Mb. Andresdottir et al., Type I membranoproliferative glomerulonephritis in a renal allograft: A recurrence induced by a cytomegalovirus infection?, AM J KIDNEY, 35(2), 2000, pp. E6-E12
A 40-year-old white woman with end-stage renal disease from idiopathic type
I membranoproliferative glomerulonephritis (MPGN) developed proteinuria an
d renal dysfunction 7 weeks after cadaveric donor renal transplantation. At
the same time, a primary cytomegalovirus (CMV) infection was diagnosed. Co
mplement levels were low, A renal biopsy disclosed an acute exudative proli
ferative glomerulonephritis with influx of polymorphonuclear granulocytes (
PMNs), with granular deposits of C3, C1q, IgG, and IgM. The immunofluoresce
nce (IF) and electron microscopy (EM) findings were compatible with an earl
y stage of a type I MPGN. CMV could not be detected in the glomeruli nor el
sewhere in the kidney by IF or EM. The patient was treated with ganciclovir
. In a renal biopsy 3 weeks later, the exudative lesions had disappeared, a
nd some glomeruli now showed the characteristic lesions of a type I MPGN wi
th an increase of mesangial cells and matrix, and reduplication of the glom
erular basement membrane. Over the following period, repeated biopsies were
performed. The activity of the glomerular inflammation and immune complex
deposits paralleled the waxing and waning of the CMV viral load. After 10.5
months, the graft was removed because of a life-threatening systemic funga
l infection. At that time, the CMV infection had cleared, and in the transp
lantectomy material, the membranoproliferative pattern of injury had disapp
eared, and in the glomeruli hardly any deposits were found. These data stro
ngly suggest that a primary CMV virus infection can induce an apparent recu
rrence of type I MPGN. (C) 2000 by the National Kidney Foundation, Inc.