nephrolithiasis
Stone type and 24-h urine guide prevention, though much therapy is empiric. Non-contrast CT is the gold-standard diagnostic study. Most stones <5 mm pass spontaneously. Metabolic workup after a first complicated or second stone. Thiazides and dietary measures for calcium stones, alkalinisation for uric acid, complete surgical removal for struvite.
acute presentation
Sudden-onset colicky flank pain radiating to groin, often with nausea/vomiting and haematuria (absent in ~15%). Pain correlates with ureteral obstruction and distension, not stone size.
Workup:
- Non-contrast CT KUB — sensitivity >95%, identifies stone size/location/density and alternative diagnoses; low-dose protocols preferred (equivalent sensitivity, lower radiation). Ultrasound first-line in pregnancy and reasonable initial study in young patients
- Urinalysis — haematuria, signs of infection
- Basic metabolic panel, calcium
- Urine culture if pyuria or fever
Fever + obstructing stone = urological emergency. Urgent decompression (ureteral stent or percutaneous nephrostomy — equivalent outcomes, choice per local expertise) + IV antibiotics. Delay ≥48 h → ~29% increased odds of death; aim for decompression within hours. Delay → urosepsis.
Acute management:
- Analgesia: NSAIDs first-line (e.g. ketorolac 15–30 mg IV, diclofenac 50 mg PO); combine with acetaminophen. Opioid for breakthrough
- IV fluids for hydration — aggressive forced fluids do not accelerate passage
- Medical expulsive therapy: tamsulosin 0.4 mg daily for distal ureteral stones 5–10 mm (modest benefit; NNT ~4–5). Little/no benefit for stones <5 mm
Disposition by stone size:
- <5 mm → >90% pass spontaneously; outpatient with strain, analgesia, urology follow-up
- 5–10 mm → ~50% pass; trial of passage 4–6 weeks with tamsulosin
- >10 mm or persistent obstruction → intervention (ureteroscopy, SWL, or PCNL depending on location/composition)
stone types
| type | radiodensity | urine pH | associations | prevention |
|---|---|---|---|---|
| calcium oxalate (75%) | radio-opaque | variable/acidic | Crohn/ileal resection (enteric hyperoxaluria), primary hyperparathyroidism, medullary sponge kidney | thiazides, low Na/animal protein, normal dietary calcium intake |
| calcium phosphate | radio-opaque | alkaline >6.0 | type I RTA, primary hyperparathyroidism | thiazides, treat underlying cause |
| uric acid (10%) | radiolucent | acidic <5.5 | gout, metabolic syndrome, myeloproliferative disorders, TLS | potassium citrate (target urine pH 6.0–6.5), allopurinol if hyperuricosuric |
| struvite (5%) | radio-opaque (staghorn) | alkaline >7.0 | urease-producing organisms (Proteus, Klebsiella, Pseudomonas) | complete surgical removal, eradicate infection |
| cystine (1%) | faintly opaque | acidic <6.5 | AR cystinuria | high fluid (>3 L/d), alkalinisation (pH >7.0), tiopronin or D-penicillamine if refractory |
Uric acid until proven otherwise. These dissolve with alkalinisation alone — potassium citrate to target urine pH 6.0–6.5. No procedure needed if non-obstructing.
metabolic workup
When: after first complicated stone (requiring intervention, bilateral, solitary kidney, recurrent), any stone in a young patient, or second lifetime stone.
24-hour urine collection (×2, on habitual diet): volume, calcium, oxalate, citrate, uric acid, sodium, pH, creatinine (adequacy check).
Serum: calcium, phosphate, PTH (if hypercalcaemic or hyperparathyroidism suspected — normocalcaemic primary hyperparathyroidism exists), uric acid, bicarbonate.
Stone analysis: send every retrieved stone — composition guides prevention. RCT data do not robustly show that matching drug to specific metabolic abnormality outperforms empiric therapy (thiazides, alkali citrate, allopurinol all reduce calcium stone recurrence), but 24-h urine identifies modifiable risk factors and guides counselling.
| finding | likely stone type | intervention |
|---|---|---|
| hypercalciuria (>7.5 mmol/d) | calcium oxalate/phosphate | hydrochlorothiazide 25 mg or indapamide 1.25–2.5 mg; low sodium diet |
| hyperoxaluria (>0.5 mmol/d; consider primary hyperoxaluria if >0.83 mmol/d) | calcium oxalate | dietary oxalate restriction; normal calcium intake (binds oxalate in gut); treat fat malabsorption |
| hypocitraturia (<1.5 mmol/d) | calcium | potassium citrate 30–60 mEq/d |
| hyperuricosuria (>4.5 mmol/d) | uric acid or calcium | allopurinol 100–300 mg/d |
| low urine volume (<2 L/d) | all types | fluid intake to target UO >2.5 L/d |
Restricting dietary calcium increases intestinal oxalate absorption → more urinary oxalate → more stones. Maintain normal calcium intake (1000–1200 mg/d from diet). Restrict sodium and animal protein instead.
traps
- Radiolucent stone missed on plain X-ray — uric acid and cystine stones are poorly seen on KUB radiograph. Non-contrast CT is the appropriate study.
- Assuming all flank pain + haematuria is renal colic — AAA and renal infarction can mimic. Consider CT with contrast if atypical.
- Ignoring struvite — no medical dissolution. Complete surgical removal required; residual fragments harbour bacteria and regrow.
- Calcium restriction for calcium stones — counterproductive; see dietary calcium callout above.