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In order to investigate the clinical usage of SNB-5001 (recombinant human erythropoietin), two types of anemic models induced by drugs were prepared. One group of rats was intravenously injected with 8 mg/kg of cisplatin. These rats temporarily showed leucopenia and thrombocytopenia. Since 2 weeks after the cisplatin injection, rats chronically showed renal failure and moderate anemia. Another group was subcutaneously injected with 15 mg/kg of puromycin, 4 times a week, for 3 weeks. These rats showed hypercholesteremia and hypoalbuminemia, and they showed chronic renal failure and severe progressive anemia. Anemic rats received SNB-5001 (50 or 500 U/kg) once a day for 7 days. In the anemic rats induced by cisplatin, more than 50 U/kg of SNB-5001 dose-dependently increased reticulocytes, red blood cells (RBC), hemoglobin (HGB) and hematocrits (HCT). SNB-5001 apparently improved the anemia induced by cisplatin. On the other hand, in anemic rats induced by puromycin, 50 U/kg of SNB-5001 increased reticulocytes, but did not increase RBC, HGB and HCT. SNB-5001 at the dose of 500 U/kg stopped the progress of anemia in puromycin treated rats. It was suggested that SNB-5001 is useful for the improvement of renal anemia induced by drugs, but the effects are affected by the uremic condition and the stage of renal anemia.

This study deals with the quantification of mRNA of basement membrane components (laminin, type IV collagen, heparan sulfate proteoglycan) and type I collagen in focal glomerular sclerosis induced by the aminonucleoside of puromycin (PAN) in rats. PAN (15 mg/100 g B.W.) was injected intraperitoneally to male Sprague-Dawley rats on day 0. On day 22, the right kidney was removed from group II and III. Rats in group III received injections of PAN (5 mg/100 g B.W.) on day 27, 34 and 41. Rats in group II received injections of 0.9% NaCl instead of PAN. Remnant kidneys were removed on days 48, 60 and 80 and processed for RNA isolation and histopathological study. Glomerular RNAs were isolated using guanidinium thiocyanate and then dotted onto nylon membrane. Filters were hybridized with specific cDNA probes and exposed to film for analysis by densitometer. FGS was detected in 70% of glomeruli on day 80 in group II. All the basement membrane components and type I collagen were accumulated in the sclerotic areas. The mRNA coding for laminin and type IV collagen continued to increase in group III till day 80. The mRNA for HSPG decreased when the urinary protein excretion was maximum on day 48, then increased with the remission of proteinuria. The type I collagen mRNA also increased during the course of the FGS. We suggest that decrease of mRNA for HSPG may play an important role in the development of proteinuria in PAN nephrosis and increase of mRNA coding for laminin, type IV collagen and type I collagen may be involved in focal glomerular sclerosis.