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Volume 55, Issue 2 , Pages 365-385 , February 2010

The Management of Diabetic Neuropathy in CKD

Rodica Pop-Busui, MD, PhD
- Department of Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor, MI
Laurel Roberts, BS
- University of Michigan Medical School, Ann Arbor, MI
Subramaniam Pennathur, MD
- Department of Internal Medicine, Division of Nephrology, University of Michigan, Ann Arbor, MI
Mathias Kretzler, MD
- Department of Internal Medicine, Division of Nephrology, University of Michigan, Ann Arbor, MI
Frank C. Brosius, MD
- Department of Internal Medicine, Division of Nephrology, University of Michigan, Ann Arbor, MI
Eva L. Feldman, MD, PhD
- Department of Neurology, University of Michigan, Ann Arbor, MI
- Address correspondence to Eva L. Feldman, MD, PhD, Russell N. DeJong Professor of Neurology, University of Michigan Department of Neurology, 5017 BSRB, 109 Zina Pitcher Pl, Ann Arbor, MI 48109-2200

Received 7 August 2009 ,Accepted 29 October 2009.

Proposed paradigm of the mechanisms inducing neurotoxicity in diabetic patients with chronic kidney disease (CKD). Abbreviations: AGE, advanced glycation end products; GSH, glutathione; GSSG, oxidized

Proposed paradigm of the mechanisms inducing neurotoxicity in diabetic patients with chronic kidney disease (CKD). Abbreviations: AGE, advanced glycation end products; GSH, glutathione; GSSG, oxidized glutathione; NADP, nicotinamide adenine dinucleotide phosphate; NADPH, reduced NADP; NF-κB, nuclear factor κB; PAI 1, plasminogen activator inhibitor 1; PARP, poly(ADP-ribose) polymerase; PKC, protein kinase C; PTH, parathyroid hormone; RNS, reactive nitrogen species; ROS, reactive oxygen species; SDH, sorbitol dehygrogenase; TCA, tricarboxylic acid; VEGF, vascular endothelial growth factor. Adapted and reproduced from Edwards et al²³ with permission of Elsevier.
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