Mechanisms of Renal Microvascular Dysfunction in Type 1 Diabetes: Potential Contribution to End Organ Damage

ISSN: 1875-6212 (Online)
ISSN: 1570-1611 (Print)


Volume 12, 6 Issues, 2014


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Editor-in-Chief:
Dimitri P. Mikhailidis
Academic Head, Deptartment of Clinical Biochemistry
Royal Free Hospital Campus
University College London Medical School
University College London (UCL)
Pond Street
London, NW3 2QG
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Mechanisms of Renal Microvascular Dysfunction in Type 1 Diabetes: Potential Contribution to End Organ Damage

Author(s): Pamela K Carmines

Affiliation: Department of Cellular & Integrative Physiology, 985850 Nebraska Medical Center, Omaha, NE 68198-5850 USA

Abstract

Although diabetes mellitus is the primary cause of end stage renal disease, the mechanisms underlying the initiation and progression of diabetic nephropathy are not well understood. The widely accepted opinion holds that events occurring early during the course of diabetes engender the progression of diabetic nephropathy. Diabetic hyperglycemia exerts an array of direct and indirect influences on the renal preglomerular microvasculature, as well as on glomeruli and tubular epithelial cells. Although the scope of these effects is not yet fully recognized, alterations in the myogenic and tubuloglomerular feedback responses, electromechanical coupling in preglomerular vascular smooth muscle, and interactions between tubular transport and vascular function all contribute to renal vascular dysfunction early after onset of T1D. These changes, which arise in environment conducive to oxidative stress and inflammation, are thought to either initiate or facilitate the eventual development of diabetic nephropathy in susceptible individuals

Keywords: Afferent arteriole, autoregulation, C-peptide, diabetes mellitus, K+ channels, oxidative stress

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Article Details

Volume: 11
First Page: 1
Last Page: 7
Page Count: 7
DOI: 10.2174/15701611113116660156
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