Renal and urology · Moderate
This case is fictional and exists for study. It describes no real patient.
24 years · male
A 24-year-old male presents to the general practice clinic complaining of dark, cola-coloured urine that began yesterday evening. He notes a 2-day history of a mild sore throat and nasal congestion. He reports a similar episode of brownish urine approximately 5 months ago following a viral cold, which resolved spontaneously after a few days. He denies dysuria, urinary frequency, fever, flank pain, or recent trauma. On physical examination, he appears well. Throat examination shows mild pharyngeal erythema without exudates. There is no peripheral oedema and no costovertebral angle tenderness.
Vital signs
- HR
- 74 bpm
- BP
- 138/86 mmHg
- RR
- 14/min
- Temp
- 37.1 °C
- SpO₂
- 99%
Examination findings
- Mild pharyngeal erythema without follicular exudates
- No peripheral oedema
- Abdomen soft, non-tender, no loin tenderness
Investigations
| Haemoglobin | 14.2 g/dL | reference: 13.5-17.5 |
| Serum Creatinine | 88 µmol/L | reference: 60-110 |
| eGFR | >90 mL/min/1.73m2 | reference: >90 |
| Urine Dipstick Blood | 3+ scale | reference: Negative |
| Urine Dipstick Protein | 1+ scale | reference: Negative |
Question 1 of 3
What is the most likely diagnosis?
IgA nephropathy (Berger disease) classically presents as visible haematuria occurring concurrently or within 1-2 days of an upper respiratory tract infection (synpharyngitic haematuria) in young adult males, often recurrent. Post-streptococcal glomerulonephritis typically occurs 1-3 weeks (post-infectious) after a streptococcal pharyngitis or skin infection. Granulomatosis with polyangiitis usually causes systemic symptoms, pulmonary involvement, and rapidly progressive glomerulonephritis. Alport syndrome presents with X-linked hereditary nephritis, sensorineural hearing loss, and ocular abnormalities.
Teaching point: IgA nephropathy characteristically presents with visible haematuria coincident with or within 1-2 days of an upper respiratory tract infection.
Question 2 of 3
If the patient's proteinuria persists above 0.75 g/day or renal function begins to decline, which of the following is the definitive diagnostic investigation?
Renal biopsy is the gold standard diagnostic investigation for IgA nephropathy, demonstrating mesangial IgA deposition on immunofluorescence. Serum IgA levels are non-specific and elevated in only about 50% of patients, so normal levels do not rule out the condition. ASOT is used to evaluate post-streptococcal glomerulonephritis. Flexible cystoscopy is used to investigate urological causes of haematuria (such as transitional cell carcinoma) rather than glomerular disease.
Teaching point: Renal biopsy showing mesangial IgA immune complex deposition is the definitive diagnostic test for IgA nephropathy.
Question 3 of 3
Repeat urinalysis 4 weeks later shows persistent proteinuria (Line 95, questions[2].prompt — replace in full with: "Repeat urinalysis 4 weeks later shows persistent proteinuria (urine protein:creatinine ratio 90 mg/mmol) and a persistent blood pressure of 142/88 mmHg. What is the most appropriate initial pharmacological management?" Companion edit, line 103, questions[2].explanation — replace "(>0.5 to 1 g/day)" with "(>0.5-1 g/day, i.e. uPCR >50-100 mg/mmol)", giving: "In IgA nephropathy, patients with persistent proteinuria (>0.5-1 g/day, i.e. uPCR >50-100 mg/mmol) or elevated blood pressure should be treated initially with an ACE inhibitor or angiotensin receptor blocker (ARB). This reduces intraglomerular pressure, decreases proteinuria, and slows renal function decline. Corticosteroids are reserved for patients who have persistent high-risk proteinuria despite maximum tolerated ACEi/ARB therapy. Cyclophosphamide is used for rapidly progressive crescentic glomerulonephritis. Antibiotics do not prevent or treat IgA nephropathy flares.") and a persistent blood pressure of 142/88 mmHg. What is the most appropriate initial pharmacological management?
In IgA nephropathy, patients with persistent proteinuria (>0.5 to 1 g/day) or elevated blood pressure should be treated initially with an ACE inhibitor or angiotensin receptor blocker (ARB). This reduces intraglomerular pressure, decreases proteinuria, and slows renal function decline. Corticosteroids are reserved for patients who have persistent high-risk proteinuria despite maximum tolerated ACEi/ARB therapy. Cyclophosphamide is used for rapidly progressive crescentic glomerulonephritis. Antibiotics do not prevent or treat IgA nephropathy flares.
Teaching point: ACE inhibitors or ARBs are the first-line treatment in IgA nephropathy to control blood pressure and reduce proteinuria.
Key learning points
- IgA nephropathy presents with synpharyngitic visible haematuria (onset < 48 hours after upper respiratory tract infection), unlike PSGN which has a 1-3 week lag period.
- Definitive diagnosis of IgA nephropathy requires a renal biopsy showing dominant mesangial IgA deposition.
- First-line disease-modifying management for IgA nephropathy with persistent proteinuria or hypertension is an ACE inhibitor or ARB.
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