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Acute Poststreptococcal GlomerulonephritisEdit

Acute Poststreptococcal Glomerulonephritis (APSGN) is a self-limited, immune-mediated inflammation of the kidney’s glomeruli that occurs after an infection with group A Streptococcus. It most commonly affects children and presents with features of nephritic syndrome, including hematuria (often dark urine), edema, hypertension, and oliguria. The usual onset is about one to three weeks after a throat infection and two to six weeks after a skin infection such as impetigo. In most cases the kidneys recover completely, but in a minority, persistent or progressive kidney problems can occur.

APSGN sits at the intersection of infectious disease, immunology, and nephrology. Understanding its course helps illuminate how simple bacterial infections can briefly trigger more complex immune and renal responses. The condition has been studied for decades, offering a window into host–pathogen interactions, the role of the complement system, and the ways the body’s immune response can both help and harm the kidneys. While the majority of cases resolve with age and supportive care, awareness of the disease remains important for clinicians, families, and health systems.

Etiology and pathogenesis

APSGN follows infection with nephritogenic strains of the group A streptococcus. The precise mechanisms involve an immune response to streptococcal antigens that forms circulating immune complexes which deposit in the glomeruli, triggering inflammation and complement activation. The classical laboratory signature includes low serum C3 with generally normal C4 early in the illness, reflecting consumption of complement by the alternative pathway. Immunofluorescence typically reveals a granular, “lumpy-bumpy” pattern of IgG, IgM, and C3 deposition along the glomerular basement membrane and mesangium, while electron microscopy may show subepithelial “humps.”

Clinical manifestations arise from glomerular inflammation and impaired filtration. Patients commonly present with cola-colored urine (hematuria), mild to moderate proteinuria, edema (often periorbital), and hypertension. Oliguria or decreased urine output can occur, particularly in more extensive disease. Most children have a favorable course with full recovery over weeks to months, whereas adults may experience a more protracted course or a somewhat higher risk of persistent renal impairment.

APSGN is distinguished from other forms of glomerulonephritis by its typical preceding infection history, age distribution, and the transient nature of complement abnormalities. In most cases, a documented antecedent throat infection or skin infection with group A Streptococcus is identified, though cases without a clear recent infection can still occur.

Clinical presentation

  • Onset: 1–3 weeks after a throat infection; 2–6 weeks after a skin infection
  • Symptoms: hematuria, edema, hypertension, oliguria, and sometimes fatigue
  • Signs: pale appearance from edema, elevated blood pressure, reduced urine output
  • Laboratory clues: microscopic or gross hematuria with red blood cell casts, proteinuria (often subnephrotic), low C3 with normal or near-normal C4, elevated antistreptolysin O (ASO) or other streptococcal antibodies

In children, APSGN is often an isolated episode with a complete recovery. In adults, the possibility of a more severe course exists, and atypical presentations require careful evaluation to exclude alternative causes of nephritic syndrome.

Diagnosis

  • Clinical suspicion guided by history and exam
  • Urinalysis showing hematuria and proteinuria
  • Serum complement testing: low C3 early, usually returning to normal within 6–8 weeks
  • Serology: elevated ASO titer or other streptococcal antibodies supports recent GAS infection
  • Imaging: renal ultrasound may be used to assess kidney size and structure when the presentation is atypical
  • Renal biopsy: rarely required in straightforward pediatric cases; reserved for atypical courses, severe, or persistent nephritic symptoms or when alternative diagnoses are considered
  • Typical differential diagnoses to consider include other causes of nephritic syndrome, such as IgA nephropathy, C3 glomerulopathy, or rapidly progressive glomerulonephritis; adjudication relies on clinical history, complement profile, and, if needed, histology

Management

  • Supportive care is the mainstay
    • Blood pressure management, often with antihypertensive therapy
    • Fluid management and edema control, including diuretics when indicated
    • Sodium restriction during the acute phase
    • Monitoring of kidney function and urine output
  • Antibacterial therapy
    • Treatment of the index streptococcal infection is important to eradicate the infection and reduce transmission, typically with penicillin or related antibiotics
    • Antibiotics given after APSGN onset do not alter the course of established glomerulonephritis but remain important to address residual infection and prevent further streptococcal spread
  • Immunomodulatory therapy
    • Corticosteroids or other immunosuppressants are not routinely recommended for APSGN and are reserved for exceptional cases with atypical histology or diagnosis
  • Dialysis
    • In rare cases with severe kidney injury or fluid overload, temporary dialysis may be necessary

Prognosis and outcomes

  • Children: the majority recover completely within weeks to months; long-term kidney function is usually preserved
  • Adults: prognosis is generally less favorable than in children, with a higher likelihood of extended recovery time and, in some instances, residual hypertension or reduced kidney function
  • Recurrence: APSGN is typically a one-time event; subsequent GAS infections are not expected to provoke identical nephritic episodes, though reinfection remains possible

Epidemiology and risk factors

  • Age distribution: most common in children, especially between ages 5 and 12
  • Geographic variation: historically more common in settings with limited access to prompt treatment of skin and throat infections; incidence has declined in many high-income regions but persists in parts of the world with limited resources
  • Sex distribution: small variations exist in different populations; overall, children of both sexes are affected
  • Race and social determinants: outcomes and access to care can be influenced by socioeconomic factors; disparities in healthcare access may affect diagnosis timing, management, and follow-up

Controversies and policy considerations

  • Antibiotic stewardship and public health
    • A tension exists between aggressive management of GAS infections to prevent complications and stewardship principles aimed at reducing unnecessary antibiotic use. The pragmatic view emphasizes treating confirmed infections to reduce transmission and prevent sequelae, while avoiding overuse in cases with uncertain infection status.
  • Vaccination and prevention
    • Some policy discussions focus on the potential for future vaccines against GAS as a way to reduce both pharyngitis and skin infections, with downstream effects on APSGN incidence. Proponents argue vaccination could lower overall disease burden; opponents emphasize cost-effectiveness and the complexity of GAS strain diversity.
  • Public health investments
    • Debates persist about how to allocate limited health resources: targeted interventions (improved access to primary care, prompt treatment of streptococcal infections, and education) versus broader, sweeping programs. A fiscally conservative approach tends to favor targeted, evidence-based prevention and treatment strategies that demonstrably reduce acute care costs and long-term kidney complications.
  • Equity and outcomes
    • Critics of health policy often point to disparities in access to care as a driver of worse outcomes in APSGN among disadvantaged populations. A balanced perspective emphasizes improving timely access to care, diagnostic accuracy, and follow-up without inflating administrative overhead or broad mandates that may not meaningfully improve outcomes.

See also