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Erschienen in: Current Diabetes Reports 4/2011

01.08.2011

Oxidative Stress and Diabetic Kidney Disease

verfasst von: Robert C. Stanton

Erschienen in: Current Diabetes Reports | Ausgabe 4/2011

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Abstract

The number of people with diabetic kidney disease continues to increase worldwide despite current treatments. Of the pathophysiologic mechanisms that have been identified in the development and progression of diabetic nephropathy, oxidative stress (more accurately described as increased levels of reactive oxygen species; ROS) is of major importance. The increase in ROS is due to both increased production and to decreased and/or inadequate antioxidant function. To date, human clinical trials with antioxidants have not been shown to be effective. This is likely due, at least in part, to the lack of specificity of current agents. Recent research has determined both major sources of high glucose–induced cellular ROS production as well as high glucose–induced changes in antioxidant function. Treatments targeted at one or more of the specific diabetes-induced alterations in the regulation of ROS levels will likely lead to effective treatments that prevent the development and progression of diabetic kidney disease.
Literatur
1.
Zurück zum Zitat USRDS: Atlas of ESRD, in, edited by System USRD, 2010 USRDS: Atlas of ESRD, in, edited by System USRD, 2010
2.
Zurück zum Zitat USRDS: Atlas of CKD, in, edited by System USRD, 2010 USRDS: Atlas of CKD, in, edited by System USRD, 2010
3.
Zurück zum Zitat Caramori ML, Mauer M. Diabetes and nephropathy. Curr Opin Nephrol Hypertens. 2003;12:273–82.PubMedCrossRef Caramori ML, Mauer M. Diabetes and nephropathy. Curr Opin Nephrol Hypertens. 2003;12:273–82.PubMedCrossRef
4.
Zurück zum Zitat Parving HH, Hovind P. Microalbuminuria in type 1 and type 2 diabetes mellitus: evidence with angiotensin converting enzyme inhibitors and angiotensin II receptor blockers for treating early and preventing clinical nephropathy. Curr Hypertens Rep. 2002;4:387–93.PubMedCrossRef Parving HH, Hovind P. Microalbuminuria in type 1 and type 2 diabetes mellitus: evidence with angiotensin converting enzyme inhibitors and angiotensin II receptor blockers for treating early and preventing clinical nephropathy. Curr Hypertens Rep. 2002;4:387–93.PubMedCrossRef
5.
Zurück zum Zitat The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med 329:977–986, 1993 The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med 329:977–986, 1993
6.
Zurück zum Zitat Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. Jama 287:2563–2569, 2002 Effect of intensive therapy on the microvascular complications of type 1 diabetes mellitus. Jama 287:2563–2569, 2002
7.
Zurück zum Zitat Sustained effect of intensive treatment of type 1 diabetes mellitus on development and progression of diabetic nephropathy: the Epidemiology of Diabetes Interventions and Complications (EDIC) study. Jama 290:2159–2167, 2003 Sustained effect of intensive treatment of type 1 diabetes mellitus on development and progression of diabetic nephropathy: the Epidemiology of Diabetes Interventions and Complications (EDIC) study. Jama 290:2159–2167, 2003
8.
Zurück zum Zitat Adler AI, Stevens RJ, Manley SE, et al. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int. 2003;63:225–32.PubMedCrossRef Adler AI, Stevens RJ, Manley SE, et al. Development and progression of nephropathy in type 2 diabetes: the United Kingdom Prospective Diabetes Study (UKPDS 64). Kidney Int. 2003;63:225–32.PubMedCrossRef
9.
Zurück zum Zitat Bakris GL, Williams M, Dworkin L, et al. Preserving renal function in adults with hypertension and diabetes: a consensus approach. National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group. Am J Kidney Dis. 2000;36:646–61.PubMedCrossRef Bakris GL, Williams M, Dworkin L, et al. Preserving renal function in adults with hypertension and diabetes: a consensus approach. National Kidney Foundation Hypertension and Diabetes Executive Committees Working Group. Am J Kidney Dis. 2000;36:646–61.PubMedCrossRef
10.
