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. 2013 Apr 4;24(8):1204–1208. doi: 10.1681/ASN.2012070665

Table 2.

Cases of anti-GBM GN in HIV-infected patients

Study (Reference) Age (yr) Sex CD4 Count (cells/ml) Organs SCr (mg/dl) Renal Pathology Treatment Outcome Anti-GBM Level Complications
Pre Post
Monteiro et al. (3) 30 Male 495 Kidney 13.5 Necrotizing crescentic (50%) GN PLEX × 14 d
Corticosteroidsa 
Cyclophosphamide, 1.5 mg/kg per d ESRD 68 U/ml NA NA
Wechsler et al. (4) 55 Male 305 Kidney 3.5 Necrotizing crescentic (10%) GN PLEX × 14 d Corticosteroidsb Resolution 8.6 EU/mlc 0 EU/ml Nausea, vomiting, hematemesis
SCr 1.1 mg/dl 6 wk after treatment
IgA nephropathy MMF
IVIG
Rituximab × 4 wk
Singh et al. (5) 33 Male 214 Kidney 19.3 Necrotizing crescentic GN PLEX × 5 d ESRD 361 AU/ml 40 AU/ml Hypoxia (atypical pneumonia versus hemorrhage)
Lung ATN Corticosteroidsd
Current report 42 Male 679 Kidney 1.89 Necrotizing crescentic GN PLEX × 14 d Corticosteroidse Cyclophosphamide, 100 mg/d ESRD 366 AU/mlf 104 AU/ml EBV and CMV viremia

SCr, serum creatinine; anti-GBM pre and post, anti-GBM antibody titers before and 4 wk after treatment; PLEX, plasmapheresis; NA, not available; MMF, mycophenolate mofetil; IVIG, intravenous immunoglobulin; ATN, acute tubular necrosis;

a

1 mg/kg per day.

b

40 mg/d.

c

Reference values, 0–5 EU/ml.

d

Methylprednisone, 1000 mg/d × 3 d; IVIG, 140 g (10% solution); rituximab, 375 mg/m2 per wk × 4 wk.

e

Methylprednisolone, 750 mg/d × 1 d, 500 mg/d × 1 day, 250 mg/d × 1 day, then prednisone, 80 mg/d × 5 d, then 60 mg/d.

f

Reference values, 0–19 AU/ml.