Post streptococcal glomerulonephritis (PSGN) is an uncommon complication of either a streptococcal throat or a streptococcal skin infection. PSGN involves inflammation of the kidney.
Post streptococcal glomerulonephritis (PSGN) is a relatively uncommon complication of certain nephritogenic strains of streptococcal pharyngitis or a streptococcal skin infection (pyoderma). It is typically associated with group A streptococci (GAS), also known as Streptococcus pyogenes, and less commonly with group C streptococci (zooepidemicus).
Post-streptococcal glomerulonephritis is the most common form of postinfectious glomerular injury. The disease occurs in 5% of those infected with streptococcal sore throat and may occur in 25% of infections with nephritogenic strains of beta-hemolytic streptococci.
Age incidence peaks at 3-12 years with an equal male for female ratio.
Recently, a systematic review of 11 population-based studies described the incidence of acute post-streptococcal glomerulonephritis.1 The authors estimated that over 470 000 cases of acute post-streptococcal glomerulonephritis occur annually. The incidence rate in children in less developed countries was found to be 24·3 cases per 100 000 person-years and 3·9 cases per 100 000 person-years in adults. Based on an Italian biopsy study, the incidence was estimated at 0·3 cases per 100 000 person-years for adults in more developed countries.2
Symptoms of PSGN develop within 10 days following a pharyngeal infection or 3 weeks following a group A streptococcal skin infection. The clinical picture ranges from asymptomatic proteinuria or hematuria to nephritic syndrome, nephrotic synrome or acute renal failure. Symptoms may include pale skin, lethargy, loss of appetite, headache and dull back pain. Clinical findings may include dark-colored urine, swelling of different parts of the body (edema), and high blood pressure.
PSGN is diagnosed by history, serology and hypocomplementinemia. A biopsy is only needed when the disease follows an atypical course.
Serology: PSGN presents as nephritic syndrome with low serum complement levels (C3 and C4). Circulating antistreptolysin O (ASO) and anti-DNAse B can be elevated.
Biopsy: The biopsy shows diffuse proliferative (mesangial and endothelial) exudative (neutrophils and monocytes) pathology with coarsely granular loop deposits of IgG and C3 and electron dense subepithelial hump like deposits detected by electron microscopy. In some cases there is evidence of crescent formation.
No specific therapy is available and most cases recover spontaneously, even in cases that develop renal failure.3, 4 Treatment of PSGN consists of supportive care. Some give antibiotics when cultures prove the presence of streptococcus. Salt and water retention are treated with diuretics and antihypertensives and salt restriction. Irreversible renal failure occurs in less than 2% and dealth in less than 1%.5
1. Carapetis JR, Steer AC, Mulholland EK, Weber M. The global burden of group A streptococcal diseases. Lancet Infect Dis. Nov 2005;5(11):685-694.
2. Stratta P, Segoloni GP, Canavese C, et al. Incidence of biopsy-proven primary glomerulonephritis in an Italian province. Am J Kidney Dis. May 1996;27(5):631-639.
3. Ferrario F, Kourilsky O, Morel-Maroger L. Acute endocapillary glomerulonephritis in adults: a histologic and clinical comparison between patients with and without initial acute renal failure. Clin Nephrol. Jan 1983;19(1):17-23.
4. Lewy JE, Salinas-Madrigal L, Herdson PB, Pirani CL, Metcoff J. Clinico-pathologic correlations in acute poststreptococcal glomerulonephritis. A correlation between renal functions, morphologic damage and clinical course of 46 children with acute poststreptococcal glomerulonephritis. Medicine (Baltimore). Nov 1971;50(6):453-501.
5. Pinto SW, Sesso R, Vasconcelos E, Watanabe YJ, Pansute AM. Follow-up of patients with epidemic poststreptococcal glomerulonephritis. Am J Kidney Dis. Aug 2001;38(2):249-255.