Zurück zum Zitat Schrier RW, Estacio RO, Esler A, et al. Effects of aggressive blood pressure control in normotensive type 2 diabetic patients on albuminuria, retinopathy and strokes. Kidney Int. 2002;61:1086–97.PubMedCrossRef Schrier RW, Estacio RO, Esler A, et al. Effects of aggressive blood pressure control in normotensive type 2 diabetic patients on albuminuria, retinopathy and strokes. Kidney Int. 2002;61:1086–97.PubMedCrossRef
11.
Zurück zum Zitat Shankar A, Klein R, Klein BE, et al. Relationship between low-normal blood pressure and kidney disease in type 1 diabetes. Hypertension. 2007;49:48–54.PubMedCrossRef Shankar A, Klein R, Klein BE, et al. Relationship between low-normal blood pressure and kidney disease in type 1 diabetes. Hypertension. 2007;49:48–54.PubMedCrossRef
12.
Zurück zum Zitat Remuzzi G, Perico N, Macia M, et al.: The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease. Kidney Int Suppl:S57-65, 2005 Remuzzi G, Perico N, Macia M, et al.: The role of renin-angiotensin-aldosterone system in the progression of chronic kidney disease. Kidney Int Suppl:S57-65, 2005
13.
Zurück zum Zitat Remuzzi G, Ruggenenti P, Perna A, et al. Continuum of renoprotection with losartan at all stages of type 2 diabetic nephropathy: a post hoc analysis of the RENAAL trial results. J Am Soc Nephrol. 2004;15:3117–25.PubMedCrossRef Remuzzi G, Ruggenenti P, Perna A, et al. Continuum of renoprotection with losartan at all stages of type 2 diabetic nephropathy: a post hoc analysis of the RENAAL trial results. J Am Soc Nephrol. 2004;15:3117–25.PubMedCrossRef
14.
Zurück zum Zitat Ritz E, Orth SR. Nephropathy in patients with type 2 diabetes mellitus. N Engl J Med. 1999;341:1127–33.PubMedCrossRef Ritz E, Orth SR. Nephropathy in patients with type 2 diabetes mellitus. N Engl J Med. 1999;341:1127–33.PubMedCrossRef
15.
Zurück zum Zitat Anderson S, Brenner BM. Pathogenesis of diabetic glomerulopathy: hemodynamic considerations. Diabetes Metab Rev. 1988;4:163–77.PubMedCrossRef Anderson S, Brenner BM. Pathogenesis of diabetic glomerulopathy: hemodynamic considerations. Diabetes Metab Rev. 1988;4:163–77.PubMedCrossRef
16.
Zurück zum Zitat Zatz R, Dunn BR, Meyer TW, et al. Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension. J Clin Invest. 1986;77:1925–30.PubMedCrossRef Zatz R, Dunn BR, Meyer TW, et al. Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension. J Clin Invest. 1986;77:1925–30.PubMedCrossRef
17.
Zurück zum Zitat Garrido AM, Griendling KK. NADPH oxidases and angiotensin II receptor signaling. Mol Cell Endocrinol. 2009;302:148–58.PubMedCrossRef Garrido AM, Griendling KK. NADPH oxidases and angiotensin II receptor signaling. Mol Cell Endocrinol. 2009;302:148–58.PubMedCrossRef
18.
Zurück zum Zitat Mehta PK, Griendling KK. Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. Am J Physiol Cell Physiol. 2007;292:C82–97.PubMedCrossRef Mehta PK, Griendling KK. Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. Am J Physiol Cell Physiol. 2007;292:C82–97.PubMedCrossRef
19.
Zurück zum Zitat Geraldes P, King GL. Activation of protein kinase C isoforms and its impact on diabetic complications. Circ Res. 2010;106:1319–31.PubMedCrossRef Geraldes P, King GL. Activation of protein kinase C isoforms and its impact on diabetic complications. Circ Res. 2010;106:1319–31.PubMedCrossRef
20.
Zurück zum Zitat Kanwar YS, Wada J, Sun L, et al. Diabetic nephropathy: mechanisms of renal disease progression. Exp Biol Med (Maywood). 2008;233:4–11.CrossRef Kanwar YS, Wada J, Sun L, et al. Diabetic nephropathy: mechanisms of renal disease progression. Exp Biol Med (Maywood). 2008;233:4–11.CrossRef
21.
