Connective-Tissue Disease and Rheumatoid Factors in Patients with Renal Transplants

Waller, Marion; Irby, Robert; Mullinax, Franklin; Toone, Elam G.

doi:10.1056/nejm196507012730103

Cited by 37 publications

(15 citation statements)

References 13 publications

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“…The reported prevalence of rheumatoid factor and heterophil antibodies in recipients after renal transplantation 16 suggests that IgM present in glomeruli may be there as part of macromolecular complexes somehow evoked by the allograft, such as IgM anti-IgG antibodies. 17 The lack of any apparent correlation between the findings of fibrinogen or fibrin and immunoglobulin in the glomeruli or between the presence of fibrin and abnormal renal function or histoincompatibility raises some question of the role of fibrin formation in the pathogenesis of glomerular injury in these transplants.…”

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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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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“…Since joint effusions and arthralgias are not uncommon posttransplant, a septic etiology may not be considered early. In 2 patients (cases 2 and 3) the symp toms were mild and indolent, and could have been confused with the connective tissue-like disorders observed after transplantation [1][2][3]. Prompt treatment may have contrib uted to survival in all, including the 2 patients with gram negative arthritis.…”

Section: Diagnosis and Treatmentmentioning

confidence: 99%

“…Treatment of these initial extra articular infections may have been inadequate or delayed. Finally, it is possible that changes occur in the synovium per se following transplantation that may predispose it to infection [1][2][3].…”

Section: Predisposing Factorsmentioning

confidence: 99%

“…Avascular bone necrosis, synovitis, and arthralgias have been described in a significant number of transplant patients [1,2]. Steroid therapy has been impli cated in some of these disorders [17].…”

Section: Diagnosis and Treatmentmentioning

confidence: 99%

“…Articular complications consisting of arthralgia, syno vitis and avascular necrosis are frequent problems follow ing renal transplantation [1][2][3]. Septic joint complications have not been previously reported, despite the frequent occurrence of bacterial infections in other sites in these immunosuppressed patients [4,5].…”

Section: Introductionmentioning

confidence: 99%

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Septic Arthritis following Renal Transplantation

Vincenti¹,

Amend²,

Feduska³

et al. 1982

Nephron

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Monoarticular septic arthritis without disseminating sepsis occurred in 4 patients following renal transplantation. The septic arthritis was preceded by an infection with the same organism in an extraarticular location (3 urinary tract, 1 upper respiratory). All patients were on prednisone-azathioprine immunosuppressive regimen but none had granulocytopenia. Prompt antibiotic therapy resulted in quick resolution of the joint infection in 3 patients. Impaired host defenses, possible inadequate prior antibiotic therapy, and intrinsic joint alterations are potential contributing factors to the development of septic arthritis following renal transplantation.

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Modification of Renal Allograft Rejection in Man

Carpenter¹,

Merrill²

1969

Arch Intern Med

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Connective-Tissue Disease and Rheumatoid Factors in Patients with Renal Transplants

Cited by 37 publications

References 13 publications

Immunofluorescent Examination of Biopsies from Long-Term Renal Allografts

Immunofluorescent Examination of Biopsies from Long-Term Renal Allografts

Septic Arthritis following Renal Transplantation

Modification of Renal Allograft Rejection in Man

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