The classic association of glomerulonephritis (GN) with infection is poststreptococcal GN, usually developing after streptococcal pharyngitis (see Glomerulonephritis, Poststreptococcal). [1, 2] However, a number of glomerular diseases are associated with other bacterial, viral, fungal, and parasitic diseases.
Most glomerular diseases associated with infection are mediated by the immune complex. The classic example observed in poststreptococcal GN involves an antigen-antibody reaction, which may occur in the circulation or in the glomerulus. Deposition in the glomerulus results in activation of the complement cascade, which may involve either the classic or alternative pathway. The immune complexes may activate endogenous glomerular cells. The reduction of chemotactic factors results in the accumulation of leukocytes and platelets within the glomerulus and, consequently, the inflammatory response.
Several possible pathogenic events occur in viral diseases associated with glomerular injury. These may include the formation of circulating immune complexes involving viral antigens and antibodies, formation of circulating immune complexes induced by the release of antigens following virally induced cellular injury, formation of in situ antigen-antibody reactions or cell-mediated injury, and autoimmune reactions to glomerular structures induced by the virus.
In protozoal infections, such as malaria, antibodies are formed against malarial antigens. The circulating immune complexes activate complement and macrophages. The complexes are primarily deposited in subendothelial areas. A cell-mediated immune response may also occur.
The various causes of infection-related GN have different prevalence rates. In endocarditis, associated GN may occur in up to 20% of cases.  Staphylococcus aureus has become a more common cause of GN than Streptococcus in developed countries. GN associated with hepatitis C is becoming a far more commonly recognized cause of GN. [4, 5]
Although specific numbers for incidence statistics are not available, in certain developing areas of the world, hepatitis B, HIV disease, malaria, and schistosomiasis are major causes of glomerulopathy.
Depending on the etiology, the outcome of GN associated with infection can be quite variable.
In GN associated with bacterial endocarditis, renal function returns after treatment with antibiotics. The GN usually resolves after the infection has cleared, with renal function beginning to improve within 1-2 weeks, complement levels normalizing within 6 weeks, and hematuria normalizing in approximately 6 months. 
The course of GNs associated with viral infection is more variable, although patients with HIV nephropathy commonly progress to end-stage renal disease. 
This condition is not limited to any particular race.
In most GNs associated with infection, no sexual predilection exists. However, HIV-associated GN is far more common in males.
Although postinfectious GN primarily occurs in childhood, it has been documented in all age groups. A study by Nasr et al examined 109 cases of postinfectious GN in patients aged 65 years or older who were diagnosed by renal biopsy.  The study determined that the most common site of infection was the skin and the most common causative agent was staphylococcus (46%). Increased risk factors included male sex, diabetes, and malignancy. The study also concluded prognosis for elderly patients is poor, with less than 25% recovering full renal function.
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