Zurück zum Zitat Tuttle KR. Protein kinase C-beta inhibition for diabetic kidney disease. Diabetes Res Clin Pract. 2008;82 Suppl 1:S70–74.PubMedCrossRef Tuttle KR. Protein kinase C-beta inhibition for diabetic kidney disease. Diabetes Res Clin Pract. 2008;82 Suppl 1:S70–74.PubMedCrossRef
22.
Zurück zum Zitat Bierhaus A, Hofmann MA, Ziegler R, et al. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept. Cardiovasc Res. 1998;37:586–600.PubMedCrossRef Bierhaus A, Hofmann MA, Ziegler R, et al. AGEs and their interaction with AGE-receptors in vascular disease and diabetes mellitus. I. The AGE concept. Cardiovasc Res. 1998;37:586–600.PubMedCrossRef
23.
Zurück zum Zitat Tan AL, Forbes JM, Cooper ME. AGE, RAGE, and ROS in diabetic nephropathy. Semin Nephrol. 2007;27:130–43.PubMedCrossRef Tan AL, Forbes JM, Cooper ME. AGE, RAGE, and ROS in diabetic nephropathy. Semin Nephrol. 2007;27:130–43.PubMedCrossRef
24.
Zurück zum Zitat Ziyadeh FN. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. J Am Soc Nephrol. 2004;15 Suppl 1:S55–57.PubMedCrossRef Ziyadeh FN. Mediators of diabetic renal disease: the case for tgf-Beta as the major mediator. J Am Soc Nephrol. 2004;15 Suppl 1:S55–57.PubMedCrossRef
25.
Zurück zum Zitat Stribling D, Armstrong FM, Harrison HE. Aldose reductase in the etiology of diabetic complications: 2. Nephropathy. J Diabet Complications. 1989;3:70–6.PubMedCrossRef Stribling D, Armstrong FM, Harrison HE. Aldose reductase in the etiology of diabetic complications: 2. Nephropathy. J Diabet Complications. 1989;3:70–6.PubMedCrossRef
26.
Zurück zum Zitat Thrailkill KM, Clay Bunn R, Fowlkes JL. Matrix metalloproteinases: their potential role in the pathogenesis of diabetic nephropathy. Endocrine. 2009;35:1–10.PubMedCrossRef Thrailkill KM, Clay Bunn R, Fowlkes JL. Matrix metalloproteinases: their potential role in the pathogenesis of diabetic nephropathy. Endocrine. 2009;35:1–10.PubMedCrossRef
27.
Zurück zum Zitat Ahn SH, Susztak K. Getting a notch closer to understanding diabetic kidney disease. Diabetes. 2010;59:1865–7.PubMedCrossRef Ahn SH, Susztak K. Getting a notch closer to understanding diabetic kidney disease. Diabetes. 2010;59:1865–7.PubMedCrossRef
28.
Zurück zum Zitat Dai C, Stolz DB, Kiss LP, et al. Wnt/beta-catenin signaling promotes podocyte dysfunction and albuminuria. J Am Soc Nephrol. 2009;20:1997–2008.PubMedCrossRef Dai C, Stolz DB, Kiss LP, et al. Wnt/beta-catenin signaling promotes podocyte dysfunction and albuminuria. J Am Soc Nephrol. 2009;20:1997–2008.PubMedCrossRef
30.
Zurück zum Zitat • Bashan N, Kovsan J, Kachko I, et al.: Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species. Physiol Rev 89:27–71, 2009 This is an excellent overview of ROS production and regulation. • Bashan N, Kovsan J, Kachko I, et al.: Positive and negative regulation of insulin signaling by reactive oxygen and nitrogen species. Physiol Rev 89:27–71, 2009 This is an excellent overview of ROS production and regulation.
31.
Zurück zum Zitat Brown MR, Miller Jr FJ, Li WG, et al. Overexpression of human catalase inhibits proliferation and promotes apoptosis in vascular smooth muscle cells. Circ Res. 1999;85:524–33.PubMed Brown MR, Miller Jr FJ, Li WG, et al. Overexpression of human catalase inhibits proliferation and promotes apoptosis in vascular smooth muscle cells. Circ Res. 1999;85:524–33.PubMed
32.
