Lucan · Conditions

Renal calculi

Australian guidance: CARI Kidney Stones + RACGP

1. Definition and epidemiology

Renal calculi (urolithiasis, nephrolithiasis) are crystalline mineral deposits forming within the renal collecting system, capable of migrating into the ureter and causing obstruction. Australian incidence data are limited; one Melbourne tertiary emergency department reported acute symptomatic urolithiasis at 6.7 per 1,000 presentations, and New Zealand data suggest incident rates of 85 to 131 per 100,000 per year. Seasonal variation is well documented, with warmer climates such as northern Australia and the Middle East carrying higher incidence, reflecting the role of dehydration and heat exposure in stone formation.

2. Pathophysiology

Stone formation begins with supersaturation of urine with stone-forming solutes, leading to nucleation and crystal growth (Robbins Ch 20). The commonest stone type is calcium oxalate (approximately 75% of stones), followed by calcium phosphate, uric acid, struvite, and cystine. Supersaturation arises from reduced urinary volume, elevated excretion of calcium (hypercalciuria), oxalate (hyperoxaluria), or uric acid (hyperuricosuria), or from deficiency of inhibitors such as citrate and magnesium. Low urine pH favours uric acid crystallisation because uric acid is insoluble below pH 5.5. Struvite stones form exclusively in the context of urease-producing organisms (Proteus, Klebsiella) that alkalinise urine and drive magnesium ammonium phosphate precipitation. Brushite (calcium phosphate) stones carry a particularly high recurrence burden due to stone density and solidity. Genetic predispositions including cystinuria, distal renal tubular acidosis, and primary hyperoxaluria create monogenic stone phenotypes that warrant targeted evaluation.

3. Clinical presentation and diagnostic criteria

Acute ureteric colic presents as severe, colicky, unilateral loin pain radiating to the groin, genitalia, or inner thigh, often accompanied by nausea, vomiting, and restlessness. The pain typically waxes and wanes as the stone migrates. Haematuria (macroscopic or microscopic) is present in up to 90% of cases but is not diagnostic. Obstructing stones may cause complete obstruction with ipsilateral hydronephrosis, and superimposed infection (pyonephrosis) is a urological emergency signalled by fever, rigors, and sepsis. Asymptomatic stones are increasingly detected incidentally on imaging performed for other indications; the majority remain asymptomatic. Spontaneous passage is strongly predicted by stone size: 87% of 1 mm stones pass spontaneously versus 27% of 10 mm stones.

4. Investigations and AU-specific cutoffs

First-line imaging: CARI Guidelines (Version 11, July 2025) issue a strong recommendation (high certainty) for low-dose non-contrast computed tomography (CT) of the kidneys, ureters, and bladder (KUB) as first-line imaging for adults presenting with acute abdominal, flank, or loin pain suspicious for kidney stones. Low-dose CT has 99% receiver operator curve accuracy compared to intravenous urogram. Ultrasound is conditionally recommended for recurrent uncomplicated stones (no infection, self-limiting pain, non-obstructive) and is strongly preferred in pregnancy and children to avoid radiation. For recurrent stone patients, repeated CT is discouraged given cumulative radiation risk (median 17.2 mSv per 6-month follow-up in one multicentre RCT). Urine should be strained for 48 hours after an acute episode to capture stone material for composition analysis.

Metabolic evaluation applies to all people with kidney stones:

Basic (all patients): serum bicarbonate, calcium, chloride, creatinine, liver function tests, parathyroid hormone, phosphate, potassium, sodium, urate, urea; midstream urine for microscopy, culture, and pH (measured with a pH meter rather than dipstick, as dipsticks are inaccurate at higher values).

Comprehensive (recurrent stones, multiple stones, high recurrence risk, or solitary kidney): two 24-hour urine collections measuring calcium, citrate, creatinine, magnesium, oxalate, pH, phosphate, potassium, sodium, urea, uric acid, and urine volume. Two collections are preferred over one to reduce variability; 32% of single-collection parameters differ by more than one standard deviation from paired means. Collections should be deferred until the acute episode has resolved and the patient has returned to their usual dietary environment. MBS item 66590 (calculus analysis) costs approximately $30.60 (October 2023 data).

