ABSTRACT
Basic fibroblast growth factor (FGF2) is generally known to induce proliferation of cultured mesangial cells and is expressed in proliferative mesangial cells in anti-Thy1.1 mesangial proliferative glomerulonephritis (anti-Thy1.1 GN). The distribution of the FGF receptor (FGFR) has not been studied in anti-Thy1.1 GN, so we used in situ hybridization to determine whether cells expressing FGFR1-4 mRNAs could be detected. In normal rats, all glomeruli were negative for FGFR1-4 mRNA, but those of the mesangial proliferative phase expressed FGFR1-4 mRNA in proliferative mesangial cells. Proliferation of mesangial cells has not been observed in normal rats injected with FGF2( )but it has been noted in anti-Thy1.1 rats injected with FGF2. These data and our results demonstrate that mesangial cells produce and release FGF2( )after injury and that during the proliferative phase these cells upregulate FGFR in vivo. This study is the first to demonstrate expression of FGFR1-4 mRNAs in pathological glomeruli of anti-Thy1.1 GN. The FGF2 and FGFR1-4 genes were expressed in the proliferative mesangial cells. Upregulation of FGFR is necessary for mesangial proliferation by FGF2.
Subject(s)
Gene Expression , Glomerulonephritis, Membranoproliferative/metabolism , Kidney Glomerulus/metabolism , Receptors, Fibroblast Growth Factor/metabolism , Animals , Antigens, Differentiation/metabolism , Cell Count , Cell Division , Disease Models, Animal , Glomerulonephritis, Membranoproliferative/immunology , Glomerulonephritis, Membranoproliferative/pathology , In Situ Hybridization , Kidney Glomerulus/pathology , Macrophages/cytology , Male , Monocytes/cytology , Proliferating Cell Nuclear Antigen/metabolism , RNA, Messenger/biosynthesis , Rats , Rats, Wistar , Receptors, Fibroblast Growth Factor/genetics , Reverse Transcriptase Polymerase Chain Reaction , Thy-1 Antigens/immunologyABSTRACT
We describe a 26-year-old male hemodialysis patient with erythropoietin (EPO) resistant anemia associated with primary hyperthyroidism. Use of the anti-hyperthyroid drug, methimazole, led to improvement of his hyperthyroidism and anemia. Before the anti-hyperthyroid therapy, he had received transfusions to maintain an adequate hematocrit during recombinant human EPO therapy. After the therapy, his hyperthyroidism improved and his hematocrit gradually increased without any transfusion. These findings suggest that the patient's EPO resistant anemia was the result of primary hyperthyroidism, and that this complication is reversible if accurate treatment is given.
