Nephrolithiasis — DCE Clinical Case

Long case

Patient scenario

Mr JR is a 48-year-old man referred to the nephrology outpatient clinic for management of recurrent kidney stones. He has a 20-year history of Crohn disease (ileocolonic), managed with azathioprine and infliximab, with a terminal ileal resection 10 years ago for stricturing disease. He currently has 4 to 6 loose stools per day despite loperamide. [1]

His first kidney stone was six years ago — a left-sided ureteric stone requiring ureteroscopy and laser lithotripsy. Stone analysis confirmed calcium oxalate. He has had three further episodes since: two passed spontaneously, and one required ESWL. His most recent episode was three months ago. [1]

He was advised by a friend to reduce his calcium intake after his first stone, and he now consumes approximately 500 mg of calcium per day (predominantly avoiding dairy). He drinks about 1.5 L of fluid per day. He does not smoke and drinks alcohol rarely. [1]

A 24-hour urine collection shows: volume 1.2 L per day, calcium 5.2 mmol per day (normal), oxalate 0.9 mmol per day (elevated), citrate 1.2 mmol per day (low), urate 3.1 mmol per day (normal), sodium 180 mmol per day (high). Serum calcium is 2.35 mmol per litre (normal), phosphate 0.95 mmol per litre (normal), PTH 3.2 pmol per litre (normal), bicarbonate 20 mmol per litre (low), potassium 3.4 mmol per litre (low), creatinine 92 micromol per litre (eGFR 82). [1]

History-taking approach

I would take a focused history covering:

• Stone history: age at first stone, frequency, side, symptoms, interventions (ESWL, URS, PCNL), complications (infection, AKI), stone analysis results
• Bowel history: Crohn disease duration, extent, surgeries (especially ileal resection — the key driver of enteric hyperoxaluria), current symptoms (stool frequency, consistency, fat malabsorption), medications
• Dietary history: fluid intake, calcium intake, oxalate-rich foods, animal protein, sodium
• Medications: any supplements (vitamin C increases oxalate, vitamin D increases calcium), current Crohn disease therapy
• Family history: stones (cystinuria, hypercalciuria), inflammatory bowel disease
• Systemic symptoms: bone pain (hyperparathyroidism), gout (tophi, podagra), weight loss [1]

Presentation

"Doctor, my patient is a 48-year-old man with Crohn disease and a prior terminal ileal resection, presenting with his fourth episode of calcium oxalate nephrolithiasis in six years. The 24-hour urine confirms enteric hyperoxaluria (oxalate 0.9 mmol per day) from fat malabsorption, hypocitraturia (citrate 1.2 mmol per day) from chronic diarrhoea and metabolic acidosis (bicarbonate 20), and a low urine volume (1.2 L per day). His low-calcium diet (500 mg per day) is actively worsening his hyperoxaluria by leaving more free oxalate available for colonic absorption. The normal serum calcium and PTH exclude primary hyperparathyroidism. [1]

His problems are:

1. Recurrent calcium oxalate nephrolithiasis from enteric hyperoxaluria
2. Hypocitraturia from chronic diarrhoea and metabolic acidosis
3. Low urine volume
4. A counterproductive low-calcium diet
5. Crohn disease with chronic diarrhoea — the underlying driver [1]

The priority is targeted dietary and pharmacological therapy to correct the metabolic abnormalities and prevent further recurrence." [1]

Problem list and integrated management plan

1. Enteric hyperoxaluria — dietary and pharmacological correction. [1]

The mechanism is fat malabsorption: unabsorbed fatty acids saponify dietary calcium in the colon, leaving free oxalate to be absorbed [1]. The correction is multi-pronged:

• Increase calcium to 1000 to 1200 mg per day, taken with meals so it binds intestinal oxalate. The Borghi trial proved that normal calcium halves recurrence compared with low calcium [2].
• Add oral calcium carbonate 500 to 1000 mg with each main meal for additional oxalate binding.
• Low-oxalate diet: restrict spinach, rhubarb, nuts, chocolate, tea.
• Low-fat diet: reducing dietary fat reduces the fatty acids that saponify calcium.
• Cholestyramine: a bile acid sequestrant for refractory cases, reducing colonic oxalate permeability.

2. Hypocitraturia — potassium citrate. [1]

Potassium citrate 10 mEq twice daily, titrated to urine pH 6.5 to 7.0. This addresses both the hypocitraturia (increasing the main calcium crystallisation inhibitor) and the metabolic acidosis (bicarbonate 20) from chronic diarrhoea [5]. I would monitor serum potassium — his potassium is already low at 3.4, and potassium citrate will help correct this. The target urine citrate is above 2.5 mmol per day.

3. Low urine volume — increase fluid intake. [1]

Target urine output above 2.5 L per day. Given his chronic diarrhoea (4 to 6 stools per day), this will require an intake of 3 to 4 L per day. I would counsel on consistent fluid intake throughout the day and monitoring urine colour (aiming for pale). Oral rehydration solution may help maintain hydration without worsening diarrhoea. [1]

4. Correct the low-calcium diet. [1]

This is a key intervention — the current 500 mg per day is actively harmful. The patient needs education that calcium binds oxalate in the gut and that a low-calcium diet increases oxalate absorption and stone risk. The Borghi trial is the evidence anchor [2].

