Acute Post-Streptococcal Glomerulonephritis

Abstract

Acute post-streptococcal glomerulonephritis is the prototype for a postinfectious immune-complex mediated glomerulonephritis. Clinical manifestations follow a latent period of 1-6 weeks after a streptococcal skin or upper respiratory tract infection. Epidemic infections have been reported. Disease prevalence tends to be highest in economically disadvantaged geographic areas and populations. Disease pathogenesis has highlighted certain cell surface M virulence proteins and several putative nephritogenic antigens have been proposed, with activation of the complement pathway playing a key role. The disease phenotype is broad, ranging from asymptomatic microhematuria to a rapidly progressive glomerulonephritis (RPGN). Peak prevalence is in young school-aged children, with a preponderance of boys affected. Gross hematuria and hypertension are the most common clinical characteristics, with a third or more of affected children with oliguria or azotemia. Nephrotic syndrome is less common than a nephritic presentation. Depression of C3 complement levels and positive anti-streptolysin O and anti-DNAse B titers help to confirm the diagnosis. Kidney biopsy is infrequently necessary, but typically reveals a proliferative and exudative glomerulonephritis on light microscopy, with C3 and IgG deposition on immunofluorescence, and subepithelial electron-dense humps as well as subendothelial deposits. Treatment is generally supportive, with focus on volume overload and hypertension, with most children recovering rapidly without long-term kidney residuals. Significant acute kidney injury requiring dialysis is usually associated with an RPGN with crescentic changes that is most commonly treated with pulse intravenous steroids, though there is no evidence-based support for immunomodulatory therapy.