Nephrology · KIMS Secunderabad
Post-Infectious Glomerulonephritis — When a Throat or Skin Infection Attacks the Kidneys
Post-infectious glomerulonephritis (PIGN) — most commonly post-streptococcal GN (PSGN) — is an immune-mediated glomerulonephritis that develops 1 to 3 weeks after a streptococcal throat infection (pharyngitis) or 3 to 6 weeks after a streptococcal skin infection (impetigo, pyoderma). It is caused not by the bacteria themselves reaching the kidney, but by immune complex formation — antibodies against streptococcal antigens form complexes that deposit in the glomeruli and trigger complement activation and glomerular inflammation.
PIGN is the most common cause of acute nephritic syndrome in children — and remains common in India where impetigo (pyoderma) from Streptococcus pyogenes (Group A Streptococcus) is endemic in tropical conditions with limited hygiene. The classic presentation — a child 6 to 12 years old with haematuria (cola-coloured urine), periorbital oedema (facial puffiness on waking), and hypertension, 2 weeks after a sore throat — is one of the most recognisable syndromes in nephrology. Most cases resolve completely and spontaneously without permanent kidney damage, making PIGN one of the few truly self-limiting causes of glomerulonephritis.
Clinical features — the nephritic syndrome
Gross haematuria — the urine appears brown, red, or cola-coloured from red blood cells passing through inflamed glomeruli. Red cell casts on urine microscopy are pathognomonic of glomerular origin.
Periorbital oedema — puffiness around the eyes, most prominent on waking. Caused by hypoalbuminaemia (from mild protein loss) and sodium retention. Particularly dramatic in children.
Hypertension — from sodium retention driven by reduced GFR and activated RAAS.
Oliguria — reduced urine output from acute glomerulonephritis reducing filtration.
Mild proteinuria — typically subnephrotic range (below 3.5g/day). Heavy nephrotic-range proteinuria in PIGN should prompt consideration of an alternative or concurrent glomerular diagnosis.
Preceding infection — throat infection 1 to 3 weeks before (post-streptococcal pharyngitis); skin infection 3 to 6 weeks before (post-streptococcal impetigo).
Investigations
Urine microscopy
Dysmorphic red blood cells and red cell casts — pathognomonic of glomerular haematuria. Pyuria is common.
ASO titre (anti-streptolysin O) and anti-DNase B
Elevated in post-streptococcal pharyngitis (ASO titre rises after throat infection). Anti-DNase B is more sensitive for post-impetigo PSGN — ASO may be normal in skin-infection-related PSGN because streptococcal lipoprotein in the skin inactivates streptolysin O. A negative ASO does not exclude PSGN — anti-DNase B or anti-hyaluronidase should be measured.
Complement C3 and C4
Low C3 (with normal C4) is characteristic — the alternative complement pathway is activated by the deposited immune complexes. C3 returns to normal within 6 to 8 weeks in typical PSGN. Persistent low C3 beyond 8 to 12 weeks is a red flag — it suggests C3 glomerulopathy or membranoproliferative GN (which may mimic PIGN at presentation but has a very different prognosis).
Throat and skin cultures
May be positive for Group A Streptococcus if performed within 1 to 2 weeks of the infection. Often negative by the time GN presents, because the infection has resolved.
Kidney biopsy — not always required
Biopsy is not necessary for a typical case of PIGN in a child (clinical diagnosis is usually sufficient). Biopsy is indicated when: the diagnosis is uncertain, recovery is atypical (no improvement after 4 weeks), complement does not normalise, or an adult patient with atypical features requires histological confirmation. The biopsy shows endocapillary proliferative GN with 'humps' — large subepithelial immune complex deposits on electron microscopy.
Treatment and prognosis
PIGN is primarily a self-limiting condition — specific immunosuppressive treatment is not required in typical cases. Management is supportive.
Antibiotics
Penicillin or amoxicillin to eradicate the causative streptococcal infection (even if culture is negative at presentation). This does not alter the course of the GN but prevents further antigenic stimulation.
Antihypertensives
Blood pressure control with calcium channel blockers or ACE inhibitors until hypertension resolves.
Diuretics
Furosemide for fluid overload and oedema. Salt restriction.
Dialysis (rarely required)
Severe oliguric AKI not responding to furosemide may require short-term dialysis support. At KIMS, CRRT is available for severe cases.
Prognosis: In children, 95 to 100% of typical PSGN resolves completely with no long-term kidney damage. Haematuria resolves within 2 to 4 weeks, proteinuria within 3 to 6 months, and hypertension within 2 to 4 weeks. In adults, complete recovery is less certain — approximately 25 to 30% of adults with PIGN develop persistent CKD, particularly those with severe initial presentation.
Persistent haematuria beyond 6 to 12 months, persistent proteinuria beyond 12 months, or failure of C3 to normalise within 8 to 12 weeks of presentation should prompt repeat nephrology evaluation and possible kidney biopsy to exclude IgA nephropathy, C3 glomerulopathy, or lupus nephritis — all of which can mimic PIGN at presentation.
Book a Nephrology Assessment for Post-Infectious Glomerulonephritis at KIMS
Frequently Asked Questions — Post-Infectious GN
Post-streptococcal GN from pharyngitis (throat infection) develops 1 to 3 weeks after the sore throat — the time required for immune complex formation and deposition in the glomeruli. Post-streptococcal GN from skin infection (impetigo, pyoderma) takes longer — 3 to 6 weeks — because skin infections generate a different antibody profile with slower kinetics. The typical presentation: a parent notices that their child's urine is brown or dark, and the child's face is puffy on waking, approximately 2 weeks after a sore throat episode. The throat infection itself may have resolved by the time GN develops, which is why parents often do not make the connection.
No — though they can be confused clinically. Both cause haematuria following an upper respiratory infection. The key distinction: PIGN haematuria appears 1 to 3 weeks after the throat infection ('latent period'), while IgA nephropathy haematuria appears within 24 to 48 hours of the same throat infection ('synpharyngitic haematuria' — simultaneous with the infection). PIGN is characterised by low C3 complement; IgA nephropathy has normal complement. PIGN typically resolves completely in children; IgA nephropathy is a chronic relapsing condition. If haematuria recurs with each subsequent upper respiratory infection, IgA nephropathy is more likely than PIGN.
In the vast majority of children with typical PSGN — no. Complete recovery is the expected outcome in 95 to 100% of paediatric cases, with no long-term kidney damage. Haematuria, hypertension, and oedema resolve over weeks, and kidney function returns to normal. Long-term follow-up studies show that children with typical PSGN have normal blood pressure and kidney function 10 to 20 years later. The rare exceptions are children with very severe acute disease (requiring dialysis) or those with atypical presentations that turn out to represent a different glomerular disease.
Yes — PIGN occurs in adults, though it is less common than in children and carries a worse prognosis. In adults, the causative organism is more variable — Staphylococcus aureus (particularly in diabetics and IV drug users — IgA-dominant staphylococcal GN, which has a different immune complex profile from streptococcal GN), Gram-negative organisms in patients with urinary tract infections, and endocarditis-associated GN. Adults with PIGN are more likely to have persistent hypertension, proteinuria, and declining eGFR than children. Kidney biopsy is more often indicated in adults to confirm the diagnosis and assess the extent of injury.
KIMS Secunderabad — Dr. E. Ravi (Senior Consultant Nephrologist), urine microscopy with red cell cast identification, ASO titre and anti-DNase B, complement C3 and C4, kidney biopsy with NABL pathology (LM + IF + EM) for atypical cases, blood pressure management, dialysis support for severe cases. NABH and NABL accredited. Call 040-4488-5000.