Zurück zum Zitat Shi M, Yang H, Motley ED, et al. Overexpression of Cu/Zn-superoxide dismutase and/or catalase in mice inhibits aorta smooth muscle cell proliferation. Am J Hypertens. 2004;17:450–6.PubMedCrossRef Shi M, Yang H, Motley ED, et al. Overexpression of Cu/Zn-superoxide dismutase and/or catalase in mice inhibits aorta smooth muscle cell proliferation. Am J Hypertens. 2004;17:450–6.PubMedCrossRef
33.
Zurück zum Zitat Rajasekaran NS, Connell P, Christians ES, et al. Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice. Cell. 2007;130:427–39.PubMedCrossRef Rajasekaran NS, Connell P, Christians ES, et al. Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice. Cell. 2007;130:427–39.PubMedCrossRef
34.
Zurück zum Zitat Feng J, Damrauer SM, Lee M, et al.: Endothelium-dependent coronary vasodilatation requires NADPH oxidase-derived reactive oxygen species. Arterioscler Thromb Vasc Biol 30:1703–1710 Feng J, Damrauer SM, Lee M, et al.: Endothelium-dependent coronary vasodilatation requires NADPH oxidase-derived reactive oxygen species. Arterioscler Thromb Vasc Biol 30:1703–1710
35.
Zurück zum Zitat Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003;52:2110–20.PubMedCrossRef Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes. 2003;52:2110–20.PubMedCrossRef
36.
Zurück zum Zitat Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54:1615–25.PubMedCrossRef Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54:1615–25.PubMedCrossRef
37.
Zurück zum Zitat • Forbes JM, Coughlan MT, Cooper ME: Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes 57:1446–1454, 2008 This is a very good, detailed review of the scientific studies on basic mechanisms of oxidative stress in diabetes and kidney disease. • Forbes JM, Coughlan MT, Cooper ME: Oxidative stress as a major culprit in kidney disease in diabetes. Diabetes 57:1446–1454, 2008 This is a very good, detailed review of the scientific studies on basic mechanisms of oxidative stress in diabetes and kidney disease.
38.
Zurück zum Zitat Bedard K, Krause KH. The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology. Physiol Rev. 2007;87:245–313.PubMedCrossRef Bedard K, Krause KH. The NOX Family of ROS-Generating NADPH Oxidases: Physiology and Pathophysiology. Physiol Rev. 2007;87:245–313.PubMedCrossRef
39.
40.
Zurück zum Zitat Kakehi T, Yabe-Nishimura C. NOX enzymes and diabetic complications. Semin Immunopathol. 2008;30:301–14.PubMedCrossRef Kakehi T, Yabe-Nishimura C. NOX enzymes and diabetic complications. Semin Immunopathol. 2008;30:301–14.PubMedCrossRef
41.
Zurück zum Zitat Xu M, Dai DZ, Dai Y. Normalizing NADPH oxidase contributes to attenuating diabetic nephropathy by the dual endothelin receptor antagonist CPU0213 in rats. Am J Nephrol. 2009;29:252–6.PubMedCrossRef Xu M, Dai DZ, Dai Y. Normalizing NADPH oxidase contributes to attenuating diabetic nephropathy by the dual endothelin receptor antagonist CPU0213 in rats. Am J Nephrol. 2009;29:252–6.PubMedCrossRef
42.
Zurück zum Zitat Kletzien RF, Harris PK, Foellmi LA. Glucose-6-phosphate dehydrogenase: a “housekeeping” enzyme subject to tissue-specific regulation by hormones, nutrients, and oxidant stress. Faseb J. 1994;8:174–81.PubMed Kletzien RF, Harris PK, Foellmi LA. Glucose-6-phosphate dehydrogenase: a “housekeeping” enzyme subject to tissue-specific regulation by hormones, nutrients, and oxidant stress. Faseb J. 1994;8:174–81.PubMed
43.
Zurück zum Zitat Maritim AC, Sanders RA, Watkins 3rd JB. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol. 2003;17:24–38.PubMedCrossRef Maritim AC, Sanders RA, Watkins 3rd JB. Diabetes, oxidative stress, and antioxidants: a review. J Biochem Mol Toxicol. 2003;17:24–38.PubMedCrossRef
44.
