The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

Faria, José B. Lopes de; Silva, Kamila Cristina; Faria, Jacqueline M. Lopes de

doi:10.1038/hr.2010.263

Cited by 56 publications

(39 citation statements)

References 153 publications

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“…Previous studies describing retinopathy in dogs with naturally occurring diabetes have reported similar prevalence values as this study, ranging from 3 to 21% 5, 7, 29, 30. Although hypertension is also a well‐known risk factor for development and progression of diabetic retinopathy in humans,28, 31 a similar correlation was not found in the present study. Time since DM diagnosis and glycemic control scores were also not correlated with presence of ophthalmoscopically visible retinopathy in this study.…”

Section: Discussionsupporting

confidence: 88%

Longitudinal Prevalence of Hypertension, Proteinuria, and Retinopathy in Dogs with Spontaneous Diabetes Mellitus

Herring

Panciera

Werre

2014

Veterinary Internal Medicne

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BackgroundThe prevalence and progression of vascular complications of spontaneous diabetes mellitus (DM) in dogs have not been described.ObjectivesTo investigate the effects of duration of disease, as estimated by time since DM diagnosis, and glycemic control on prevalence of systemic hypertension, proteinuria, and diabetic retinopathy in dogs with spontaneous DM.AnimalsSeventeen client‐owned dogs with spontaneous DM.MethodsProspective, longitudinal observational study. Dogs with DM of less than 1 year's duration were recruited and evaluated once every 6 months for 24 months. Recorded measures included indirect BP, urine albumin, protein and creatinine concentrations, serial blood glucose and serum fructosamine concentrations, ophthalmic examination, and a standardized behavioral questionnaire.ResultsEleven dogs completed the 2‐year follow‐up period, during which the highest recorded prevalence of systolic and diastolic hypertension was 55 and 64%, respectively. Prevalence of microalbuminuria and elevated urine protein:creatinine ratio (UPC) ranged up to 73 and 55%, respectively. Prevalence of retinopathy ranged up to 20%. No significant effect of time since DM diagnosis or glycemic control was detected for any of the measures examined. Additionally, no significant associations between BP, urine albumin concentration, UPC and retinopathy were detected.Conclusions and Clinical RelevanceWith the exception of proteinuria, which was substantial in some cases, clinically deleterious diabetic vascular complications were not identified in dogs in this study.

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Section: Discussionsupporting

confidence: 88%

Longitudinal Prevalence of Hypertension, Proteinuria, and Retinopathy in Dogs with Spontaneous Diabetes Mellitus

Herring

Panciera

Werre

2014

Veterinary Internal Medicne

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“…The diabetic rats either did or did not receive tempol treatment (Calbiochem, La Jolla, Calif., USA), as previously reported [7]. We have chosen to use SHR rats because others and we have shown that diabetic SHR display features of accelerated nephropathy and also because of the frequent association of hypertension with DM in human DN [8,9]. …”

Section: Methodsmentioning

confidence: 99%

Tempol Reduces Podocyte Apoptosis via PARP Signaling Pathway in Experimental Diabetes Mellitus

Peixoto

Papadimitriou²,

Faria³

et al. 2012

Nephron Exp Nephrol

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Background/Aims: In diabetic hypertensive rats, tempol reduces albuminuria by restoring the redox imbalance. Increased formation of reactive oxygen species leading to activation of poly(ADP-ribose) polymerase (PARP)-1 and podocyte loss by apoptosis contribute to albuminuria in diabetes mellitus (DM). In the present study, we investigated the hypothesis that in DM tempol reduces albuminuria by inhibition of PARP-induced podocyte apoptosis. Methods: DM was induced in 4-week-old spontaneously hypertensive rats by streptozotocin. Mouse and human podocyte cell lines were cultured in normal or high-glucose conditions, with or without tempol and/or a PARP-1 inhibitor, PJ34. Results: In diabetic rats, tempol treatment did not affect plasma glucose levels or systolic blood pressure. Albuminuria was higher in diabetic rats, and it was reduced by tempol. DM leads to an elevation of glomerular apoptotic cells and to podocyte loss; both were prevented by tempol treatment. DM increases the expression of poly(ADP-ribose)-modified proteins in isolated glomeruli, and it was reduced by tempol. In vitro, high glucose increased caspase-3 activity and led to a higher number of apoptotic cells that were prevented by tempol and the PARP-1 inhibitor. Conclusion: In DM, tempol reduces albuminuria associated with reduction of podocyte apoptosis and decreasing oxidative stress via PARP signaling.

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“…Nevertheless, one essential mechanism seems to be oxidative stress, which mediates glomerular and interstitial damage in diabetic nephropathy [9,10,11]. Indeed, oxidative stress was detected in murine mesangial and proximal tubular epithelial cells, in rats and in patients with hyperglycemia, suggesting that oxidative stress may play a pathological role in the development of diabetic nephropathy [12,13]. …”

Section: Introductionmentioning

confidence: 99%

Telmisartan Attenuates Diabetic Nephropathy by Suppressing Oxidative Stress in <b><i>db/db</i></b> Mice

Sato-Horiguchi¹,

Ogawa²,

Wada³

et al. 2013

Nephron Exp Nephrol

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Background/Aims: Telmisartan, an angiotensin II type 1 receptor blocker, is widely used to treat hypertension and kidney diseases, including diabetic nephropathy, because of its renoprotective effects. However, the mechanism by which telmisartan prevents proteinuria and renal dysfunction in diabetic nephropathy is still unclear. In this study, we examined the effects of telmisartan against diabetic nephropathy in db/db mice. Methods: Telmisartan was administered at a dose of 5 mg/kg/day for 3 weeks to db/db (diabetic) and db/m (control) mice. Urinary albumin excretion, renal histology, and the gene expression of oxidative stress and inflammatory markers in renal tissue were determined. To evaluate the effects of telmisartan on reactive oxygen species (ROS) production, superoxide was detected by dihydroethidium (DHE) staining in vivo and in vitro. Results: Telmisartan reduced albuminuria, mesangial matrix expansion, macrophage infiltration, and the expression of ROS markers (NADPH oxidase 4- and 8-hydroxydeoxyguanosine) and inflammatory cytokines (monocyte chemoattractant protein-1, osteopontin, and transforming growth factor-β) in the kidney. DHE staining showed that telmisartan decreased ROS generation in the kidney and in cultured mesangial and proximal tubular epithelial cells. Conclusions: Taken together, these findings indicate that telmisartan protects against diabetic nephropathy by reducing diabetes-induced oxidative stress.

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The contribution of hypertension to diabetic nephropathy and retinopathy: the role of inflammation and oxidative stress

Cited by 56 publications

References 153 publications

Longitudinal Prevalence of Hypertension, Proteinuria, and Retinopathy in Dogs with Spontaneous Diabetes Mellitus

Longitudinal Prevalence of Hypertension, Proteinuria, and Retinopathy in Dogs with Spontaneous Diabetes Mellitus

Tempol Reduces Podocyte Apoptosis via PARP Signaling Pathway in Experimental Diabetes Mellitus

Telmisartan Attenuates Diabetic Nephropathy by Suppressing Oxidative Stress in <b><i>db/db</i></b> Mice

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