Poststreptococcal Glomerulonephritis

Poststreptococcal glomerulonephritis (PSGN) is characterized by rapid deterioration of kidney functions due to an inflammatory response (type III hypersensitivity reaction) following streptococcal infection. This condition results from specific strains of group A beta-hemolytic streptococci called nephrogenic streptococci. The disease affects the glomeruli and the small blood vessels of the kidneys. PSGN most frequently presents in children 1 to 2 weeks after a sore throat, or 6 weeks after a skin infection (impetigo). Though the incidence of PSGN has declined in developed countries, the incidence of non-streptococcal organisms is emerging. Nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B (SPeB) are the two common antigens associated with the pathogenesis of PSGN. They not only activate the alternate complement pathway, resulting in hypocomplementemia, but they also have an affinity towards the plasmin and glomerular proteins. The clinical presentation of PIGN can vary from no symptoms to renal failure requiring renal replacement therapy (RRT). When symptomatic, PSGN typically presents with features of the nephritic syndrome such as hematuria, oliguria, hypertension, and edema. Less commonly presentation can mimic nephrotic syndrome with significant proteinuria.