Vitamin D deficiency is a prominent feature of chronic kidney disease (CKD) even in its early stages. While vitamin D deficiency leads to mineral imbalance and bone problems in CDK patients, it also accelerates the progression of kidney disease. Ever since the observation that vitamin D analogs reduce proteinuria in CKD patients, it has been postulated that podocytes are major target of the reno-protective action of vitamin D. Recent large randomized clinical trials have confirmed the potent anti-proteinuric activity of vitamin D therapy. Studies from various animal models of kidney disease have demonstrated that vitamin D prevents podocyte injury and cell loss, promotes the expression of slit diaphragm proteins and maintains the integrity of the glomerular filtration barrier. Emerging experimental data suggest that vitamin D may protect podocytes by targeting multiple pathways, including the renin-angiotensin system, Wnt/β-catenin pathway and pro-apoptotic pathway.
Keywords: Vitamin D, Vitamin D analog, Podocyte, Diabetic nephropathy, Chronic kidney disease, 7-dehydrocholesterol, D 25-hydroxylase, 25-hydroxyvitamin, D3 (25OHD3), hydroxyvitamin D 1-hydroxylase (CYP27B1), parathyroid hormone, fibroblast growth factor (FGF), CYP24, rular filtration rate (GFR), DBP-25OHD3, receptor (VDR), PCNA, desmin, streptozotocin (STZ), actinin-4, losartan, Wnt/-catenin pathway, apoptotic pathway, hyper-glycemia, NF-B pathway, hyperreninemia, catenin, adriamycin injury, ameliorates podocyte lesio, p38, keratinocytes, Podocyte gene expression
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