Immunofluorescent Localization of Staphylococcos aureus Antigen in Acute Bacterial Endocarditis Nephritis

Abstract

A 75-year-old man with Staphylococcus aureus endocarditis in whom acute diffuse proliferative glomerulonephritis developed is described. The light- and electron-microscopic changes of the glomeruli in this case were identical to those of acute poststreptococcal glomerulonephritis. Immunofluorescence revealed deposition of immunoglobulins and complement in the glomeruli. In addition, bacterial antigenic material was demonstrated in the glomeruli by indirect immunofluorescence. These observations further support the hypothesis of an immune-complex pathogenesis in this form of glomerulonephritis.

Rapidly Progressive Glomerulonephritis Associated with Bacterial Endocarditis: Efficacy of Antibiotic Therapy Alone

“…In the literature, the use of electron microscopy re vealed electron-dense deposits located in subepithelial and subendothelial deposits and mesangial areas [3,4,7,20,23,24], The size of the deposits could be related to the nature of the organism; small intramembranous or subepithelial deposits were usually encountered in staphylo coccal endocarditis [4], whereas the larger ones were dem onstrated mostly in streptococcal-related endocarditis [23]. In our patient, small intramembranous and suben dothelial deposits were present, endocarditis being related to 5. mitis.…”

“…Some authors reported that failure of antibiotic therapy was correlated with the pres ence of persistent or increasing levels of circulating im mune complexes [ 13,14]. Antibody to or soluble antigens of the infecting organism have been demonstrated in the glomeruli, leading to the conclusion that renal lesion is the result of immune complex deposition [6,[19][20][21][22].…”

Renal Complications of Bacterial Endocarditis

“…Initially, the clinical and morphologic features of the renal involvement were attributed to emboli from an infected valve with the kidney lesions representing injury and reaction to repeated microembolization. However, the presumed embolic etiology of the renal lesions was questioned particularly when focal glomerulonephritis was reported in cases of right-sided endocarditis [16,17], Indirect evidence for an immune etiology of the renal lesion was first advanced from the observation of low serum complement in 8 cases of endocarditis with mod erate to severe renal disease, in whom the complement level became normal as renal insufficiency abated [18], Subsequently, the demonstration of circulating immune complexes [19], electron-dense, immunoglobulin and complement deposits along the glomerular basement membrane [20], and ultimately the isolation of bacterial antigen [21] and antibody [22] from the glomerular eluate provided convincing evidence for an immune-mediated etiology of the glomerulonephritic lesions of bacterial endocarditis [23].…”

“…and complement deposition along the capillary basement membrane and mesangium [23,52], but cases that have no demonstrable immunoglobulins have also been re ported [48. 55], Staphylococcal antigenic material has been demonstrated in the capillary wall of a patient with .S' , aureus endocarditis and diffuse glomerulonephritis [21]. Thus, the evidence for an immunologically me diated mechanism is quite convincing [23].…”

Identification of bacterial antigens in circulating immune complexes of infective endocarditis.

“…Localization of IgG (1) and bacterial antigens (2) in glomeruli have implicated immune complexes (IC) in the pathogenesis of the glomerulonephritis associated with IE, but it has not been resolved whether such extracardiac manifestations of the disease derive from in situ formation or from deposition of circulating IC. Circulating IC have been documented in IE by several methods, using cryoprecipitation (3), polyethylene glycol (PEG) precipitation and Clq binding (4), and binding to Raji cells (5), but the relationship of the IC to exogenous vs. endogenous antigens of the host has not been clarified.…”