Glomerulonephritis, Postinfectious



Postinfectious glomerulonephritis (PIGN) is an immune complex disease associated with nonrenal infection by certain strains of bacteria, most commonly Streptococcus and Staphylococcus. The most common form of PIGN, poststreptococcal glomerulonephritis (PSGN), is preceded by infection with Streptococcus spp. and predominantly affects children. The clinical presentation can be asymptomatic or with an acute nephritic syndrome, characterized by gross hematuria, proteinuria, edema, hypertension (HTN), and acute kidney injury.


PIGN is declining globally, especially in developed countries, in large part due to better hygiene and a decreased incidence of streptococcal skin infections. There are an estimated 470,000 new cases per annum of PSGN worldwide, and it remains the most common cause of acute nephritis in children globally, with 97% of cases occur in developing countries. PSGN is primarily a pediatric disease, but a recent increase in cases has been seen in nonstreptococcal GN in adults.

Etiology and Pathophysiology

  • Glomerular immune complex disease induced by specific nephritogenic strains of bacteria:
    • >95% of cases are caused by group A β-hemolytic Streptococcus (GAS) (1)
    • Staphylococcus (predominantly Staphylococcus aureus; more commonly methicillin-resistant S. aureus [MRSA], occasionally coagulase-negative Staphylococcus)
    • Gram-negative bacteria including Escherichia coli, Yersinia, Pseudomonas, and Haemophilus (2)
    • Occasionally viral, fungal, helminthic or protozoal causes
  • Proposed mechanisms for the glomerular injury (3) relates to the deposition of circulating immune complexes with streptococcal or staphylococcal antigens—although these complexes can be detected in patients with streptococcal- or staphylococcal-related GN, they do not correlate to disease activity. IgG is the most frequent immunoglobulin in PSGN (2).
  • These glomerular immune complexes result in complement activation and inflammation:
    • Nephritis-associated plasmin receptor (NAPlr): activates plasmin; contributes to activation of the alternative complement pathway
    • Streptococcal pyrogenic exotoxin B (SPE B): binds plasmin and acts as a protease; promotes the release of inflammatory mediators
  • Activation of the alternative complement pathway causes initial glomerular injury as evidenced by C3 deposition and decreased levels of serum C3. The lectin pathway of complement activation has also been recently implicated in glomerular injury (1).

Risk Factors

  • Children 5 to 12 years of age
  • Older patients (>65 years of age) with immunocompromising comorbid conditions such as diabetes and alcohol abuse

General Prevention

  • Early antibiotic treatment for streptococcal and staphylococcal infections, although efficacy in preventing GN is uncertain
  • Improved hand hygiene and respiratory etiquette
  • Prophylactic penicillin treatment to be used in closed communities and household contacts of index cases in areas where PIGN is prevalent

Commonly Associated Conditions

Streptococcal or staphylococcal infection

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