Recurrent Antibasementmembrane Nephritis after Renal Homotransplantation

Abstract

Introduction

Morphological alterations of the transplanted kidney are in most instances caused by homograft rejection. So far only very few cases with recurrent glomerulonephritis of the transplanted organ have been reported. This paper deals with a recurrent glomerulonephritis indicated by the presence of circulating antibodies and histological, immunhistologic and electronmicroscopic changes in the patient's own as well as in the transplanted kidney.

Material and methods

Autoantibodies directed against glomerular basement membrane antigens could be demonstrated in double diffusion gelprecipitation-tests. Immunofluorescence and microscopic examinations as well as electronmicroscopic studies were performed using kidney biopsy material or material obtained during the operation. In all instances the direct immunofluorescence method was used. Part of the kidney tissue was fixed in formalin for light microscopic studies. Other specimens were fixed in 2.5% glutaraldehyde and postfixed in 1.33% Osmic acid. The material was then embedded in Epon 812 for electronmicroscopic examination.

Results

Autoantibodies against glomerular basement membrane antigens were demonstrable before nephrectomy and approximately half a year after the transplantation whereas few months after transplantation such antibodies could not be observed.

Light and electronmicroscopic studies of the patient's own as well as the transplanted kidney revealed scarring of most of the glomerula, the capillaries showed cell proliferation and numerous leucocytes. In some instances, proliferation of the capsular epithelium could be observed. The lobular alterations of the glomerular lesions were characteristic. Electronmicroscopic examinations revealed splitting of the basement membrane with cellular infiltrations in the areas of the altered basement membrane as well as in the mesangium. Between the cellular fragments and the outer part of the basement membrane electron dense deposits could be observed. The epithelial cells of the glomerular capillaries were in most instances markedly swollen, the foot processes were diminished. In some instances vacuoles could be observed in the plasma of podocytes. The changes in the patient's own kidney as well as in the transplanted kidney were quite similar.

Immunhistological studies revealed marked fluorescence at the basement membrane as well as in the mesangium. By immunofluorescence deposits consisting predominantly of IgA and IgG, but also C'3 and C'4 could be demonstrated.

Discussion

These immunological, immunhistological, mircoscopical and electronmicroscopical findings indicate that membranoproliferative glomerulonephritis can occur in the transplanted kidney if it had been present in the patient's own kidney. In the case reported here the patient suffered from a progressive membranoproliferative glomerulonephritis. After removal of both kidneys and homotransplantation the same renal disease occurred in the transplanted organ approximately six months after transplantation.