5. Optimise Crohn disease management. [1]

Reducing diarrhoea and fat malabsorption addresses the root cause. This involves the gastroenterology team — optimising immunosuppressive therapy, managing high-output diarrhoea, and nutritional support. [1]

Not indicated: Thiazide diuretics — his urinary calcium is normal. Thiazides are for hypercalciuria and would not address the primary abnormality. They could also worsen volume depletion. [1]

Follow-up: Annual 24-hour urine re-evaluation to confirm the biochemistry has normalised, annual bloods (eGFR, electrolytes, calcium), and a DEXA scan for bone density (malabsorption and metabolic acidosis increase osteoporosis risk). [1]

Defence of key decisions

Examiner: "Why is the low-calcium diet harmful in this patient?" [1]

Calcium normally binds intestinal oxalate, forming insoluble calcium oxalate that is excreted in the stool. A low-calcium diet — especially in the setting of fat malabsorption where fatty acids compete for calcium binding — leaves more free oxalate available for colonic absorption, increasing urinary oxalate. The Borghi 2002 NEJM trial randomised 120 men with hypercalciuria to a normal-calcium (1200 mg), low-sodium, low-protein diet versus a low-calcium (400 mg) diet. The normal-calcium group had half the recurrence rate at five years (20 per cent versus 38 per cent, RR 0.49). This is the single most important dietary principle in stone prevention and is the most commonly tested fact [2].

Examiner: "How would you manage this patient if he presents with acute renal colic?" [1]

NSAIDs first-line — diclofenac 75 mg IM. I would check renal function first because his chronic diarrhoea may cause volume depletion and NSAIDs can worsen AKI. Non-contrast CT KUB confirms the stone. For a stone below 5 mm, expectant management. For 5 to 10 mm distal ureteric stones, I would consider tamsulosin — the SUSPEND trial (Pickard 2015, Lancet, 1167 patients) found no overall benefit for stones below 10 mm [4], but the Hollingsworth 2016 BMJ meta-analysis suggested modest benefit for larger distal stones [6]. For stones above 10 mm, intervention (ESWL for upper tract stones below 2 cm, ureteroscopy for ureteric stones, PCNL for stones above 2 cm). The critical emergency is obstructive pyelonephritis — an infected obstructed system requires urgent decompression (stent or nephrostomy), not antibiotics alone.

Examiner: "What imaging would you use?" [1]

Non-contrast CT KUB is the gold standard — sensitivity 97 to 100 per cent, detects all stone types except indinavir, measures size and density, and identifies hydronephrosis and alternative diagnoses. The STONE trial (Smith-Bindman 2014, NEJM) showed that ultrasound is a safe first-line alternative with no significant difference in adverse events [3]. I would use ultrasound in pregnancy, children, and for known recurrences to limit cumulative radiation.

Short-case discussion — examination of the patient with acute flank pain

Examiner: "What are the key bedside observations in a patient presenting with suspected renal colic?" [1]

The most important bedside observation is whether the patient is writhing and moving (visceral pain from ureteric spasm — classic renal colic) or lying still and resisting movement (somatic pain from peritoneal inflammation — appendicitis, cholecystitis, perforation). This single observation is one of the most valuable discriminating signs in the acute abdomen. [1]

Vital signs: fever suggests infection (obstructive pyelonephritis if there is an obstructing stone), hypotension suggests sepsis or AAA in the older patient. Abdominal examination: costovertebral angle tenderness (renal), peritoneal signs (surgical abdomen), pulsatile mass (AAA). Urinalysis: haematuria in 85 to 90 per cent of stones, leucocytes and nitrites suggest infection. [1]

Examiner: "What are the red flags that mandate urgent urological referral?" [1]

Fever with obstruction (obstructive pyelonephritis), AKI from bilateral obstruction or a solitary kidney, intractable pain or vomiting, stone above 10 mm, failure of conservative management after 4 weeks, and pregnancy with obstruction. These require urgent decompression or intervention, not expectant management. [1]

Branching discussion — obstructive pyelonephritis

Examiner: "If this patient presented with fever of 39 degrees, rigors, and an obstructing stone on CT with hydronephrosis, what would you do?" [1]

This is obstructive pyelonephritis — a urological emergency. The principles are:

1. Resuscitate — intravenous fluids, broad-spectrum antibiotics (covering Gram-negatives including Proteus), vasopressor support if septic.
2. Urgent decompression — ureteric stent (retrograde, via cystoscopy) or percutaneous nephrostomy (image-guided), within hours. The choice depends on local expertise and the patient's stability.
3. Defer definitive stone treatment — ESWL, ureteroscopy, or PCNL is performed only after the infection and sepsis have resolved (typically 48 to 72 hours after decompression). [1]

The rationale is that an obstructed infected collecting system cannot be sterilised with antibiotics alone — the obstruction prevents antibiotic penetration, and the infected urine under pressure drives bacteria into the bloodstream. Attempting definitive stone removal in the setting of active sepsis risks worsening the sepsis by manipulating the infected system. The lesson is: decompress first, treat the stone later. [1]

Summary

This case illustrates the principles of recurrent stone prevention: identify the specific metabolic abnormality through 24-hour urine evaluation, correct it with targeted dietary and pharmacological therapy (not empiric treatment), correct dietary misconceptions (the low-calcium diet is harmful), and address the underlying systemic disease (Crohn disease). With sustained adherence, the recurrence rate can be reduced by 50 to 80 per cent. The emergency of obstructive pyelonephritis requires urgent decompression, not antibiotics alone — a principle that applies to all stone types and all patients. [1]