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Immunofluorescent examination of open renal biopsies revealed clear-cut glomerular localization of immunoglobulins not related clearly to the quality of donor-recipient histocompatibility in 19 of 34 renal allografts. The biopsies were obtained 18 to 31 months after transplantations primarily from related donors with a variable quality of histocompatibility match. IgG was the predominant immunoglobulin class fixed in 13 biopsies, and IgM in six. The pattern of immunoglobulin deposition was linear, connoting anti-GBM antibody in four of the 19; it was granular and discontinuous, connoting antigen-antibody-complex deposits, in 13. An immune process may affect glomeruli of renal allografts by mechanisms comparable to those that cause glomerulonephritis in native kidneys. The transplant glomerulonephritis may represent a persistence of the same disease that originally destroyed the host kidneys or the consequence of a new humoral antibody response to allograft antigens.The occurrence of glomerular lesions in viable renal allografts has been well documented by light and electron microscopy of biopsy material. [1][2][3][4] Understanding of the pathogenesis for the morphologic changes, however, is not clear. In particular, uncertainty exists concerning the role of well defined mechanisms 5,6 known to mediate glomerulonephritis in native kidneys in causing glomerular disease in the transplanted kidney.It is the purpose of this report to present results of immunofluorescent examinations of 34 human renal allografts. These observations are derived from a series of renal grafts, functional 18 to 31 months after implantation. All but three of the kidneys were from living, related donors, and all the recipients were treated initially with antilymphocyte globulin (ALG). 7 The results indicate considerable focal or generalized immunoglobulin deposits in glomeruli of over half the allograft biopsies studied, and document the occurrence of antiglomerular basement-membrane (anti-GBM) antibodies, in 20 per cent of the glomeruli showing such fixation. Although immunoglobulin M (IgM) occasionally was found in the absence of immunoglobulin G (IgG), IgM deposits were usually in the company of IgG deposits, often of a different distribution and distinctly less extensive.The data are compatible with the hypothesis that the glomerular lesions observed are the result of conventional mechanisms known to cause glomerulonephritis in native kidneys. Such a hypothesis suggests that the glomerular injury in the allografts is either a result of the same antibody responsible for the pre-existing processes that originally destroyed the patient's own kidneys or a de novo humoral-antibody response to the alien antigens of the new organ. MATERIALS AND METHODSThirty-five patients receiving renal allografts at Colorado University Medical Center between June 21, 1966, and August 25, 1967, were readmitted to the Center in January, 1969, for routine re-evaluation and biopsy of the transplants. An additional patient with cystinosis who had had a t...

In summary, IgA-associated glomerulonephritis is an interesting clinical problem. The immunohistochemical identification of renal IgA deposits is the sine qua non of its diagnosis, although most of the patients reported have had hematuric syndromes, particularly recurrent gross hematuria. The importance of this immunopathologic entity devolves from the crucial use of special stains to identify IgA, the enigmatic role of IgA, the usual mesangioapthic expression of histologic response, and the ill-defined relationship of this clinical problem to nephropathies associated with systemic diseases that also have glomerular IgA deposits. Although still unproven, it is likely that the usual instance of IgA-associated glomerulonephritis is due to deposition of circulating immune complexes containing IgA. The nature of the exciting antigen(s), quantitative measures and characteristics of such complexes, and the role of mediating systems, including coagulation, have not yet been elucidated.

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