NDT Advance Access originally published online on November 22, 2006
Nephrology Dialysis Transplantation 2007 22(2):321-328; doi:10.1093/ndt/gfl595
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Potential role of active vitamin D in retarding the progression of chronic kidney disease
1Renal Global Project Team, GPRD, Abbott Laboratories, Abbott Park, Illinois, 2Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA, and 3Departments of Clinical Pharmacology and Nephrology, University Medical Center Groningen, University of Groningen, The Netherlands
Correspondence and offprint requests to: Dick de Zeeuw, Departments of Clinical Pharmacology and Nephrology, University Medical Center Groningen, University of Groningen, The Netherlands. Email: d.de.zeeuw@med.umcg.nl
Keywords: chronic kidney diseases; proteinuria; renal fibrosis; renin; vitamin D
| The first 150 words of the full text of this article appear below. |
| Introduction |
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Delay up the progression of chronic kidney disease (CKD) is still an unsolved problem. The suppression of known causes of progression by targeting high blood pressure as well as the reninangiotensin system (RAS) has met with some success in REIN, RENAAL, IDNT, and other clinical trials [13]. However, although these therapies slow the progression of CKD, the residual risk of these patients for both renal and cardiovascular end points remains high. Since the pathogenesis of renal progressive disease is multifactorial, a combined therapy strategy may be the way for the future to completely block renal disease progression. An interesting result of such a combined therapy strategy came from the COOPERATE trial [combining ACE-inhibition with angiotensin-II-receptor-blockade (ACEi/ARB)], targeting the same hormonal systems from different angles [4]. Other strategies target different pathophysiologically important systems at the same time, such as RAS and glycosaminoglycans [5], and RAS
| Vitamin D |
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| Current concepts for progressive renal function loss and the potential role of vitamin D |
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| Experimental evidence for a role of active vitamin D in CKD |
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Effect on renal compensation and RAS
Effects on podocytes and mesangial cells
Effect on renal inflammation
Vitamin D and tubular interstitial fibrosis
Vitamin D deficiency and the progression of CKD
| Clinical evidence |
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| Conclusion |
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