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lüll Decreased renal alpha-Klotho expression in early diabetic nephropathy in humans and mice and its possible role in urinary calcium excretion Asai O; Nakatani K; Tanaka T; Sakan H; Imura A; Yoshimoto S; Samejima K; Yamaguchi Y; Matsui M; Akai Y; Konishi N; Iwano M; Nabeshima Y; Saito YKidney Int 2012[Mar]; 81 (6): 539-47Hypercalciuria is one of the early manifestations of diabetic nephropathy. We explored here the role of alpha-Klotho, a protein expressed predominantly in distal convoluted tubules that has a role in calcium reabsorption. We studied 31 patients with early diabetic nephropathy and compared them with 31 patients with IgA nephropathy and 7 with minimal change disease. Renal alpha-Klotho expression was significantly lower and urinary calcium excretion (UCa/UCr) significantly higher in diabetic nephropathy than in IgA nephropathy or minimal change disease. Multiple regression analyses indicated that alpha-Klotho mRNA was inversely correlated with calcium excretion. We next measured these parameters in a mouse model of streptozotocin (STZ)-induced diabetic nephropathy, characterized by glomerular hyperfiltration, as seen in early diabetic nephropathy. We also confirmed a reduction of renal alpha-Klotho mRNA down to almost 50% and enhanced calcium excretion in mice with STZ-induced diabetic nephropathy in comparison with nondiabetic mice. Hypercalciuria was exacerbated in heterozygous alpha-Klotho knockout mice in comparison with wild-type mice, each with STZ-induced diabetic nephropathy. Thus, alpha-Klotho expression was decreased in distal convoluted tubules in diabetic nephropathy in humans and mice. Renal loss of alpha-Klotho may affect urinary calcium excretion in early diabetic nephropathy.|Adult[MESH]|Animals[MESH]|Calcium Channels/genetics/metabolism[MESH]|Calcium/*urine[MESH]|Diabetes Mellitus, Experimental/chemically induced/*complications/metabolism/urine[MESH]|Diabetic Nephropathies/*etiology/genetics/metabolism/urine[MESH]|Down-Regulation[MESH]|Glucuronidase/genetics/*metabolism[MESH]|HEK293 Cells[MESH]|Heterozygote[MESH]|Humans[MESH]|Hypercalciuria/*etiology/genetics/metabolism/urine[MESH]|Kidney Tubules, Distal/*metabolism[MESH]|Klotho Proteins[MESH]|Male[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Middle Aged[MESH]|RNA, Messenger/metabolism[MESH]|Receptors, Cell Surface/deficiency/genetics/*metabolism[MESH]|TRPV Cation Channels/genetics/metabolism[MESH]|Time Factors[MESH]|Transfection[MESH]|Young Adult[MESH] |