Peripheral Vascular Dysfunction in Chronic Kidney Disease

Martens, Christopher R.; Edwards, David G.

doi:10.4061/2011/267257

Cited by 59 publications

(43 citation statements)

References 82 publications

(99 reference statements)

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“…Skeletal muscle hypotrophy during the late stages of chronic kidney disease may release into the blood, amino acids and ureamic toxins, which in cultured endothelial cells inhibit L-arginine transport, 52 thereby elevating L-arginine levels. 53 This has not yet been confirmed in humans. In our study, the average eGFR for a minority of participants was slightly below normal without any indication of kidney disease.…”

Section: Discussionmentioning

confidence: 92%

Ethnicity-specific differences in L-arginine status in South African men

et al. 2011

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The aetiology for an increasing incidence of hypertensive cardiovascular disease amongst Africans in southern Africa is unclear. Hypertension may be induced by inadequate release of L-arginine-derived nitric oxide impairing vascular tone regulation. In addition, asymmetric dimethylarginine (ADMA) is associated with cardiovascular disease. We compared profiles of L-arginine in African and Caucasian men of similar age with cardiovascular risk factors. We studied 163 Caucasian and 132 African men, respectively, (20 to 70 years) measuring serum L-arginine, ADMA, creatinine, urea, symmetric dimethylarginine (SDMA) and blood pressure. L-arginine levels were significantly lower, whereas blood pressure and pulse wave velocity were significantly higher in African men. Simple linear regression showed ADMA more strongly associated with L-arginine in Caucasians (r ¼ 0.59 vs 0.19), whereas association of SDMA with L-arginine was significant only in Caucasians (r ¼ 0.43 vs 0.001). The stronger association of L-arginine with ADMA in Caucasian men was confirmed by multiple regression analysis (b ¼ 0.46 vs 0.25). Our findings show that the relationship of cardiovascular risk factors with serum L-arginine and some of its catabolites is different in African and Caucasian men and that this may be associated with a relatively higher prevalence of hypertension in African men.

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Section: Discussionmentioning

confidence: 92%

Ethnicity-specific differences in L-arginine status in South African men

et al. 2011

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“…Nitric oxide (NO • ) has been implicated in the development of DN (Martens and Edwards 2011) and has been associated with increased production of NO • , hyperfiltration and microalbuminuria (Schena and Gesualdo 2005;NoriegaCisneros et al 2013). Conversely, advanced DN is characterized by decreased NO • production, which in turn may drives to hypertension, progressive renal failure and proteinuria (Baylis 2012).…”

Section: Introductionmentioning

confidence: 97%

Effects of diabetes on oxidative and nitrosative stress in kidney mitochondria from aged rats

Pérez-Gallardo

Noriega‐Cisneros

Esquivel‐Gutiérrez

et al. 2014

J Bioenerg Biomembr

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Diabetes mellitus (DM) is characterized by chronic hyperglycemia resulting from defects in the secretion and/or action of insulin. Diabetic nephropathy (DN) develops in diabetic patients and is characterized by a progressive deterioration of renal function. The mitochondrial electron transport chain (ETC) produces most of the reactive oxygen species (ROS) that are involved in diabetic nephropathy. Due to the high incidence of DM in the elderly, the aim of this study was to evaluate oxidative and nitrosative stress in kidney mitochondria from aged rats. We evaluated lipid peroxidation (LPO), nitric oxide (NO(•)) production, S-nitrosylation profiles, glutathione levels, and glutathione reductase and aconitase activities under streptozotocin (STZ)-induced experimental diabetes in kidney mitochondria from aged rats. The results showed an increase in LPO, NO(•) production, and S-nitrosylated proteins in rats with STZ-induced diabetes. A decrease in glutathione (GSH) levels and glutathione reductase (GR) and aconitase activities in the rats that received the STZ-induced diabetes treatment was also observed, when compared with the age-related controls. The data suggest that oxidative and nitrosative stresses promote mitochondrial oxidative dysfunction in the more advanced age rat kidney in STZ-induced diabetes.

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“…It is well known that the incidence of cardiovascular events increases in patients with chronic kidney disease (CKD) [1][2][3][4] . Epidemiological cases suggest that renal dysfunction may result in arterial calcification, stiffness and impairment of endothelium-dependent actions.…”

Section: Introductionmentioning

confidence: 99%

Reduction of NO-mediated Relaxing Effects in the Thoracic Aorta in an Experimental Chronic Kidney Disease Mouse Model

Mori-Kawabe

Yasuda

Ito

et al. 2015

JAT

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Aim: Chronic kidney disease (CKD) is known to frequently cause cardiovascular events. However, it is unclear how renal dysfunction affects the vascular response. We herein studied the effects of renal dysfunction on the aortic behavior in adenine-fed mice, investigating mechanisms underlying the occurrence of cardiovascular events in CKD patients. Methods: Biochemical analyses of the plasma creatinine, blood urea nitrogen (BUN) and glucose levels and measurements of the blood pressure were performed using C57BL/6 mice fed with and without an adenine-containing diet. The relaxing effects of acetylcholine (ACh) or sodium nitropurusside (SNP) and effects of NO synthase (NOS) inhibitors on the contractions induced by phenylephrine (PE) were measured in endothelium-intact aortas obtained from both mice. Results: The mice fed 0.25% adenine for four weeks showed greater plasma creatinine and BUN concentrations than the control mice, suggesting that adenine-fed mice are a useful CKD model. Furthermore, ACh relaxed the PE-stimulated, endothelium-intact aortas, the effect of which was less potent in the adenine-fed mice than in the control mice. In contrast, the degree of SNP-induced relaxation of the aortas was the same in the adenine-fed mice and control mice. The 1-adrenergic agonist, PE, induced more potent absolute tension of the endothelium-intact aortas in the CKD model mice than in the control mice, while the NOS inhibitors, N-nitro-L-arginine (LNA) and asymmetric dimethylarginine (ADMA) enhanced the contraction effects of PE in both mice. Conclusions: The findings of this study indicate that spontaneous and stimulated NO release from the endothelium is decreased in the CKD model mouse aorta. The NO-mediated correlation between renal and elastic arterial endothelial dysfunction is suggested to be a cause of cardiovascular events in patients with CKD. J Atheroscler Thromb, 2015; 22: 845-853.

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Peripheral Vascular Dysfunction in Chronic Kidney Disease

Cited by 59 publications

References 82 publications

Ethnicity-specific differences in L-arginine status in South African men

Ethnicity-specific differences in L-arginine status in South African men

Effects of diabetes on oxidative and nitrosative stress in kidney mitochondria from aged rats

Reduction of NO-mediated Relaxing Effects in the Thoracic Aorta in an Experimental Chronic Kidney Disease Mouse Model

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