Concurrent Antiglomerular Basement Membrane Disease and Immune Complex Glomerulonephritis

Figures & data

Table 1 Comparison of clinical and laboratory data of patients with anti-GBM disease, with and without glomerular immune complexes

	With glomerular immune complexes (n = 10)	Anti-GBM diseasealone (n = 37)
M/F	6/4	28/9
Mean age; yr (range)	40 (18–67)	32 (13–66)
Anti-GBM antibodies (%)	106.3 ± 59.5	92.7 ± 44.8
With ANCA positive	2 (20%)	8 (22%)
Exposure to hydrocarbons	1 (10%)	5 (14%)
Smoker	4 (40%)	19 (51%)
Upper respiratory tract infection	4 (40%)	21 (57%)
Hemoptysis	3 (30%)	19 (51%)
Hematuria	10 (100%)	36 (97%)
Proteinuria	10 (100%)	36 (97%)
Nephrotic syndrome	4 (40%)	11 (30%)
Oligo-anuria	4 (40%)	20 (54%)
Serum creatitine at presentation(μmol/L)	861.3 ± 274.1	823.4 ± 410.1
Hemoglobin (g/L)	83.0 ± 28.0	79.3 ± 25.3
Percentage of crescents (%)	93.8 ± 13.1	84.0 ± 26.3
Plasma exchange	3 (30%)	20 (54%)
MP + Pred + CTX	10 (100%)	32 (86%)
Dialysis independent	1 (10%)	9 (24%)

MP: methylprednisolone pulse; Pred: prednisolone; CTX: cyclophosphamide.

Figure 1. Subepithelial electron-dense deposits were seen by electron microscope (arrowheads).

Figure 2. Subepithelial electron-dense deposits were seen by electron microscope (arrowheads).

Figure 3. Electron-dense deposits in mesangium were seen by electron microscopy (arrowheads).

Figure 4. Subendothelial and subepithelial electron-dense deposits were seen by electron microscopy (arrowheads).

Figure 5. Electron-dense deposits in mesangium were seen by electron microscopy (arrowheads).

Figure 6. Electron-dense deposits in GBM and mesangium were seen by electron microscopy (arrowheads).