Zurück zum Zitat Tian WN, Braunstein LD, Pang J, et al. Importance of glucose-6-phosphate dehydrogenase activity for cell growth. J Biol Chem. 1998;273:10609–17.PubMedCrossRef Tian WN, Braunstein LD, Pang J, et al. Importance of glucose-6-phosphate dehydrogenase activity for cell growth. J Biol Chem. 1998;273:10609–17.PubMedCrossRef
45.
Zurück zum Zitat Locigno R, Castronovo V. Reduced glutathione system: role in cancer development, prevention and treatment (review). Int J Oncol. 2001;19:221–36.PubMed Locigno R, Castronovo V. Reduced glutathione system: role in cancer development, prevention and treatment (review). Int J Oncol. 2001;19:221–36.PubMed
46.
Zurück zum Zitat Xu Y, Osborne BW, Stanton RC. Diabetes causes inhibition of glucose-6-phosphate dehydrogenase via activation of PKA, which contributes to oxidative stress in rat kidney cortex. Am J Physiol Renal Physiol. 2005;289:F1040–1047.PubMedCrossRef Xu Y, Osborne BW, Stanton RC. Diabetes causes inhibition of glucose-6-phosphate dehydrogenase via activation of PKA, which contributes to oxidative stress in rat kidney cortex. Am J Physiol Renal Physiol. 2005;289:F1040–1047.PubMedCrossRef
47.
Zurück zum Zitat Fujita H, Fujishima H, Chida S, et al. Reduction of renal superoxide dismutase in progressive diabetic nephropathy. J Am Soc Nephrol. 2009;20:1303–13.PubMedCrossRef Fujita H, Fujishima H, Chida S, et al. Reduction of renal superoxide dismutase in progressive diabetic nephropathy. J Am Soc Nephrol. 2009;20:1303–13.PubMedCrossRef
48.
Zurück zum Zitat Drel VR, Pacher P, Stevens MJ, et al. Aldose reductase inhibition counteracts nitrosative stress and poly(ADP-ribose) polymerase activation in diabetic rat kidney and high-glucose-exposed human mesangial cells. Free Radic Biol Med. 2006;40:1454–65.PubMedCrossRef Drel VR, Pacher P, Stevens MJ, et al. Aldose reductase inhibition counteracts nitrosative stress and poly(ADP-ribose) polymerase activation in diabetic rat kidney and high-glucose-exposed human mesangial cells. Free Radic Biol Med. 2006;40:1454–65.PubMedCrossRef
49.
Zurück zum Zitat Srivastava SK, Ramana KV, Bhatnagar A. Role of aldose reductase and oxidative damage in diabetes and the consequent potential for therapeutic options. Endocr Rev. 2005;26:380–92.PubMedCrossRef Srivastava SK, Ramana KV, Bhatnagar A. Role of aldose reductase and oxidative damage in diabetes and the consequent potential for therapeutic options. Endocr Rev. 2005;26:380–92.PubMedCrossRef
50.
Zurück zum Zitat Kashihara N, Haruna Y, Kondeti VK, et al.: Oxidative stress in diabetic nephropathy. Curr Med Chem 17:4256–4269 Kashihara N, Haruna Y, Kondeti VK, et al.: Oxidative stress in diabetic nephropathy. Curr Med Chem 17:4256–4269
51.
Zurück zum Zitat Koya D, Hayashi K, Kitada M, et al. Effects of antioxidants in diabetes-induced oxidative stress in the glomeruli of diabetic rats. J Am Soc Nephrol. 2003;14:S250–253.PubMedCrossRef Koya D, Hayashi K, Kitada M, et al. Effects of antioxidants in diabetes-induced oxidative stress in the glomeruli of diabetic rats. J Am Soc Nephrol. 2003;14:S250–253.PubMedCrossRef
52.
Zurück zum Zitat Siu B, Saha J, Smoyer WE, et al. Reduction in podocyte density as a pathologic feature in early diabetic nephropathy in rodents: prevention by lipoic acid treatment. BMC Nephrol. 2006;7:6.PubMedCrossRef Siu B, Saha J, Smoyer WE, et al. Reduction in podocyte density as a pathologic feature in early diabetic nephropathy in rodents: prevention by lipoic acid treatment. BMC Nephrol. 2006;7:6.PubMedCrossRef
53.
