Demonstration of a passive Heymann nephritis-like mechanism in a human kidney transplant.

The underlying mechanism of human extramembranous glomerulonephritis (EMGN) is generally thought to involve circulating immune complexes. Data presented here suggest that "in situ" formation of immune deposits may also be important in the pathogenesis of EMGN. We describe a patient with a "de novo" EMGN in a kidney transplant a few months after the graft placement. Before transplantation, the patient's serum contained antibodies reacting in vitro with rat kidney brush-border, but serum concentration of these antibodies rapidly decreased prior to the onset of proteinuria. No circulating immune complexes were detected on serial serum samples from the patients. Antibodies which were eluted from the kidney transplant biopsy were shown to react with the brush-border of the proximal convoluted tubule of rat kidney. We postulate that "in situ" formation of immune complexes within the glomerular capillary walls, and not circulating immune complexes, is the pathogenic mechanism responsible for the glomerular lesions of this case of EMGN.