Kidney stones: acute colic, passing the stone, and preventing the next one

Kidney stones — what they are and why they hurt

Kidney stones form when minerals in concentrated urine crystallise into hard deposits. Most sit silently in the kidney until a stone enters the ureter, causing acute obstruction. The resulting pain — renal colic — is among the most severe encountered in general practice.

Kidney Health Australia estimates a lifetime stone prevalence of approximately 12% in Australian men and 6% in women, with incidence rising alongside rates of obesity, type 2 diabetes, and dehydration in a hot climate. Without preventive measures, about half of first-time stone-formers will have another episode within ten years.

Stone types vary: calcium oxalate accounts for 70–80% of all stones; calcium phosphate, uric acid, struvite (infection-related), and cystine make up the remainder. Each type has different drivers and different preventive strategies, which is why stone analysis matters after every retrievable episode.

The GP’s role spans rapid triage of acute colic, appropriate imaging and analgesia, deciding who needs emergency intervention, coordinating metabolic workup for recurrent stone-formers, and delivering prevention counselling aligned with current Australian guidance.

A. Core clinical — the AU general-practice framework

Recognising acute renal colic

The history is usually distinctive. Pain begins suddenly in the flank or costovertebral angle, radiates anteriorly and inferiorly toward the groin, ipsilateral testis, or labium majus as the stone progresses distally, and waxes and wanes with ureteric peristalsis. Unlike peritoneal irritation — where the patient lies rigidly still — those with renal colic are restless, unable to settle. Nausea and vomiting are common. Frequency, urgency, and dysuria may emerge when the stone approaches the vesicoureteric junction.

The must-not-miss differentials before attributing pain to stone:

• Ruptured abdominal aortic aneurysm — older male, back or flank pain, haemodynamic instability, pulsatile mass on examination; CT angiography urgently
• Ectopic pregnancy — any reproductive-age woman with flank or pelvic pain; β-hCG is mandatory before proceeding
• Pyelonephritis — fever, costovertebral angle tenderness, pyuria; may coexist with an obstructing stone
• Biliary colic or cholecystitis — right upper quadrant, post-prandial; ultrasound
• Appendicitis — right iliac fossa migration, peritonism on examination; CT
• Testicular torsion — acute scrotal pain referred from a distal ureteric stone; Doppler ultrasound

Investigations

Per eTG Genitourinary and RACGP guidance:

• Urine dipstick — haematuria (absent in ~10–15% of confirmed stones, so its absence does not exclude a stone), leucocytes, nitrites
• β-hCG — mandatory in any reproductive-age woman with flank or abdominal pain
• Urea, electrolytes, creatinine, eGFR — renal function before NSAID administration and for disposition decisions
• FBC, CRP — if infection is clinically suspected
• Calcium, urate, phosphate — first-stone metabolic screen at time of acute presentation
• Non-contrast CT KUB (low-dose) — gold standard; sensitivity >97%, specificity >95%; defines stone size, location, density in Hounsfield units, and degree of hydronephrosis; standard of care in non-pregnant adults
• Renal tract ultrasound — first-line imaging in pregnancy and young patients minimising radiation; detects hydronephrosis reliably but has lower sensitivity for ureteric stones than CT

Acute pain management

eTG and AMH both position NSAIDs as first-line analgesia for renal colic, provided eGFR is ≥45–60 mL/min and there is no peptic ulcer disease, significant cardiovascular contraindication, or allergy:

• Diclofenac 75 mg intramuscularly or 50 mg orally or rectally; or ketorolac 10–30 mg intravenously in the emergency setting
• Paracetamol 1 g as adjunct
• Antiemetic: metoclopramide 10 mg intravenously or intramuscularly

Opioid analgesia (morphine 0.1 mg/kg IV titrated, or oxycodone 5–10 mg orally) is appropriate when NSAIDs are contraindicated or insufficient — they are the backup, not the first choice.

Forced intravenous fluid administration is not recommended — there is no evidence of benefit and it may worsen pain by increasing intraluminal pressure proximal to the obstruction. Cautious rehydration addresses dehydration from vomiting.

Medical expulsive therapy. Tamsulosin 400 mcg daily for up to four weeks is used selectively for distal ureteric stones 5–10 mm in size. The SUSPEND trial (NEJM 2015) was negative for the primary endpoint. Subsequent Cochrane meta-analyses suggest a modest benefit for stones ≥5 mm in the distal ureter. Use is selective rather than routine; counsel patients that benefit is marginal and the medication is off-label for this indication on the PBS.