Zurück zum Zitat Yi X, Nickeleit V, James LR, et al.: alpha-Lipoic acid protects diabetic apolipoprotein E-deficient mice from nephropathy. J Diabetes Complications, 2010 Yi X, Nickeleit V, James LR, et al.: alpha-Lipoic acid protects diabetic apolipoprotein E-deficient mice from nephropathy. J Diabetes Complications, 2010
54.
Zurück zum Zitat Winiarska K, Malinska D, Szymanski K, et al. Lipoic acid ameliorates oxidative stress and renal injury in alloxan diabetic rabbits. Biochimie. 2008;90:450–9.PubMedCrossRef Winiarska K, Malinska D, Szymanski K, et al. Lipoic acid ameliorates oxidative stress and renal injury in alloxan diabetic rabbits. Biochimie. 2008;90:450–9.PubMedCrossRef
55.
Zurück zum Zitat Thallas-Bonke V, Coughlan MT, Bach LA, et al. Preservation of kidney function with combined inhibition of NADPH oxidase and angiotensin-converting enzyme in diabetic nephropathy. Am J Nephrol. 2010;32:73–82.PubMedCrossRef Thallas-Bonke V, Coughlan MT, Bach LA, et al. Preservation of kidney function with combined inhibition of NADPH oxidase and angiotensin-converting enzyme in diabetic nephropathy. Am J Nephrol. 2010;32:73–82.PubMedCrossRef
56.
Zurück zum Zitat Bursell SE, Clermont AC, Aiello LP, et al. High-dose vitamin E supplementation normalizes retinal blood flow and creatinine clearance in patients with type 1 diabetes. Diabetes Care. 1999;22:1245–51.PubMedCrossRef Bursell SE, Clermont AC, Aiello LP, et al. High-dose vitamin E supplementation normalizes retinal blood flow and creatinine clearance in patients with type 1 diabetes. Diabetes Care. 1999;22:1245–51.PubMedCrossRef
57.
Zurück zum Zitat Lonn E, Yusuf S, Hoogwerf B, et al. Effects of vitamin E on cardiovascular and microvascular outcomes in high-risk patients with diabetes: results of the HOPE study and MICRO-HOPE substudy. Diabetes Care. 2002;25:1919–27.PubMedCrossRef Lonn E, Yusuf S, Hoogwerf B, et al. Effects of vitamin E on cardiovascular and microvascular outcomes in high-risk patients with diabetes: results of the HOPE study and MICRO-HOPE substudy. Diabetes Care. 2002;25:1919–27.PubMedCrossRef
58.
Zurück zum Zitat Endo K, Miyashita Y, Sasaki H, et al. Probucol delays progression of diabetic nephropathy. Diabetes Res Clin Pract. 2006;71:156–63.PubMedCrossRef Endo K, Miyashita Y, Sasaki H, et al. Probucol delays progression of diabetic nephropathy. Diabetes Res Clin Pract. 2006;71:156–63.PubMedCrossRef
59.
Zurück zum Zitat • Alkhalaf A, Klooster A, van Oeveren W, et al.: A double-blind, randomized, placebo-controlled clinical trial on benfotiamine treatment in patients with diabetic nephropathy. Diabetes Care 33:1598–1601, 2010 This paper is the first to use a physiologically targeted treatment in clinical trials in diabetic kidney disease. It illustrates both an interesting approach but also the concern of translating animal data to human clinical trials as this is a negative study. • Alkhalaf A, Klooster A, van Oeveren W, et al.: A double-blind, randomized, placebo-controlled clinical trial on benfotiamine treatment in patients with diabetic nephropathy. Diabetes Care 33:1598–1601, 2010 This paper is the first to use a physiologically targeted treatment in clinical trials in diabetic kidney disease. It illustrates both an interesting approach but also the concern of translating animal data to human clinical trials as this is a negative study.
Metadaten
Titel
Oxidative Stress and Diabetic Kidney Disease
verfasst von
Robert C. Stanton
Publikationsdatum
01.08.2011
Verlag
Current Science Inc.
Erschienen in
Current Diabetes Reports / Ausgabe 4/2011
Print ISSN: 1534-4827
Elektronische ISSN: 1539-0829
DOI
https://doi.org/10.1007/s11892-011-0196-9

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