Glomerulonephritis with anti-glomerular basement membrane antibody during pregnancy: potential role of the placenta in amelioration of disease.
A case of rapidly progressive glomerulonephritis with glomerular deposition of anti-glomerular basement membrane (anti-GBM) antibody during pregnancy is described. Development of precipitous renal failure postpartum raised the possibility that the placenta may have served as an adsorptive surface for the autoantibody, thereby ameliorating its manifestations antepartum. Sera from the patient obtained during pregnancy contained low titers of anti-GBM immunoglobulin G. No antibody was identified in the serum from the healthy infant. Additional studies of this patient's sera, as well as sera from other patients with documented anti-GBM antibody-mediated glomerulonephritis, demonstrated that binding of anti-GBM antibody to placental membranes can occur, although it appears weaker than binding to basement membranes in renal glomeruli. We postulate that the patient's accelerated decline in renal function postpartum may have been due to removal of the ameliorating influence of the placenta.
Department of Pathology, University of Washington, Seattle 98195.
H
H
Deubner
J P
JP
Wagnild
M H
MH
Wener
C E
CE
Alpers
D000328:Adult; D001323:Autoantibodies / Q000378:metabolism*; D001485:Basement Membrane / Q000276:immunology; D005260:Female; D005921:Glomerulonephritis / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D007678:Kidney Glomerulus / Q000276:immunology*; D010920:Placenta / Q000276:immunology / Q000502:physiology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology*
D001323:Autoantibodies; D007074:Immunoglobulin G