Renal Osteodystrophy
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New findings from K. Kusano and co-researchers in the area of renal osteodystrophy described
2009 JUN 1 - (NewsRx.com) -- "Phosphorus is one of the important factors that accelerate the progression of chronic kidney disease. Phosphorus restriction or phosphate binders have been reported to have the ability to prevent the progression of chronic kidney disease," researchers in Shizuoka, Japan report. "FGF23 is a circulating factor that regulates renal phosphorus reabsorption and 1 alpha-hydroxylase activity. We focused on the phosphaturic activity of FGF23 and investigated whether a pharmacological dose of FGF23 is beneficial to the Progression of renal insufficiency in uremic rats. To this end, we administered one of the mutant FGF23 expression plasmids into irreversible Thy1 rats. Chronic renal failure rats were established by intravenous injection of anti-rat CD90 (Thy1.1) monoclonal antibody to unilaterally nephrectomized Wistar rats. The rats were then intravenously injected every 2 wk with a naked DNA Solution containing 10 mu g of MOCK vector or a mutant FGF23 expression plasmid for 13 wk. Renal function was assessed biochemically and histopathologically, Mutant FGF23 significantly decreased serum creatinine and serum urea nitrogen. The marked glomerular sclerosis observed in uremic rats receiving the MOCK vector was ameliorated in rats treated with mutant FGF23. However. mutant FGF23 not only significantly decreased serum 1,25(OH)(2)D and calcium but also aggravated high-turnover renal osteodystrophy from extremely high levels of PTH. These results might: be a result of the mechanisms of FGF23 such as phosphaturic activity and lowering the level of 1,25(OH)(2)D," wrote K. Kusano and colleagues. The researchers concluded: "Mutant FGP23 prevented the progression of chronic renal failure by regulating serum phosphorus but aggravated renal osteodystrophy from the lowered levels of 1,25(OH)(2)D." Kusano and colleagues published their study in the Journal of Nutritional Science and Vitaminology (Mutant FGF23 Prevents the Progression of Chronic Kidney Disease but Aggravates Renal Osteodystrophy in Uremic Rats. Journal of Nutritional Science and Vitaminology, 2009;55(2):99-105). For additional information, contact K. Kusano, Chugai Pharmaceutical Co. Ltd, Pharmaceutical Research Department, 1-135 Komakado, Shizuoka 4128513, Japan. Publisher contact information for the Journal of Nutritional Science and Vitaminology is: Center Academic Publ Japan, 2-4-16 Yayoi, Bunkyo-Ku, Tokyo, 113-0032, Japan. Keywords: Japan, Shizuoka, Alternative Medicine, Biotechnology, Chronic Kidney Failure, Chronic Renal Failure, DNA, Enzyme Research, Hydroxylase, Kidney, Kidney Disease, Medical Device, Monoclonal Antibody, Nephrology, Pharmaceuticals, Pharmacological, Renal Failure, Renal Insufficiency, Renal Osteodystrophy, Therapy, Treatment, Vitaminology. This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2009, Biotech Business Week via NewsRx.com.
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