Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 43-year-old man developed the nephrotic syndrome 26 months after allogeneic bone-marrow transplantation for chronic myeloid leukemia. This occurred during an exacerbation of graft-versus-host disease (GVHD) and both problems remitted after therapy with cyclosporine and prednisolone. Renal biopsy showed ultrastructural and immunofluorescence evidence of membranous nephropathy. Anti-nuclear antibodies (but not antiglomerular or anti-renal tubular epithelial antibodies) were detected in his serum. Experimental GVHD in mice has been associated with immune complex glomerulonephritis and the presence of IgG autoantibodies which has been attributed to abnormal T (donor)/B (recipient) cell co-operation. This association can be extrapolated to the human GVHD where autoantibody formation is better described than immune complex glomerulonephritis.
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PMID:Membranous nephropathy with graft-versus-host disease in a bone marrow transplant recipient. 156 14

The pathogenesis of renal involvement was studied in murine chronic graft-versus-host disease (GVHD), which is a model for human systemic lupus erythematosus. GVHD was induced by four i.v. injections of lymphocytes from DBA/2 donor mice into (C57BL/10 x DBA/2)F1 hybrids at 3-4-day intervals. Two weeks after the first injection, antibodies were found to have been deposited in the mesangium and along the glomerular basement membrane (GBM) in a linear arrangement, which changed to a granular pattern after 6-8 weeks. In this stage, large electron-dense complexes were present both subepithelially and subendothelially along the GBM. Proteinuria increased up to 11,300 +/- 2140 micrograms/18 h. Indirect immunofluorescence studies and ELISA showed that sera and kidney eluates contained autoantibodies directed against nuclear antigens and GBM component laminin as well as against renal tubular epithelial antigens (RTE). The specificity of the anti-RTE antibodies was further characterized by the use of absorption techniques as well as immunoblotting. The early linear immunofluorescence pattern seems to be associated with glomerular binding of anti-GBM antibodies, while electron-dense complex formation in later stages may be induced by the superimposed deposition of anti-RTE antibodies. Similar phenomena were recently described in Heymann's nephritis in the rat, a model for human membranous nephropathy.
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PMID:Pathogenesis of experimental lupus nephritis: a role for anti-basement membrane and anti-tubular brush border antibodies in murine chronic graft-versus-host disease. 230 29

A bone marrow transplant recipient is described who had development of nephrotic syndrome in association with chronic graft-versus-host disease (GVHD) and on cyclosporine (CsA) treatment withdrawal. Renal biopsy revealed a membranous glomerulonephritis (MG). The possible relationship between this autoimmune disorder, the immunological features of GVHD in experimental animals, and the influence of CsA is discussed.
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PMID:Membranous nephropathy in a bone marrow transplant recipient. 327 9

A 21-year-old male developed massive proteinuria and microscopic hematuria, 1 year after allogeneic BMT for acute lymphoblastic leukemia. These symptoms occurred during an exacerbation of chronic cutaneous graft-versus-host disease (GVHD). Renal biopsy revealed granular deposits of IgG and IgM along the glomerular basement membrane, and subepithelial electron dense deposits. A diagnosis of membranous nephropathy was made. With prednisolone therapy proteinuria decreased gradually, and amelioration of cutaneous lesions was also noted. It was speculated that the disordered immune regulation of chronic GVHD resulted in the development of immune complex nephritis.
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PMID:Nephrotic syndrome in a bone marrow transplant recipient with chronic graft-versus-host disease. 758 Nov 52

A 13-yr-old boy was diagnosed as T cell lymphoma. After the second remission, he underwent BMT from an HLA-identical, MLC negative sibling donor. After BMT, he developed grade II acute GVHD. GVHD was improved by pulsed steroid therapy using prednisolone. About 12 months after BMT, he developed bronchiolitis obliterans, sicca syndrome, and leukoderma, which were related to chronic GVHD. Pulsed steroid therapy was carried out twice, and his condition improved. Twenty-seven months after BMT, he developed nephrotic syndrome. A renal biopsy was performed, and the diagnosis was histologically membranous nephropathy and focal glomerular sclerosis. The response to steroids was not satisfactory. After 5 weeks, dipyridamole was added, but proteinuria persisted. Proteinuria disappeared 8 weeks after the addition of cyclosporine. The second biopsy after 5 months of treatment revealed an improvement in the renal lesions. The patient showed a low T4 to T8 ratio of T-lymphocytes at the onset of nephrotic syndrome. However after treatment with cyclosporine, the ratio gradually increased. These findings suggested the nephrotic syndrome in this patient was related to renal involvement in the course of chronic GVHD.
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PMID:[Nephrotic syndrome related to chronic graft versus host disease after allogeneic bone marrow transplantation in a patient with malignant lymphoma]. 899 26

