Table 3.

Characteristics of glomerulonephritis associated with endocarditis due to Capnocytophaga species.

Characteristic	Present Case	Archer, 1985 [3]	Kannan, 2001 [4]
Cr at presentation, mg/dL	2.9	1.2	3.2
Urine WBC/hpf	396	Not described	Not described
Urine RBC/hpf	1450	60	20–40
Proteinuria, g/24-h	3.6	3.0	2+ proteinuria
Serum C3 level	Low	Low	Normal
Serum C4 level	Low	Normal	Normal
Cryoglobulins	Present; IgM monoclonal protein with kappa light chain specificity	Absent	Not described
ANA	Absent	Absent	Absent
Light microscopy	Glomeruli show endocapillary proliferation with abundant neutrophil infiltrate; reactive visceral and parietal epithelial cells are present forming minicrescents; Fibrin occ. associated w/the crescents; duplication of the glomerular basement membrane not identified; mild intimal thickening of arteries w/o vasculitis; moderate lymphoplasmacytic and neutrophil infiltrate of interstitium with occ. aggregates of eosinophils; neutrophil infiltrates of tubules w/occ. WBC casts. Rare necrotic tubules associated with WBC casts; moderate interstitial fibrosis	Increased mesangium pushing into capillary loops.	Glomeruli show segmental necrosis and crescents of varying sizes. Heavy infiltrate of inflammatory cells seen in the interstitium. No vascular lesions seen.
Fluorescence microscopy	Glomeruli are granularly stained: IgG 2-3+, IgA 1+, IgM 1+, C3 3+, C1q 1+, Fibrin Negative, Kappa 1+ and Lambda 1+	Negative results for IgG and IgM and weakly positive results for complement.	2+ granular IgM and C3 in a global mesangial and capillary wall distribution, and IgA, IgG, CIq, 1+ granular in a segmental mesangial distribution.
Electron microscopy	Ultrastructural study of parts of two glomeruli shows prominent endocapillary proliferation with numerous neutrophils in glomerular capillary lumen and mesangial matrix; poorly formed immune complex deposits primarily within the mesangial and paramesangial portions of glomeruli. Hump subepithelial deposits not identified; effacement of the overlying visceral epithelial foot processes associated w/ swelling of visceral epithelial cell cytoplasm and occ. poorly formed pseudovillous transformation. Vacuolar degeneration of the tubular epithelia.	Features consistent with type 1 membranoproliferative GN and not with type 2, or “dense deposit” disease	Glomeruli show cellular crescents, one associated w/ the rupture of the capillary wall. Finely granular and microfibrillary deposits seen in mesangium and paramesangium. Interstitium contained an inflammatory cell infiltrate. No vasculitis seen.
Overall impression	Resembles postinfectious GN	Type 1 membranoproliferative GN (decreased serum C3 level, increased mesangial tissue and capillary wall thickening; milder course than type 2); resembles postinfectious GN	Necrotizing and crescentic immune-complex glomerulonephritis.
Outcome	Required hemodialysis; no indication of improvement over 12 weeks at the time of death	Recovered	Recovered

Abbreviations: Cr, creatinine; WBC, white blood cells; RBC, red blood cells; C3, complement 3; C4, complement 4; ANA, anti-nuclear antibody; occ., occasional; w/, with; w/o, without; IgG, immunoglobulin G; IgM, immunoglobulin M; IgA, immunoglobulin A; C1q, complement 1q; GN, glomerulonephritis.