Post-infectious glomerulonephritis: Case

This girl has typical post-streptococcal glomerulonephritis. The diagnosis rests on the acute nephritic syndrome of haematuria, oedema, and hypertension, arising two weeks after an untreated sore throat, with dysmorphic red cells and red cell casts, a low C3 with a normal C4, and a raised antistreptolysin O titre. The latency of two weeks after pharyngitis and the low-C3-normal-C4 pattern together confirm the diagnosis and distinguish it from IgA nephropathy and from the other hypocomplementaemic glomerulonephritides. [1]

Clinical findings

The pattern is unequivocally that of pharyngitis-associated PSGN. The temporal sequence is classic: a sore throat two weeks before the haematuria, which is the expected one to three week latency after throat infection. The smoky brown urine reflects glomerular bleeding with dysmorphic red cells and red cell casts, the periorbital and ankle oedema reflects salt and water retention from the nephritic syndrome, and the hypertension is volume-dependent and renin-mediated from the renal injury. The mild acute kidney injury with a creatinine of 88 is consistent with the typical course. [2]

The low C3 with a normal C4 is the serological fingerprint of PSGN. It reflects consumption of C3 downstream of the alternative-pathway C3 convertase, with the lectin pathway also contributing, while the classical pathway is relatively spared so that C4 is preserved. The raised antistreptolysin O titre confirms a recent group A streptococcal throat infection, even though the throat swab is negative, because the organism is often cleared by the time PSGN declares itself. The negative throat swab therefore does not exclude the diagnosis. [3]

Investigations and diagnosis

The diagnosis is typical post-streptococcal glomerulonephritis, confirmed by the clinical and serological picture. The key investigations already sent are the urinalysis, the complement profile, and the streptococcal serology. To complete the workup I would check renal function and electrolytes for acute kidney injury and hyperkalaemia, albumin, a full blood count, and a renal ultrasound to exclude obstruction. A renal biopsy is not needed in this typical case; it is reserved for atypical features such as a rapidly progressive course with crescents, nephrotic-range proteinuria, a low C4, no streptococcal evidence, or a C3 that fails to recover by eight weeks. [1]

The differential diagnosis was considered and excluded. IgA nephropathy was excluded by the post-infectious latency (rather than synpharyngic haematuria) and by the low C3 (rather than a normal C3). Lupus nephritis was excluded by the normal C4, because lupus nephritis lowers both C3 and C4, though I would check an autoimmune screen if the C4 were low. C3 glomerulopathy and membranoproliferative glomerulonephritis remain in the differential only if the C3 fails to recover by eight weeks, which is why the recheck at six to eight weeks is essential. [1]

Management and outcome

Management began with supportive care, because typical PSGN resolves spontaneously and no immunosuppression changes its course. Fluid and salt balance was the cornerstone: she was restricted to insensible losses plus urine output and given a no-added-salt diet, with daily weights to guide fluid removal. Her oedema and her volume-dependent hypertension were treated with oral frusemide at 1 to 2 mg per kg per dose, and her blood pressure of 126 over 83 was treated with amlodipine, starting at 0.1 mg per kg once daily and titrating to a maximum of 10 mg per day. [2]

She received streptococcal eradication with phenoxymethylpenicillin orally for 10 days at 500 mg twice daily, because she is over 20 kg. This does not change the established glomerulonephritis but clears the nephritogenic strain and prevents spread to her household contacts. She was not given corticosteroids or other immunosuppression, because typical PSGN is self-limiting and immunosuppression exposes a resolving disease to harm. Over the following week her oedema settled, her blood pressure normalised, and her macroscopic haematuria resolved. [2]

At discharge her C3 was rechecked and was recovering. The family was counselled that over 95 percent of children recover completely, that the C3 will normalise within eight weeks, and that microscopic haematuria and low-grade proteinuria may persist for months or even one to two years before disappearing. The C3 was rechecked at six to eight weeks and had normalised, confirming the diagnosis. She was given a plan for follow-up of blood pressure and urinalysis, with longer surveillance weighted toward the risk factors for chronicity, namely heavier proteinuria, persistent hypertension, persistent low C3, and a higher presenting creatinine, none of which she carried. [1]

The counterfactual: if the C3 had not recovered by eight weeks

If this girl's C3 had not normalised by eight weeks, the diagnosis would change. 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 rather than a self-limiting one. I would check the C4 and an autoimmune screen, refer her urgently to a paediatric nephrologist, and arrange a renal biopsy to confirm the diagnosis histologically, because these conditions may require immunosuppression and long-term nephrology care. This counterfactual illustrates why the single most important confirmatory step in PSGN is rechecking the C3 at six to eight weeks, because it separates the self-limiting typical case from the chronic complement-mediated disease. [1]