Disposition. Stones under 5 mm in a single non-obstructed, non-infected kidney with controlled pain and adequate oral intake can be managed as outpatients with GP follow-up and repeat imaging at 4–6 weeks. Hospital admission or urgent urology referral is indicated for: fever with stone (infected obstruction — urological emergency), acute kidney injury, intractable pain, bilateral obstruction, or a solitary functioning kidney.

B. Stone types and the evidence for prevention

The calcium oxalate majority

Calcium oxalate stones (70–80%) are driven by low urinary volume, hypercalciuria, hyperoxaluria, and low urinary citrate — all of which are modifiable. The single most effective intervention is increasing fluid intake to produce at least 2 litres of urine per day, consistently supported across observational cohorts and endorsed by NHMRC and Kidney Health Australia.

Counterintuitively, dietary calcium restriction increases stone risk. Calcium binds oxalate in the gut, reducing intestinal oxalate absorption and urinary oxalate excretion. Patients should maintain normal dietary calcium (~1000–1200 mg/day) rather than restricting it. Calcium supplements taken away from meals may slightly increase urinary oxalate and are worth reviewing.

Additional dietary targets for calcium oxalate stone prevention:

• Reduce sodium to under 2.3 g/day — this lowers urinary calcium excretion
• Moderate animal protein — high purine and acid load increases both calciuria and uricosuria
• Limit excessive oxalate foods (spinach, rhubarb, beetroot, almonds, dark chocolate in very large amounts) — moderation, not elimination
• Avoid vitamin C supplementation >500 mg/day — high-dose vitamin C metabolises to oxalate

Potassium citrate supplementation is indicated for hypocitraturic recurrent stone-formers; it alkalinises the urine and directly inhibits calcium oxalate crystal formation. Thiazide diuretics (indapamide, hydrochlorothiazide) reduce urinary calcium and halve recurrence in hypercalciuric patients.

Uric acid and other stone types

Uric acid stones form in acidic, concentrated urine — particularly in patients with gout, type 2 diabetes, and high purine intake. Treatment targets urinary alkalinisation (potassium citrate to maintain pH 6.5–7.0) and, where hyperuricaemia is present, allopurinol. Unlike calcium oxalate stones, uric acid stones are radiolucent on plain X-ray — only visible on CT.

Struvite stones (5–10%) are infection-related, driven by urease-producing organisms (Proteus, Klebsiella). They have a tendency to form staghorn calculi. Management requires eradication of the underlying infection plus surgical removal of the stone, which acts as a persistent nidus.

Metabolic workup for recurrent stone-formers

Two or more stone episodes, a positive family history, young age at first stone, or atypical stone composition warrant metabolic investigation. USANZ recommends:

• 24-hour urine collection ×2 — calcium, oxalate, citrate, urate, sodium, creatinine, urine volume
• Serum PTH if hypercalcaemia is present or calcium stones are recurrent
• Spot urine cystine in young patients with recurrent stones
• Fasting serum biochemistry — calcium, urate, bicarbonate, eGFR

C. Surgical intervention — what the options mean

When stones are too large to pass spontaneously or conservative management fails, USANZ specialist urologists advise on intervention:

• Extracorporeal shock-wave lithotripsy (ESWL) — non-invasive outpatient procedure; most suited to renal or proximal ureteric stones under 2 cm with favourable HU density; moderate stone-free rate; may require repeat sessions
• Ureteroscopy with laser lithotripsy (URS) — most widely used for ureteric stones; high stone-free rate; typically performed under general anaesthesia with a temporary ureteric stent
• Percutaneous nephrolithotomy (PCNL) — for stones over 2 cm or staghorn calculi; inpatient procedure; highest stone-free rate for large or complex stones
• Emergency drainage — obstructed infected stone requires immediate ureteric stent or percutaneous nephrostomy for decompression before any definitive stone treatment; this is a surgical emergency where sepsis can develop within hours

D. Australian operations

MBS items most relevant in general practice:

Standard GP consultations (MBS items 23, 36, 44) cover the initial acute assessment, analgesia, investigation ordering, and follow-up review. For recurrent stone-formers with comorbid chronic conditions such as CKD, type 2 diabetes, or gout, the GP Chronic Condition Management Plan (GPCCMP — items 965 and 967, replacing the former GPMP/TCA structure from 1 July 2025) enables referral to a dietitian under Medicare for stone-prevention counselling. Multidisciplinary case conferencing (item 707) is available for complex cases coordinating with urology, nephrology, and dietetics.

