Epidemiology

Bimodal age distribution; mostly affects children (between the ages of 3–12 years) and patients > 60 years of age

Etiology

• Prior infection with group A beta-hemolytic streptococci (GAS, S pyogenes)
  • In children
    • Infection of the mouth and pharynx (tonsillitis, pharyngitis): PSGN typically arises 1–2 weeks following infection.
    • Soft tissue infections (erysipelas, impetigo): PSGN typically arises 4–6 weeks following infection.

Pathophysiology

Infection with nephritogenic strains of group A beta-hemolytic streptococci → streptococcal antigen deposit within the glomerular basement membrane → immune complexes formation (Type III hypersensitivity reaction) → complement activation (↑ consumption of complement factors) → destruction of the glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome

Clinical features

Approx. 50% of patients remain asymptomatic. Symptoms occur approximately 1–6 weeks following an acute infection.

• Nephritic syndrome
  • Hematuria: tea- or cola-colored urine
  • Hypertension: can lead to headaches
  • Edema (prominent facial edema)
  • Oliguria
• Influenza-like symptoms
• Flank pain

Diagnostics

Initial evaluation

• Urinalysis with microscopy: nephritic sediment
• C3 complement, C4 complement levels: classically shows ↓ C3 complement with normal C4 complement

Evidence of preceding GAS infection

• Antistreptococcal antibody titers
  • Findings: ↑ ASO, ↑ anti-DNase B antibodies
• Isolation of group A beta-hemolytic streptococci
  • Pharyngitis: rapid strep test, throat culture
  • Skin lesions: wound cultures

Microscopy

• LM: hypercellular glomeruli

Treatment

Prognosis

Increased age is the most important poor prognostic factor

• Recovery usually occurs within 6–8 weeks.
  • In children: restitution of kidney function in > 90% of cases
• In adults, about 50% of patients suffer from persistently reduced renal function.