Algodystrophy after kidney grafting.
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Biomedical subjects
Publications and source records attributed to D Morel.
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Recently, a new lymphokine called HILDA (human interleukin for DA cells) has been described and cloned. This cytokine, initially described to be produced by alloreactive T lymphocyte clones grown from a rejected human kidney allograft, is identical to other factors termed D-factor, differentiation-inducing factor, differentiation inhibitory activity, hepatocyte-stimulating factor III, and leukemia inhibitory factor. HILDA/LIF induces various effects on neural, hemopoietic, embryonic cells as well as on bone remodeling and acute phase protein synthesis in hepatocyte. In this study we demonstrate the presence of HILDA/LIF in the urine but not in the serum of kidney graft recipients during acute rejection episodes, whereas this lymphokine was detectable neither in the serum nor in the urine of kidney transplanted patients with stable renal function. These data reinforce the notion of a possible role for this lymphokine in the inflammatory and/or the immune response.
The development of necrosis and macrophage infiltration increases the risk of renal graft rejection. But the macrophages secrete the alpha form of the tumour necrosing factor (TNF) which is also involved in several immunologic and inflammatory phenomena. We therefore studied the expression of the gene TNF alpha by in situ hybridization during advanced stage rejection after renal transplantation: the grafts were infiltrated with macrophage-like cells expressing the mRNA of the TNF alpha gene, particularly deep in the cortex and in the medulla. These cells then secrete the TNF alpha molecule since they are recognized by anti-TNF alpha antibodies. These antibodies also recognize certain other glomerular endothelial and tubular epithelial cells which do not express the TNF alpha gene: these cells are undoubtedly the TNF target cells. These findings confirm the synthesis of TNF alpha in advanced stage renal graft rejection.
One hundred ninety-five color Doppler flow (CDF) examinations were performed in 146 renal allografts to assess the capabilities of this technique in detecting intra- or extrarenal vascular complications. Conventional angiography was also performed in 44 transplants. In the group of transplants with angiographic correlation, CDF sonography enabled correct identification of 30 of 34 vascular complications. CDF showed 10 of 11 significant stenoses of the renal artery or of one of its main branches. There were two false-positive renal artery stenoses (one normal artery and one 40% stenosis). Nine of nine renal artery thromboses and the single pseudoaneurysm were also identified. Within the parenchyma, CDF sonography demonstrated five of five segmental infarcts, two of two postbiopsy arteriovenous fistulas, and three of six segmental or interlobar artery stenoses. Measurement of peak systolic velocity showed a significant difference (P less than .05) between a group (n = 8) with significant stenosis of the renal artery or one of its main branches (mean, 215.2 cm/sec +/- 32) and a group (n = 14) without stenosis (mean, 99.2 cm/sec +/- 19).
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