Duchenne muscular dystrophy is a severe muscular disorder, often complicated with osteoporosis, and impaired renal function has recently been featured. We aimed to clarify the involvement of renal function in the pathogenesis of mineral and bone disorder in mdx mice, a murine model of the disease. We clearly revealed renal dysfunction in adult mdx mice, in which dehydration and hypercalcemia were contributed. We also examined the effects of dietary phosphorus (P) overload on phosphate metabolism. Serum phosphate and parathyroid hormone (PTH) levels were significantly increased in mdx mice by dietary P in a dose-dependent manner; however, bone alkaline phosphatase levels were significantly lower in mdx mice. Additionally, bone mineral density in mdx mice were even worsened by increased dietary P in a dose-dependent manner. These results suggested that the uncoupling of bone formation and resorption was enhanced by skeletal resistance to PTH due to renal failure in mdx mice.

中文翻译：

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肾脏参与肌营养不良蛋白缺陷型mdx小鼠的矿物质和骨骼疾病的发病机理。

杜兴氏肌营养不良症是一种严重的肌肉疾病，通常并发骨质疏松症，并且最近已表现出肾功能受损。我们旨在阐明肾脏功能与该疾病的小鼠模型mdx小鼠的矿物质和骨骼疾病的发病机理有关。我们清楚地揭示了成年mdx小鼠的肾功能不全，其中有脱水和高钙血症。我们还检查了饮食中磷（P）超载对磷酸盐代谢的影响。饮食P通过剂量P显着增加mdx小鼠的血清磷酸盐和甲状旁腺激素（PTH）水平；但是，mdx小鼠的骨碱性磷酸酶水平明显降低。另外，饮食中P的增加以剂量依赖的方式使mdx小鼠的骨矿物质密度更加恶化。