期刊
KIDNEY INTERNATIONAL
卷 68, 期 2, 页码 642-652出版社
ELSEVIER SCIENCE INC
DOI: 10.1111/j.1523-1755.2005.00442.x
关键词
chloride channel; hypercalciuria; nephrocalcinosis; renal insufficiency; Dent's disease; citrate
资金
- NIDDK NIH HHS [DKO64388, DK32753] Funding Source: Medline
Background. Dent's disease, an X-linked renal tubular disorder, is characterized by low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, nephrolithiasis, and progressive renal failure. Dent's disease results from mutations of the voltage-gated chloride channel CLC-5. Methods. We studied the effect of zero and high citrate diet on renal function of ClC-5 knockout mice and wild-type mice. The mice were placed in metabolic cages from which the urine was collected. Mice were sacrificed to obtain serum and tissues for analysis. Results. ClC-5 knockout mice fed zero or high citrate diet had significantly increased urinary calcium excretion compared with wild-type mice fed the same diets. Nine-month-old ClC-5 knockout mice on a zero citrate diet had significantly decreased glomerular filtration rate (GFR), whereas 9-month- old ClC-5 knockout mice on a high citrate diet had normal renal function. ClC-5 knockout mice fed a zero citrate diet had significantly increased tubular atrophy, interstitial fibrosis, cystic changes, and nephrocalcinosis compared to ClC-5 knockout mice fed a high citrate diet. Transforming growth factor-b1 (TGF-b1) was significantly increased in 9-month- old ClC-5 knockout mice on zero citrate diet compared to 9-month- old wild-type mice on the same diet. Conclusion. High citrate diet preserved renal function and delayed progression of renal disease in ClC-5 knockout mice even in the apparent absence of stone formation. We conclude from this that long-term control of hypercalciuria is an important factor in preventing renal failure in these mice.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据