Value of Diabetes as an Independent Predictor of Death in Subjects with End-Stage Renal Disease

BackgroundAbnormal ankle-brachial index (ABI) has been found to be a strong predictor of mortality in some hemodialysis populations in studies with relatively short periods of follow-up, lower than 2 years.ObjectiveThis study aimed to assess the predictive value of abnormal ABI as a risk factor for death among patients on maintenance hemodialysis after a 5-year follow-up.MethodsA total of 478 patients on hemodialysis for at least 12 months were included in the study. ABI measurement was performed using a mercury column sphygmomanometer and portable Doppler. Patients were divided into 3 groups according to ABI (low: <0.9; normal: 0.9 to 1.3; and high: >1.3) and followed for a 60-month period.ResultsThe prevalence rates of low, normal and high ABI were 26.8%, 64.6% and 8.6%, respectively. The 5-year survival rate was lower in the groups with low ABI (44.1%, P<0.0001) and high ABI (60.8%, P= 0.025) than in the group with normal ABI (71.7%). Cox regression was used to evaluate the association between ABI and mortality, adjusting for potential confounders. Using normal ABI as reference, a low, but not a high ABI was found to be an independent risk factor for all-cause mortality (HR2.57; 95% CI, 1.84-3.57 and HR 1.62; 95% CI, 0.93-2.83, respectively).Conclusionslong-term survival rates of patients with either low or high ABI were lower than the one from those with normal ABI. However, after adjustment for potential confounders, only low ABI persisted as an independent risk factor for all-cause mortality among hemodialysis patients.

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“…Moreover, diabetes was not a risk factor for death in hemodialysis when patients with PAD were excluded from the sample. 23 …”

Section: Discussionmentioning

confidence: 99%

Ankle-Brachial Index as a Predictor of Mortality in Hemodialysis: A 5-Year Cohort Study

Miguel¹,

Matos²,

Lugon³

2017

Arquivos Brasileiros De Cardiologia

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“…Additive or synergistic effects of urea and hyperglycemia might explain the 2-fold increase in 5-year mortality of ESRD patients with diabetes compared with those without diabetes (35). …”

Section: Discussionmentioning

confidence: 99%

Urea-induced ROS cause endothelial dysfunction in chronic renal failure

D’Apolito

Pisanelli

et al. 2015

Atherosclerosis

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Objective The pathogenic events responsible for accelerated atherosclerosis in patients with chronic renal failure (CRF) are poorly understood. Here we investigate the hypothesis that concentrations of urea associated with CRF and increased ROS production in adipocytes might also increase ROS production directly in arterial endothelial cells, causing the same pathophysiologic changes seen with hyperglycemia. Methods Primary cultures of human aortic endothelial cells (HAEC) were exposed to 20 mM urea for 48 hrs. C57BL/6J wild-type mice underwent 5/6 nephrectomy or a sham operation. Randomized groups of 5/6 nephrectomized mice and their controls were also injected i.p. with a SOD/catalase mimetic (MnTBAP) for 15 days starting immediately after the final surgical procedure. Results Urea at concentrations seen in CRF induced mitochondrial ROS production in cultured HAEC. Urea-induced ROS caused the activation of endothelial pro-inflammatory pathways through the inhibition of GAPDH, including increased protein kinase C isoforms activity, increased hexosamine pathway activity, and accumulation of intracellular AGEs (advanced glycation end products). Urea-induced ROS directly inactivated the anti-atherosclerosis enzyme PGI2 synthase and also caused ER stress. Normalization of mitochondrial ROS production prevented each of these effects of urea. In uremic mice, treatment with MnTBAP prevented aortic oxidative stress, PGI2 synthase activity reduction and increased expression of the pro-inflammatory proteins TNFα, IL-6, VCAM1, Endoglin, and MCP-1. Conclusions Taken together, these data show that urea itself, at levels common in patients with CRF, causes endothelial dysfunction and activation of proatherogenic pathways.

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“…Like urea, hyperglycemia also increases intracellular oxidative stress, modification of insulin signaling molecules by O-GlcNAc, and insulin resistance in arterial endothelial cells (35). Additive or synergistic effects of urea and hyperglycemia might explain the 2-fold increase in 5-year mortality of ESRD patients with diabetes compared with those without diabetes (36).…”

Section: Discussionmentioning

confidence: 99%

Urea-induced ROS generation causes insulin resistance in mice with chronic renal failure

et al. 2010

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Value of Diabetes as an Independent Predictor of Death in Subjects with End-Stage Renal Disease

Abstract: Diabetes is not an independent predictor of death in the ESRD study group presented here. Prevention of CAD and CLI in diabetic subjects is most important to improve survival.

Cited by 7 publications

References 15 publications

Ankle-Brachial Index as a Predictor of Mortality in Hemodialysis: A 5-Year Cohort Study

Ankle-Brachial Index as a Predictor of Mortality in Hemodialysis: A 5-Year Cohort Study

Urea-induced ROS cause endothelial dysfunction in chronic renal failure

Urea-induced ROS generation causes insulin resistance in mice with chronic renal failure

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