Write a short note on nephritic syndrome and acute glomerulonephritis, including post-streptococcal glomerulonephritis.

Definition

Nephritic syndrome is a clinical syndrome resulting from glomerular inflammation, characterised by:

1. Haematuria — classically with dysmorphic red cells and RED CELL CASTS (the hallmark of glomerular bleeding)

2. Proteinuria — usually sub-nephrotic (< 3.5 g/day)

3. Hypertension

4. Oedema — typically periorbital and facial

5. Oliguria with azotaemia (rising urea and creatinine)

The underlying process is inflammatory damage to the glomerular capillary wall with proliferation of glomerular cells, in contrast to the non-inflammatory podocyte injury of nephrotic syndrome.

NEPHRITIC versus NEPHROTIC — the fundamental contrast

Causes of Nephritic Syndrome

Post-streptococcal Glomerulonephritis (PSGN)

The classic cause of acute nephritic syndrome, and still common in India, where streptococcal skin and throat infection remain prevalent.

Aetiology: follows infection with nephritogenic strains of group A beta-haemolytic *Streptococcus pyogenes*:

• After PHARYNGITIS: latent period of 1–3 weeks
• After SKIN infection (pyoderma, impetigo, scabies with secondary infection): latent period of 3–6 weeks

Pathogenesis: immune complex-mediated (type III hypersensitivity) — circulating and in-situ immune complexes deposit in the glomerulus, activating complement and recruiting inflammatory cells. Histology shows diffuse endocapillary proliferative glomerulonephritis with "lumpy-bumpy" granular subepithelial deposits of IgG and C3 on immunofluorescence, and subepithelial "humps" on electron microscopy — a classic examination triad.

Clinical features:

• Affects predominantly children aged 2–12 years; more severe in adults.
• Abrupt onset of facial and periorbital oedema, worst on waking.
• "Smoky", "cola-coloured" or tea-coloured urine — macroscopic haematuria.
• Hypertension — from salt and water retention; may cause hypertensive encephalopathy with headache, seizures and visual disturbance, which is a major early danger in children.
• Oliguria; malaise, headache, loin pain.
• Pulmonary oedema and circulatory congestion from volume overload.

Investigations:

• Urinalysis: dysmorphic red cells and RED CELL CASTS, proteinuria, granular casts.
• Raised urea and creatinine; mild normocytic anaemia (dilutional).
• Evidence of streptococcal infection: raised or rising ASO titre (better after pharyngitis) and anti-DNase B (better after skin infection — important, since ASO is often normal in post-pyoderma cases); throat or skin swab culture.
• LOW C3 with normal or mildly low C4 — and crucially, C3 returns to NORMAL within 6–8 WEEKS. Persistent hypocomplementaemia beyond 8–12 weeks suggests membranoproliferative GN or lupus instead, and mandates biopsy.
• Renal biopsy is NOT usually required in a typical case; it is indicated for atypical features — persistent low C3, nephrotic-range proteinuria, progressive renal failure, no evidence of streptococcal infection, or failure to improve.

Management — supportive, as the disease is self-limiting in the great majority:

• Salt and water restriction; fluid balance and daily weight.
• Loop diuretics for oedema and volume overload — these also control the hypertension, which is volume-dependent.
• Antihypertensives as needed (calcium channel blockers; ACE inhibitors used cautiously given the risk of hyperkalaemia and AKI).
• Penicillin to eradicate residual streptococcal infection — it does NOT alter the course of the nephritis but reduces transmission; treat close contacts.
• Dialysis for severe AKI, refractory overload or hyperkalaemia.
• Immunosuppression has no role in typical PSGN.

Prognosis: excellent in children — over 95% recover completely. Adults do less well, with a higher rate of persistent proteinuria, hypertension and progression to CKD.

OTHER IMPORTANT CAUSES — key distinguishing features

• IgA nephropathy (Berger's disease) — the commonest primary glomerulonephritis worldwide. Presents with macroscopic haematuria occurring DURING or 1–2 DAYS AFTER an upper respiratory infection ("synpharyngitic") — in sharp contrast to the 1–3 week latent period of PSGN. Complement is NORMAL. Biopsy shows mesangial IgA deposition. Management: ACE inhibitor/ARB for proteinuria, blood pressure control, and immunosuppression for progressive disease.
• Henoch–Schönlein purpura (IgA vasculitis) — the systemic form of IgA nephropathy: palpable purpura on the buttocks and legs, arthralgia, abdominal pain and nephritis, typically in children after an upper respiratory infection.
• Lupus nephritis — low C3 AND C4, positive ANA and anti-dsDNA; biopsy classifies into ISN/RPS classes I–VI, which determines treatment.
• Infective endocarditis-associated GN — low complement, positive blood cultures; treat the infection.
• Rapidly progressive glomerulonephritis — see the separate answer.