Post-infectious glomerulonephritis: Viva

Branch 1: Diagnosis and the streptococcal latency

The candidate should recognise that this girl has post-streptococcal glomerulonephritis and state the acute nephritic syndrome of haematuria, oedema, and hypertension. A strong candidate should emphasise the latency of two weeks between the sore throat and the haematuria as the key discriminator from IgA nephropathy, which produces haematuria during rather than after an infection. The candidate should link the low C3 with the normal C4 and the raised antistreptolysin O titre to confirm the diagnosis, and should state that the C3 is expected to recover within six to eight weeks. [1]

If the examiner asks about the differential, the candidate should distinguish PSGN from the other hypocomplementaemic glomerulonephritides. IgA nephropathy has a normal C3 and synpharyngic haematuria. Lupus nephritis lowers both C3 and C4, so a low C4 mandates an autoimmune screen. C3 glomerulopathy and membranoproliferative glomerulonephritis produce persistently low C3 that does not recover by eight weeks. The candidate should name the streptococcal antigens: the nephritis-associated plasmin receptor and streptococcal pyrogenic exotoxin B. [1]

Branch 2: The mechanism and the low C3

If asked about the pathophysiology, the candidate should explain that PSGN is an immune-complex glomerulonephritis. Streptococcal antigens lodge in the glomerulus and activate complement in situ: the nephritis-associated plasmin receptor activates plasmin, which drives alternative-pathway complement activation and C3-dominant injury, and streptococcal pyrogenic exotoxin B colocalises with the deposits. [3]

The candidate should explain why the C3 falls while the C4 stays normal. Because the alternative and lectin pathways are engaged while the classical pathway is relatively spared, C3 is consumed downstream of the alternative-pathway C3 convertase while C4 is preserved. This low-C3-normal-C4 pattern is the serological fingerprint of PSGN, and it recovers within six to eight weeks as the immune injury resolves. The candidate should state that the inflamed capillary wall leaks red cells and protein, giving the haematuria and proteinuria, and retains salt and water, giving the oedema and hypertension. [3]

Branch 3: Acute management and streptococcal eradication

If asked about immediate management, the candidate should state that the treatment is supportive because typical PSGN resolves spontaneously and no immunosuppression changes its course. The candidate should address fluid and salt balance first: restrict fluids to insensible losses plus urine output, give a no-added-salt diet, and use the daily weight to guide removal. The oedema and the volume-dependent hypertension respond to a loop diuretic such as oral frusemide 1 to 2 mg per kg per dose. [2]

The candidate should treat the hypertension with a calcium channel blocker, amlodipine 0.1 to 0.2 mg per kg once daily up to a maximum of 10 mg per day. For a hypertensive emergency with encephalopathy, the candidate should describe controlled lowering with an intravenous infusion of labetalol or nicardipine, reducing the pressure by no more than 25 percent in the first hours. The candidate should state the indications for dialysis: refractory hyperkalaemia, severe metabolic acidosis, or pulmonary oedema unresponsive to diuretics, all of which are rare in typical PSGN. [2]

The candidate should give streptococcal eradication with phenoxymethylpenicillin orally for 10 days (250 mg twice daily under 20 kg, 500 mg twice daily at 20 kg and over), or a single intramuscular dose of benzathine penicillin if adherence is uncertain, or a macrolide if penicillin-allergic. The candidate should stress that antibiotics do not change the established glomerulonephritis but clear the nephritogenic strain and prevent spread, and that there is no role for corticosteroids in typical PSGN. [1]

Branch 4: The persistent hypocomplementaemia scenario

If the examiner changes the scenario so that the C3 has not normalised by eight weeks, the candidate should shift the diagnosis. Persistent hypocomplementaemia after eight weeks is not a slow recovery; it raises C3 glomerulopathy, membranoproliferative glomerulonephritis, or lupus nephritis. C3 glomerulopathy can follow an apparent streptococcal illness and behaves as a chronic complement-mediated disease. The candidate should check the C4 and an autoimmune screen, and refer urgently to a paediatric nephrologist for renal biopsy. [1]

A strong candidate should close on prognosis and disposition. Over 95 percent of children with typical PSGN recover completely, and mortality is under 1 percent. The candidate should recheck the C3 at six to eight weeks to confirm recovery, monitor blood pressure and urinalysis, and weight follow-up toward the risk factors for chronicity: heavier proteinuria, persistent hypertension, persistent low C3, crescents, and a higher presenting creatinine. The candidate should emphasise that rechecking the C3 at eight weeks is the single most important confirmatory step, because it separates the self-limiting typical case from the chronic complement-mediated disease. [1]