Imaging: low-dose CT KUB and renal ultrasound are Medicare-rebatable under relevant MBS items when clinically indicated. KUB plain X-ray (item 58100) has limited utility — uric acid stones are radiolucent and most ureteric stones are not reliably seen.

Pathology: urea and electrolytes, FBC, calcium, urate, and 24-hour urine collections (MBS items in the 66500 and 66536 ranges) are all rebatable as part of acute workup and ongoing metabolic monitoring.

PBS medications:

Diclofenac, ibuprofen, and naproxen are general schedule. Tamsulosin is general schedule for BPH; off-label for medical expulsive therapy. Allopurinol is general schedule. Indapamide and hydrochlorothiazide are general schedule. Potassium citrate (Urocit-K) is not PBS-listed; compounded preparations are available privately for prevention in hypocitraturic patients.

Opioids prescribed for acute stone pain attract Real Time Prescription Monitoring (RTPM) obligations; document rationale and liaise with the patient’s usual GP.

Telehealth is appropriate for stone-prevention counselling, 24-hour urine result review, and ongoing monitoring once an existing-relationship rule is met.

E. Special populations

Pregnancy. Renal colic in pregnancy is managed conservatively wherever possible. Renal tract ultrasound is the preferred first-line imaging modality (no ionising radiation). NSAIDs are avoided after 20 weeks’ gestation because of risks of premature ductus arteriosus closure and oligohydramnios; paracetamol and opioids are used instead. Any stone causing obstruction or infection in a pregnant patient requires urgent urology input.

Paediatric patients. Stones in children are uncommon in Australia but increasing in frequency alongside childhood obesity and dietary changes. Metabolic workup is essential at any age of presentation. Cystinuria, primary hyperoxaluria, and distal renal tubular acidosis should be excluded in young patients with recurrent disease.

Single functioning kidney. Any stone event in a patient with a solitary functioning kidney warrants immediate urological involvement regardless of stone size, as obstruction threatens the only source of renal clearance.

Occupational and climate risk. Mining workers, outdoor labourers in northern and remote Australia, and people with limited access to water during working hours have significantly elevated stone risk from occupational dehydration. Stone-prevention counselling must account for realistic fluid replacement strategies in hot-climate occupations.

Older adults. Thiazide diuretics used for stone prevention require monitoring for hypokalaemia, hyponatraemia, and gout exacerbation in older patients with multiple comorbidities. NSAID use for acute pain is more hazardous with declining eGFR — check renal function at every stone event.

When to escalate

Call 000 or send to emergency immediately for: fever with flank pain or rigors (obstructed infected stone), haemodynamic instability, acute kidney injury at presentation, bilateral ureteric obstruction, or a known single functioning kidney with any obstruction.

Same-week urology referral is appropriate for stones 5–10 mm not passing after 4 weeks, any stone larger than 10 mm, stones in pregnancy, and recurrent disease in young patients or unusual stone types.

Routine urology referral is appropriate for complex stone anatomy, failed metabolic prevention, or stones requiring surveillance imaging.

What this article is and is not

This is general health information drawn from eTG, AMH, RACGP, Kidney Health Australia, USANZ, and NHMRC guidance. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about imaging, analgesia, surgical referral, and long-term prevention are made with your own GP and treating clinicians.

For AU consumer resources: Kidney Health Australia, HealthDirect — Kidney stones, and Better Health Channel.

For fever with flank pain or severe pain that does not settle — this is a potential emergency. Present to an emergency department or call 000.

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Sources cited

1. RACGP — Acute flank pain and renal colic
2. Therapeutic Guidelines (eTG) — Genitourinary/Renal
3. Australian Medicines Handbook
4. NHMRC — Dietary guidelines
5. Kidney Health Australia — Kidney stones
6. USANZ — Urolithiasis position statement
7. EAU Guidelines — Urolithiasis
8. Cochrane — Alpha-blockers for ureteric stones
9. HealthDirect — Kidney stones
10. Better Health Channel — Kidney stones