Stone composition analysis is recommended for all recurrent stone formers (strong recommendation, CARI Guidelines); infrared spectroscopy is preferred over chemical analysis in Australian laboratories due to lower error rates (1 to 5% versus greater than 10% for common substances).

5. Management

Acute phase: analgesia is the immediate priority; NSAIDs (ibuprofen 400 mg orally or diclofenac 75 mg intramuscularly) are first-line where renal function permits, with opioids as adjuncts. Adequate hydration supports passage but forced high-volume fluids have not been shown to accelerate stone passage. Alpha-1 blockers (tamsulosin 400 micrograms daily) are used as medical expulsive therapy for distal ureteric stones of 5 to 10 mm to increase spontaneous passage rates, though evidence is of moderate quality.

Intervention thresholds: stones less than 4 mm have a high likelihood of spontaneous passage (38 to 71%) and can be managed conservatively with analgesia and close follow-up. Stones greater than 10 mm, stones causing complete obstruction, stones with concurrent infection, or stones in a solitary kidney require urgent urological referral. Intervention options include ureteroscopy with laser lithotripsy, extracorporeal shock wave lithotripsy (ESWL), and percutaneous nephrolithotomy (PCNL) for large or staghorn calculi.

Preventive management is guided by metabolic evaluation results. All patients benefit from fluid intake targeting urine output of at least 2 to 2.5 litres per day. Dietary calcium intake should be maintained at normal levels (approximately 1,000 mg per day) because restricting dietary calcium paradoxically increases oxalate absorption and stone risk. High oxalate foods (spinach, nuts, chocolate) and high sodium intake should be limited. Animal protein restriction reduces acid load and uricosuria.

6. Pharmacology and AU PBS notes

Thiazide diuretics (hydrochlorothiazide 25 mg daily or indapamide 1.25 to 2.5 mg daily) reduce urinary calcium excretion and are first-line medical prophylaxis for recurrent calcium oxalate stones with hypercalciuria. Available on PBS for hypertension; stone prophylaxis use may be off-label in some contexts.

Potassium citrate (Urocit-K, various generics; 20 to 60 mEq per day in divided doses) alkalinises urine and raises urinary citrate, inhibiting calcium oxalate and uric acid crystallisation. It is first-line for uric acid stones and used adjunctively for hypocitraturic calcium stones. Not currently PBS-listed for stone prophylaxis; available as a private prescription.

Allopurinol (100 to 300 mg daily) reduces uric acid production and is indicated for recurrent uric acid or calcium oxalate stones with hyperuricosuria. PBS-listed (Streamlined Authority code 4190) for gout; stone prophylaxis indications require GP or specialist initiation.

Acetohydroxamic acid is used for struvite stones secondary to urease-producing bacteria; rarely used in Australian practice and not PBS-listed. Appropriate antibiotic treatment of causative organisms is the primary approach.

Cystinuria is managed with high fluid intake, urine alkalinisation with potassium citrate, and tiopronin or D-penicillamine in refractory cases.

7. Complications and monitoring

Acute complications include ureteric obstruction with post-renal acute kidney injury, urinary tract infection progressing to pyelonephritis or urosepsis, and pyonephrosis requiring emergency drainage. Chronic sequelae of recurrent obstructive stones include progressive chronic kidney disease from tubular atrophy and interstitial fibrosis (Robbins Ch 20). Staghorn calculi composed of struvite can fill the entire renal pelvis and cause progressive renal destruction without adequate treatment.

Surveillance after a first stone event should include repeat metabolic evaluation if stone recurrence occurs. 24-hour urine collection should be repeated after any change in preventive treatment to assess response, and should not be delayed for stent removal or other urological procedures. Renal function (serum creatinine and estimated glomerular filtration rate) should be monitored annually in patients with recurrent stone disease or known chronic kidney disease. Parathyroid hormone should be checked in conjunction with serum calcium to exclude primary hyperparathyroidism as an underlying cause in any patient with hypercalciuria. Imaging surveillance interval is guided by stone burden; most patients with a single passed stone and no metabolic abnormality do not require routine annual imaging.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.