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March 1976

Immune-Complex Nephritis in Bacterial Endocarditis

Author Affiliations

From the Department of Medicine, University of Miami School of Medicine, and the Veterans Administration Hospital, Miami, Fla (Dr Perez); the Department of Medicine, Veterans Administration Hospital, University of Connecticut (Dr Rothfield); and the Department of Medicine, University of New Mexico School of Medicine, Albuquerque (Dr Williams).

Arch Intern Med. 1976;136(3):334-336. doi:10.1001/archinte.1976.03630030066012

Patients with subacute bacterial endocarditis (SBE) may develop focal or diffuse proliferative glomerulonephritis.1 These lesions were believed originally to be secondary to emboli that originated from the heart valves. Recent evidence, coupled with the rarity of bacterial isolation from the glomerular lesions, suggests that they are immunological in origin. Deposits of immunoglobulins and complement on the glomerular basement membrane and depressed serum complement levels have been taken as indirect evidence that renal disease in SBE represents a form of immunecomplex nephritis.2-4 This theory of the pathogenesis of SBE nephritis is further supported by the recent demonstration by Levy and Hong5 that eluates from a kidney of a patient dying of SBE specifically combined with the bacteria cultured from the patient's blood antemortem. The present study constitutes further evidence that glomerular immunecomplex deposition may be involved in SBE nephritis, since streptococcal bacterial antigen has been identified in glomerular

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