Expansion of the glomerular mesangial matrix (MM), thickening of the glomerular basement membrane (GBM), and eventually the development of glomerulosclerosis are often seen in immunologically mediated kidney diseases. In addition to quantitative changes in the extracellular matrix (ECM), qualitative changes in ECM molecules may contribute to alterations in the composition of the glomerular matrix. The expression of collagen IV, alpha 1-5(IV) mRNA, and polypeptides was therefore investigated during the development of chronic graft-versus-host disease (GvHD) in mice, a model for lupus nephritis, and in chronic serum sickness (CSS) in rats, a model for membranous nephropathy. Immunohistochemical studies showed increased mesangial expression of alpha 1 and alpha 2 early in the disease, but only late in the GBM. In contrast, alpha 3 and alpha 4 increased in the GBM during disease, but not in the MM. The mRNA levels for all collagen IV chains were increased in isolated glomeruli before morphological alterations were detectable. The mRNA increase was earlier and more profound for alpha 3, alpha 4 and alpha 5 than for alpha 1 and alpha 2. Expression of alpha 3(IV) was greatest in GvHD, whereas expression of alpha 4 was greatest in CSS. As determined by in situ hybridization (ISH), alpha 1 mRNA was observed dispersed in the glomerulus, but alpha 3, alpha 4, and alpha 5 mRNAs were mainly located in cells at the periphery of the glomerular tuft. The changes in the relative abundance of collagen IV mRNA in disease states may perturb the collagen IV network, altering glomerular structure and function, and may thereby play a central role in the development of glomerulonephritis and glomerulosclerosis.
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PMID:Differential expression of collagen IV isoforms in experimental glomerulosclerosis. 961 84

A 42-year-old man with chronic myelogenous leukemia underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) from an unrelated donor in January 1998. About 100 days later, he developed skin eruption and a diagnosis of chronic graft-versus-host disease (cGVHD) was made by skin biopsy. The eruption improved with steroid therapy, and the dose of steroid was gradually tapered. On day 151, the patient developed nephrotic syndrome with proteinuria up to 20 g/day. A renal biopsy carried out on day 160 showed minimal change in the glomeruli. The proteinuria disappeared 19 days after the onset of nephrotic syndrome without any additional therapy, and no recurrence was observed upon re-tapering of the steroid. In this case, cGVHD might have been related to development of the nephrotic syndrome. Nephrotic syndrome after allo-HSCT is a rare complication, and only ten cases have been reported. The histological findings were mainly membranous nephropathy, and immunosuppressive therapy was effective. As seen in this case, transient nephrotic syndrome with cGVHD may occur after allo-HSCT, and care is necessary to ensure that treatment of cGVHD is sufficient.
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PMID:[Transient nephrotic syndrome after allogeneic bone marrow transplantation for chronic myelogenous leukemia]. 1140 Mar 4

Renal involvement during graft-versus-host disease following haematopoietic cell transplantation for multiple myeloma has never been described. We report a case of a recipient who developed nephrotic syndrome and membranous glomerulonephritis 22 months after the graft and 6 months after cyclosporine withdrawal. Symptoms resolved when immunosuppressive therapy was reinstituted.
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PMID:Membranous glomerulonephritis after haematopoietic cell transplantation for multiple myeloma. 1142 58

A 15-year-old boy developed nephrotic syndrome and acute renal failure 4 years after allogenic bone marrow transplantation (BMT) for lymphoid crisis of chronic myelocytic leukemia. On admission, he presented with clinical features of chronic GVHD including transient exacerbation of cholestatic liver injury. Renal biopsy showed diffuse proliferative glomerulonephritis with cellular crescents. The patient was treated with methylprednisolone pulse therapy (1 g/day, for 3 days) followed by oral prednisolone. Renal function gradually improved but nephrotic state was persistent. A second renal biopsy showed improvement of acute tubular necrosis and endocapillary proliferation and transformation of crescents into a fibrous form. After tapering of oral prednisolone, cyclophosphamide was started, which resulted in a gradual improvement of proteinuria. Several cases of nephrotic syndrome occurring after BMT have already been reported, but most cases had membranous nephropathy. In our case, renal biopsy revealed diffuse proliferative glomerulonephritis with findings of active cellular immunity, and aggressive treatment resulted in attenuation of these findings. Moreover, chronic GVHD-related liver injury was noted at the time of this episode. Our findings suggest that chronic GVHD may be complicated with diffuse proliferative glomerulonephritis through unknown cellular immune mechanism.
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PMID:Diffuse proliferative glomerulonephritis after bone marrow transplantation. 1235 94

Nephrotic syndrome has been described as one of the clinical forms of chronic graft-versus-host disease (cGVHD), but a limited number of cases have been described. We experienced a young female patient with nephrotic syndrome developed 22 months after allogeneic hematopoietic stem cell transplantation (HSCT) for severe aplastic anemia. She had been well after successful management for gut-limited cGVHD until she developed a clinical nephrotic syndrome with hypoalbuminemia of 2.0 g/dL and 24-hr urine protein of 6.88 g/dL. On physical examination and laboratory findings, there was no other evidence of cGVHD. Clinical and renal biopsy findings were consistent with cGVHD-related membranous nephropathy, and immunosuppressive agents with cyclosporine and prednisone were prescribed. After 3 month of treatment, the proteinuria decreased to normal range; and the patient from nephrotic syndrome nearly recovered. We recommend cGVHD-related glomerulonephritis should be considered in all patients with hypoalbuminemia following allogeneic HSCT, even if there is no other evidence of clinical GVHD.
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PMID:Membranous nephropathy after allogeneic hematopoietic stem cell transplantation in a patient with aplastic anemia: a case report. 1269 32


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