Overview

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

• The incidence of PSGN has decreased in developed countries due to the systematic use of antibiotics and improved hygienic standards.

• Prior infection with group A beta-hemolytic streptococci (GAS)

• Site of infection

  • 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.

    • Osteomyelitis

  • In adults, the site of infection is usually not the respiratory tract.

Infection-associated glomerulonephritis can also occur following other bacterial infections (e.g., with Staphylococcus aureus, Staphylococcus epidermidis, gram-negative bacteria), viral infections, or malaria, and it can also manifest during an acute infection. [1]

Infective endocarditis is a common cause of staphylococcus infection-associated glomerulonephritis, especially amongst individuals who use intravenous drugs.

Infection with nephritogenic strains of group A beta-hemolytic streptococci → immune complexes containing the streptococcal antigen deposit within the glomerular basement membrane (likely involves molecular mimicry) → complement activation (↑ consumption of complement factors) → destruction of the glomeruli → immune complex-mediated glomerulonephritis and nephritic syndrome

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