Update on endocarditis-associated glomerulonephritis

Abstract

Glomerulonephritis (GN) due to infective endocarditis (IE) is well documented, but most available data are based on old autopsy series. To update information, we now present the largest biopsy-based clinicopathologic series on IE-associated GN. The study group included 49 patients (male-to-female ratio of 3.5:1) with a mean age of 48 years. The most common presenting feature was acute kidney injury. Over half of the patients had no known prior cardiac abnormality. However, the most common comorbidities were cardiac valve disease (30%), intravenous drug use (29%), hepatitis C (20%), and diabetes (18%). The cardiac valve infected was tricuspid in 43%, mitral in 33%, and aortic in 29% of patients. The two most common infective bacteria were Staphylococcus (53%) and Streptococcus (23%). Hypocomplementemia was found in 56% of patients tested and ANCA antibody in 28%. The most common biopsy finding was necrotizing and crescentic GN (53%), followed by endocapillary proliferative GN (37%). C3 deposition was prominent in all cases, whereas IgG deposition was seen in <30% of cases. Most patients had immune deposits detectable by electron microscopy. Thus, IE-associated GN most commonly presents with AKI and complicates staphylococcal tricuspid valve infection. Contrary to infection-associated glomerulonephritis in general, the most common pattern of glomerular injury in IE-associated glomerulonephritis was necrotizing and crescentic glomerulonephritis.

Figure 1

Light microscopy findings in endocarditis-associated glomerulonephritis. (a) Cellular crescents with necrotizing foci (Jones methenamine silver; original magnification × 400). (b) Segmental cellular crescent with no underlying proliferation (periodic acid–Schiff; original magnification × 400). (c) Diffuse crescentic glomerulonephritis (Jones methenamine silver; original magnification × 400). (d) Acute focal proliferative glomerulonephritis (hematoxylin and eosin; original magnification × 400). (e) Diffuse proliferative glomerulonephritis (periodic acid–Schiff; original magnification × 400). (f) Mesangial proliferative glomerulonephritis (periodic acid–Schiff; original magnification × 400).

Figure 2

Immunofluorescence microscopy findings in endocarditis-associated glomerulonephritis. (a) Glomerulus with predominantly mesangial staining by C3 (fluorescein-conjugated anti-human C3; original magnification × 400). (b) Glomerulus with mesangial and capillary wall reaction with C3 (fluorescein-conjugated anti-human C3; original magnification × 400).

Figure 3

Electron microscopy findings in endocarditis-associated glomerulonephritis. (a) Mesangial electron-dense deposits (arrow) in diffuse crescentic glomerulonephritis (original magnification × 12,000). (b) Subendothelial electron-dense deposits (arrow) in focal proliferative glomerulonephritis (original magnification × 12,000).