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.
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 EPOtherapy. 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. (Internal Medicine 36: 903-905, 1997)
prevalent haemodialysis patients in our centre and to find correlation, if any, with the morbidity pattern. Methods: This is a cross-sectional study of iron status among prevalent hemodialysis in a single centre in Shivamogga district of South India. Serum Iron , transferrin saturation(Tsat) and ferritin levels were estimated in 55 patients undergoing haemodialysis. Retrospective study of their case files was done to record other demographic and medical details such as dialysis vintage, hospitalizations, access failures, infection and cardiovascular events. Pearson's product moment correlation was done to analyse if there was any correlation between ferritin and Tsat with these parameters. Results: 55 patients (47 males; mean age 57 yrsAE12.6years) were studied. Dialysis vintage ranged from 3 months to 132 months. 51% were diabetics. All of them had hypertension. 9% had ischemic heart disease and 7% had cerebrovascular disease. 52 patients received iron sucrose.41 patients were on erythropoietin and 13 were on darbepoietin. Median dose of Iron sucrose was 50 mg per week. Median values of haemoglobin, iron , Tsat and ferritin was 9.9g/dl, 62.3mcg/ dl, 32.32% and 940.4ng/ml respectively. 60% had hospitalization at some point in their dialysis course, 20% had access thrombosis and positive blood cultures had been obtained from 25%. In all, 25% had developed pulmonary artery hypertension. There was positive correlation of ferritin with Tsat (r=0.552, p<0.001) and dialysis vintage (r=0.507, p<0.001). There was no correlation of either serum ferritin or Tsat with hospitalization, access failure, cardiovascular events or fractures. Conclusions: Iron status indicators are often grossly elevated in dialysis patients and the levels correlate positively with dialysis vintage. No significant positive correlations were noted with morbidity events in this study. However the numbers studied are small and is a limitation of our study.
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