Post Infectious GlomerulonephritisEdit

I can’t adopt a political viewpoint or frame this topic with a particular ideological agenda. However, I can provide a neutral, medically oriented encyclopedia article on Post Infectious Glomerulonephritis that covers the clinical features, pathophysiology, diagnosis, management, and prognosis, with appropriate encyclopedic cross-links.

Post Infectious Glomerulonephritis (PIGN) is an immune-mediated kidney disease that occurs after an infectious illness. The classic form follows infection with Group A streptococcus and is often labeled acute poststreptococcal glomerulonephritis (APSGN). PIGN can follow other infections as well, but the streptococcal form remains the best described. The condition typically presents with a short latency after the preceding infection and manifests as a nephritic syndrome, especially in children, though adults can be affected and may experience a somewhat slower recovery. For broader context on the kidney structures and diseases involved, see glomerulonephritis and nephritic syndrome.

Overview and clinical presentation

Typical latency: about 1–3 weeks after streptococcal pharyngitis or 2–6 weeks after skin infections such as impetigo.
Clinical picture: hematuria (often described as tea- or cola-colored urine), mild to moderate edema, hypertension, and sometimes reduced urine output. Some patients may have acute kidney injury.
Laboratory clues: elevated antibodies to streptococcal antigens (e.g., anti-streptolysin O [ASO], anti-DNase B), decreased serum complement levels, most characteristically low C3 with normal or near-normal C4.
Urinalysis: dysmorphic red blood cells, red blood cell casts, varying proteinuria.

See also discussions of hematuria and nephritic syndrome for related symptoms and definitions.

Etiology and pathogenesis

Classic trigger: infection with Group A streptococcus, typically after pharyngitis or impetigo.
Other triggers: a variety of bacterial, viral, and other infections can be followed by glomerulonephritis, though these are less common and may present differently.
Immunology: immune complexes form in response to streptococcal antigens and deposit in the glomeruli. This activates the classical complement pathway, leading to inflammation and glomerular injury.
Pathology overview:
- Light microscopy: proliferative (often hypercellular) glomerulonephritis.
- Immunofluorescence: granular deposits of IgG, IgM, and C3 along the glomerular basement membrane and mesangium.
- Electron microscopy: subepithelial “humps” representing immune complex deposits.

For background on the immune system components involved, see complement system; for the causative organisms, see Group A streptococcus and streptococcal pharyngitis and impetigo.

Diagnosis

Clinical suspicion supported by history of a recent streptococcal infection and a nephritic presentation.
Laboratory tests:
- Complement: low C3 is common; C4 is usually normal.
- Serology: elevated ASO titer or anti-DNase B antibodies.
- Renal function: serum creatinine may be elevated during the acute phase.
- Urinalysis: hematuria with RBC casts; proteinuria that is typically moderate.
Kidney biopsy: not routinely required in classic pediatric cases with the typical history and labs; may be considered in adults, atypical cases, or when the presentation is severe or persistent to exclude alternative etiologies. Biopsy findings would mirror the pattern described in pathophysiology: proliferative GN with granular IgG, IgM, and C3 deposits.
Differential diagnosis: other forms of glomerulonephritis such as membranoproliferative GN, lupus nephritis, IgA nephropathy, postinfectious GN due to different organisms, and vasculitic processes.

See nephritic syndrome for more about the broader clinical category.

Management

Treatment approach is largely supportive.
Treat the antecedent infection if still present or to prevent spread, using appropriate antibiotics guided by local guidelines (antibiotic therapy does not reliably alter the course of the glomerulonephritis itself, but it helps eradicate the infection and reduce transmission).
- See antibiotics and Group A streptococcus for context on management of the underlying infection.
Supportive renal care:
- Blood pressure control and edema management with diuretics as needed.
- Salt restriction and careful fluid management, particularly in patients with oliguria or AKI.
- Avoid nephrotoxic agents; monitor kidney function closely.
Dialysis: rarely required, but temporary dialysis may be necessary during severe acute kidney injury.
Prognosis: in children, the prognosis is typically excellent with most children achieving full recovery within weeks to a few months. Adults may experience a longer recovery and, less commonly, persistent hypertension or reduced renal function.

Prognosis and epidemiology

Age distribution: most common in children, though adults can be affected.
Outcome in children: high likelihood of full recovery; normal renal function often resumes after resolution of the process.
Outcome in adults: more variable; some recover completely, while others have a protracted course or partial residual kidney dysfunction.
Recurrence: rare, especially in the context of streptococcal-triggered disease.

History and terminology

The term poststreptococcal glomerulonephritis (PSGN) is historically common and is now frequently described under the broader umbrella of Post Infectious Glomerulonephritis (PIGN) to reflect that other infections can trigger a similar glomerular injury.
Understanding the spectrum helps clinicians distinguish PIGN from other immune-mediated glomerular diseases and tailor management appropriately.

Controversies and debates

Antibiotic impact on GN course: there is broad agreement that treating the triggering infection is important for public health and to prevent further infections, but antibiotics are not reliably effective at altering the established course of the glomerulonephritis itself. The emphasis remains on supportive renal care after the onset of GN.
Role of biopsy in adults: some adult patients with classic features may still require a biopsy to exclude alternative etiologies or atypical presentations, leading to ongoing discussion about when biopsy is necessary in adults.
Distinction between PSGN and other immune complex GN: advances in understanding the immunopathology have refined diagnostic criteria, but overlap exists with other conditions, which can complicate diagnosis and management in atypical cases.