalinises urine, increases citrate excretion, and inhibits crystallisation; hydrochlorothiazide (12.5-25mg daily) reduces urinary calcium in absorptive hypercalciuria. Uric acid stone prevention: alkalinise urine with potassium citrate (target urine pH 6.5-7.0 — uric acid dissolves at higher pH); allopurinol (for hyperuricosuria and gout); dietary purine restriction (reduce organ meats, red meat, shellfish). Struvite: treat and eliminate UTI with urease-producing organisms; complete surgical clearance of stone material (residual infected stone fragments perpetuate infection and stone growth); long-term low-dose antibiotics. Cystine: very high fluid intake (greater than 3.5L/day); alkalinise urine aggressively (target pH above 7.0-7.5); D-penicillamine or tiopronin (chelate cystine — reduce free cystine excretion).

Go to an emergency department immediately for: severe flank or loin pain with fever and rigors (obstructed infected kidney/pyonephrosis — a urological emergency that can cause septic shock and death within hours without drainage); ureteric colic in a single-functioning kidney (immediate risk of AKI from complete obstruction — urological emergency); severe intractable pain not controlled with oral analgesia at home; ureteric colic in a pregnant woman (risk to fetus from untreated obstruction and infection; imaging and management must be expedited); and symptoms suggesting bilateral obstruction (absence of urine output — anuria — or very low urine output from both kidneys). Call your GP or go to A&E for: any first episode of suspected ureteric colic (requires imaging confirmation and analgesia); haematuria with flank pain; frank haematuria without pain (also requires urgent urological evaluation to exclude malignancy); and failure to pass a stone within 4 weeks despite conservative management. After passing a kidney stone: always send passed stones for analysis (stone catcher/sieve or save in a container to bring to clinic); follow up with a urologist or nephrologist for metabolic stone work-up (24-hour urine) and recurrence prevention guidance.