Nephrolithiasis — Viva Defence

Long case viva — enteric hyperoxaluria from Crohn disease

Candidate's opening statement (SASPOP)

"Doctor, my patient is a 48-year-old man with Crohn disease and a prior terminal ileal resection, who has had four episodes of calcium oxalate nephrolithiasis in six years. His problems are: enteric hyperoxaluria from fat malabsorption (24-hour urine oxalate 0.9 mmol per day), hypocitraturia from chronic diarrhoea (citrate 1.2 mmol per day), low urine volume (1.2 L per day), and a counterproductive low-calcium diet that is worsening his oxalate absorption. The priority is to correct the metabolic abnormalities with targeted dietary and pharmacological therapy to prevent further stone recurrence, which can be reduced by 50 to 80 per cent with sustained adherence." ^[1]

Problem list

1. Recurrent calcium oxalate nephrolithiasis — four episodes in six years
2. Enteric hyperoxaluria from Crohn disease with ileal resection (fat malabsorption)
3. Hypocitraturia from chronic diarrhoea and metabolic acidosis
4. Low urine volume from chronic diarrhoea
5. Low-calcium diet (500 mg per day) — actively harmful, increasing oxalate absorption
6. Crohn disease — the underlying driver, requiring optimisation ^[1]

Integrated management plan

Dietary modification. Increase fluid intake to produce above 2.5 L of urine per day (given his diarrhoeal losses, this will require 3 to 4 L intake). Correct the low-calcium diet — increase to 1000 to 1200 mg per day, taken with meals so that calcium binds intestinal oxalate. The Borghi trial proved that normal calcium with reduced sodium and protein halves stone recurrence compared with low calcium ^[2]. Add a low-oxalate diet (restrict spinach, nuts, chocolate, tea) and a low-fat diet to reduce the fatty acids that saponify calcium.

Pharmacotherapy. Potassium citrate 10 mEq twice daily, titrated to urine pH 6.5 to 7.0 — this addresses both the hypocitraturia and the metabolic acidosis from chronic diarrhoea ^[5]. Oral calcium carbonate 500 to 1000 mg with each main meal to bind intestinal oxalate. Cholestyramine for refractory hyperoxaluria (binds bile acids and fatty acids so less calcium is saponified).

Not indicated. Thiazide diuretics — his urinary calcium is normal. Thiazides are for hypercalciuria, not hyperoxaluria. ^[1]

Underlying disease. Optimise the Crohn disease management to reduce diarrhoea and fat malabsorption. ^[1]

Follow-up. Annual 24-hour urine re-evaluation to confirm the biochemistry has normalised. The goal is not just prescribing therapy but confirming it works. ^[1]

Examiner probing questions

Examiner: "Why does a low-calcium diet increase stone risk in this patient?" ^[1]

Dietary calcium normally binds intestinal oxalate in the gut lumen, forming insoluble calcium oxalate that is excreted in the stool. When calcium intake is low, or when fat malabsorption saponifies the available calcium (as in Crohn disease), free oxalate is absorbed from the colon into the portal circulation and excreted by the kidney, producing hyperoxaluria. A low-calcium diet therefore increases oxalate absorption and urinary oxalate, which is the primary driver of calcium oxalate stone formation. The Borghi 2002 NEJM trial proved this: men with hypercalciuria on a normal-calcium, low-sodium, low-protein diet had half the recurrence rate of those on a low-calcium diet (relative risk 0.49) ^[2].

Examiner: "How would you manage this patient's acute renal colic if he presents to the emergency department?" ^[1]

NSAIDs are first-line — diclofenac 75 mg intramuscularly or intravenously, which reduces prostaglandin-mediated ureteric inflammation and pain. I would check his renal function first, as patients with chronic diarrhoea may be volume-depleted and NSAIDs can worsen AKI. If NSAIDs are contraindicated, I would use morphine. Non-contrast CT KUB confirms the stone. For a stone below 5 mm, expectant management is appropriate. For 5 to 10 mm distal ureteric stones, I would consider tamsulosin — the SUSPEND trial showed no overall benefit ^[4], but the Hollingsworth meta-analysis suggested modest benefit for larger distal stones ^[6]. For stones above 10 mm, intervention is needed (ESWL, ureteroscopy, or PCNL depending on size and location). The critical emergency to recognise is obstructive pyelonephritis — fever with an obstructing stone requires urgent decompression, not antibiotics alone.

Examiner: "What imaging would you use in this patient, and when would you use ultrasound?" ^[1]

Non-contrast CT KUB is the gold standard — it detects all stone types except indinavir, measures size and density, identifies hydronephrosis, and excludes alternative diagnoses. The STONE trial showed ultrasound is a safe first-line alternative with no significant difference in adverse events ^[3]. I would use ultrasound as the first imaging in pregnancy, children, and recurrent stone formers to limit cumulative radiation. In this patient with recurrent stones, I would use ultrasound for known recurrences where the diagnosis is clear, reserving CT for atypical presentations or pre-operative planning.