In the present study, two series of experiments were done with PAN nephropathy rats given fibroblast growth factor 2 (FGF2) or FGF2 neutralizing antibodies. In the first series of experiments, a dose of 10 micrograms of FGF2 (FGF2 group), 40 micrograms of an FGF2 neutralizing antibody (Anti-FGF2 group) or an equal volume of physiological saline (Control group) was administered for four days after PAN injection. Urinary protein increased more in the FGF2 group than in the other two groups. PCNA (+) glomerular cells were found in decreasing order in groups FGF2, Control and Anti-FGF2. Most of the PCNA (+) cells were podocytes and epithelial cells of Bowman's capsule. Staining for desmin, a marker of podocyte injury, was significantly reduced in the Anti-FGF2 group. Glomerular adhesive lesions were found in decreasing order in groups FGF2, Control and Anti-FGF2. The second series of experiments was designed to study the effects of FGF2 neutralizing antibody (40 micrograms for 5 days after PAN injection, in MoAb group) on severely damaged podocytes caused by repeated (two courses) injections in the PAN nephropathy rats. The results were the same as those in series 1. An increase in urinary protein excretion was observed in both groups, but on the 40th day, the level of proteinuria in the MoAb group decreased abruptly. It was observed that the MoAb group had few adhesive glomeruli compared to the IgG group (administration of mouse IgG) and the PCNA (+) epithelial cells of Bowman's capsule were also few. It was supposed that FGF2 would promote the formation of adhesive lesions by stimulating the proliferation of podocytes and epithelial cells of Bowman's capsule. Additionally, FGF2 itself was thought to impair podocytes because of the increasing desmin score and proteinuria.
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)
Abstract. Cultured, rat glomerular podocytes were examined by electron microscopy and immunohistochemistry in order to determine their origin. The outgrowth of polygonal cells was noted first. Large arboroid ceils were occasionally observed around the polygonal cells. Immunostaining of these large arboroid cells for the intermediate filament proteins showed an intensely positive reaction for vimentin, whereas cytokeratin was not detected. In the polygonal cells, however, both cytokeratin and vimentin were sometimes detected. Although scanning electron microscopy did not detect any specific irregularities in podocytes on the surface of the glomerulus, developing polygonal cells were observed. Both transmission and scanning electron microscopies revealed the polygonal cells to be similar to Bowman's capsule epithelial cells in situ. The vascular poles of the cultured glomeruli were always in contact with the culture dish. A residual Bowman's capsule was also observed. These results suggest that polygonal cells originate from the epithelial cells of the residual Bowman's capsule, whereas large arboroid cells arise from podocytes.
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