Deposits of immunoglobulin and fibrin in human allografted kidneys

McKenzie, Ifc; Whittingham, Senga

doi:10.1097/00007890-196910000-00036

Cited by 11 publications

(13 citation statements)

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“…The presence of such complexes in the circulation was shown by a 1251-Clq binding assay, the sensitivity and reproducibility of which has been previously validated in other laboratories in studies of sera from patients with systemic lupus erythematosus, carriers of hepatitis-associated antigen (10), rheumatoid arthritis (13), and by our studies of sera from patients with lupus nephritis, membranoproliferative glomerulonephritis, and other types of nephritides (14). (2)(3)(4).…”

Section: Discussionmentioning

confidence: 81%

Circulating Immune Complexes after Renal Transplantation

Ooi¹,

Ooi²,

Vallota³

et al. 1977

J. Clin. Invest.

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A B S T R A C T To assess the role ofcirculating immune complexes in the pathogenesis of acute rejection, sera were measured for such complexes by the 125I-Clq binding assay in 45 normal subjects, 24 allografted patients undergoing acute rejection, and in 11 allografted patients in a quiescent phase. Increased Clqbinding activity (Clq-BA) was detected in 14 patients with acute rejection, 9 of whom had renal biopsies showing fibrin deposition in the vasculature together with cellular infiltrates in the tubulo-interstitial structures; renal histology was not available in the other 5 patients. The other 10 patients with acute rejection, whose biopsies showed only cellular infiltrates, and the 11 patients in a quiescent phase posttransplantation did not have increased levels of serum Clq-BA.Of the group with increased serum Clq-BA, serial studies in eight patients showed a correlation between increased serum Clq-BA and the occurrence of rejection; with reversal by therapy, serum Clq-BA returned to within normal levels. Complexes from six patients were analyzed by sucrose density gradient ultracentrifugation to have sedimentation coefficients ranging from 15S to 18.4S. After acid dissociation and analysis by double-diffusion techniques, Clq-reactive complexes were shown to contain IgG. Immunofluorescent studies done in five renal biopsies from this group revealed granular deposits of immunoThis work has been previously published in abstract form: 1976. Kidney Int. 10: 608. (Abstr.)

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Section: Discussionmentioning

confidence: 81%

Circulating Immune Complexes after Renal Transplantation

Ooi¹,

Ooi²,

Vallota³

et al. 1977

J. Clin. Invest.

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“…A cute vascular, or humoral, rejection is the occasional cause of irreversible rejection of allografts [1][2][3][4] and a frequent cause of irreversible rejection of xenografts. [5][6][7][8] Studies in human subjects, 9 -13 nonhuman primates, 14,15 and rodents 16 -19 suggest that acute vascular rejection is initiated when antibodies and possibly natural killer cells, platelets, and macrophages directed by antibodies of the recipient react with the endothelial lining of blood vessels in the graft, inducing pathophysiological changes in the cells.…”

mentioning

confidence: 99%

Apoptosis and Cellular Activation in the Pathogenesis of Acute Vascular Rejection

Holzknecht

Kuypers

Plummer

et al. 2002

Circulation Research

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Abstract-Acute vascular or humoral rejection, a vexing outcome of organ transplantation, has been attributed by some to activation and by others to apoptosis of endothelial cells in the graft. We asked which of these processes causes acute vascular rejection by tracing the processes during the development of acute vascular rejection in porcine cardiac xenografts performed in baboons. Apoptosis, assayed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), expression of activated caspase-3, and proapoptotic genes Bax and Bcl-x L , was not detected until acute vascular rejection was well advanced, and even then, apoptosis was largely confined to myocytes. Activation of the endothelium, as evidenced by expansion of rough endoplasmic reticulum and increased ribosomal antigen and phospho-p70 S6 kinase, occurred early in the course of acute vascular rejection and progressed through the disease process. These findings suggest that acute vascular rejection is caused by an active metabolic process and not by apoptosis in the endothelium.

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“…12,13 This study sought to establish with clarity immunofluorescent observations in a relatively homogeneous group of long-term renal allografts at a point in time remote from recent rejection episodes. Such an attempt was made here in a large series of patients with surviving allografts, The data indicate that appreciable immunoglobulin deposition in glomeruli is found in over half of such allografted kidneys.…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports of immunofluorescent observations of human renal allografts have been weakened by three principal qualifications: failure to define the patterns of immunoglobulin deposition and their relative frequency 12 ; failure to define the class as well as the intensity of immunoglobulins in the deposit 13 ; and confusion introduced by the acute events relating to active or recent surges of allograft immunity as reflected in clinical episodes of rejection. 12,13 This study sought to establish with clarity immunofluorescent observations in a relatively homogeneous group of long-term renal allografts at a point in time remote from recent rejection episodes.…”

Section: Discussionmentioning

confidence: 99%

Immunofluorescent Examination of Biopsies from Long-Term Renal Allografts

McPhaul¹,

Dixon²,

Brettschneider³

et al. 1970

N Engl J Med

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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...

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Deposits of immunoglobulin and fibrin in human allografted kidneys

Cited by 11 publications

References 0 publications

Circulating Immune Complexes after Renal Transplantation

Circulating Immune Complexes after Renal Transplantation

Apoptosis and Cellular Activation in the Pathogenesis of Acute Vascular Rejection

Immunofluorescent Examination of Biopsies from Long-Term Renal Allografts

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