7 Oct 2026

Case #032

1

Presenting complaint

Patient history

A 24-year-old man attends after two days of passing visibly red-brown urine. It is painless (no burning, no urgency and no loin pain) and the discolouration is present throughout the stream rather than only at the beginning or the end.

2Clue sealed:Patient history
3Clue sealed:Vital signs
4Clue sealed:Laboratory results
5Clue sealed:Laboratory results
6Clue sealed:Pathology

Pick a diagnosis from the suggestion list, then tap Submit to lock it in.

Reveal the answer (counts as a forfeit)

Diagnosis

IgA nephropathy

Key clinical clues

  • Painless haematuria throughout the stream, with dysmorphic red cells and red cell casts, a glomerular bleed, not a urological one
  • Haematuria starting within 48 hours of a sore throat, not after the one-to-three-week latent period of post-streptococcal disease
  • An earlier self-limiting episode triggered by a previous infection
  • Normal C3 and C4, which excludes post-streptococcal glomerulonephritis and lupus nephritis
  • Negative ANCA and anti-GBM, a raised serum IgA, and dominant mesangial IgA on immunofluorescence

First-line treatment

ACE inhibitor or ARB with blood pressure control

Visible haematuria in a young adult is either urological or glomerular, and the microscopy settles it: dysmorphic red cells and casts can only form as blood crosses an inflamed glomerulus, so stones, infection and bladder pathology fall away. Which glomerulonephritis is then answered by the timing. IgA nephropathy produces haematuria synpharyngitically, within one to three days of a mucosal infection and while the sore throat is still present, because the circulating galactose-deficient IgA1 complexes are already there and deposit in the mesangium as soon as production surges. Post-streptococcal glomerulonephritis, its closest mimic, runs the other way: it needs one to three weeks after a pharyngitis for immune complexes to form, so a throat still sore when the urine turns red argues strongly against it. Complement seals the split: post-streptococcal disease consumes complement and drives C3 down, whereas C3 and C4 are normal in IgA nephropathy, as they are here. Negative ANCA and anti-GBM exclude the small-vessel vasculitides and Goodpasture disease; a negative ANA with normal complement excludes lupus nephritis, which would stain as a full house with IgG and C1q rather than IgA-dominant. The self-limiting episode two years ago fits the characteristic recurrent, infection-triggered course, and the biopsy is definitive. Although this episode looks benign, a quarter to a third of patients reach end-stage kidney disease over two to three decades, and that is why the treatment is not immunosuppression but hard supportive control of the two drivers, both abnormal here. An ACE inhibitor or angiotensin receptor blocker is titrated to the maximum tolerated dose against a systolic target near 120, well under his 142, with an SGLT2 inhibitor for proteinuria that persists. His albumin:creatinine ratio of 148 mg/mmol is roughly 1.5 g a day, above the level at which corticosteroids enter the conversation, but they wait until several months of optimised supportive therapy have been tried, because the benefit is modest and the infection risk is not.