Glomerulonephritis in bacterial endocarditis.
The introduction of antibiotic therapy and changing epidemiologic patterns have altered the nature of glomerulonephritis as it occurs during the course of bacterial endocarditis. Observations made predominantly in the pre-antibiotic era suggested that infections with less virulent organisms, by virtue of their indolent subacute course, favored an antibody response predisposing to immune complex glomerulonephritis. Although antibiotic prophylaxis and therapy have reduced the incidence of both Streptococcus viridans bacterial endocarditis and concomitant glomerulonephritis, Staphylococcus aureus has become a major cause of acute bacterial endocarditis with a high incidence of glomerulonephritis. Parenteral drug abuse itself, which has emerged as a major factor predisposing to endocarditis, may also favor the development of glomerulonephritis. The course of glomerulonephritis has been altered in association with these changes in etiology and epidemiology. This review summarizes the clinical and morphologic features of glomerulonephritis as it currently occurs during the course of bacterial endocarditis.
D000936:Antigen-Antibody Complex / Q000032:analysis; D003176:Complement C3 / Q000032:analysis; D004697:Endocarditis, Bacterial / Q000150:complications* / Q000276:immunology / Q000473:pathology; D005921:Glomerulonephritis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007263:Infusions, Parenteral / Q000009:adverse effects; D007676:Kidney Failure, Chronic / Q000150:complications; D007678:Kidney Glomerulus / Q000648:ultrastructure; D013203:Staphylococcal Infections / Q000150:complications / Q000276:immunology / Q000473:pathology; D013290:Streptococcal Infections / Q000150:complications / Q000276:immunology / Q000473:pathology; D019966:Substance-Related Disorders / Q000150:complications; D014511:Uremia / Q000209:etiology
D000936:Antigen-Antibody Complex; D003176:Complement C3; D007136:Immunoglobulins