Arterial Stiffness: A Nexus between Cardiac and Renal Disease

Jia, Guanghong; Aroor, Annayya R.; Sowers, James R.

doi:10.1159/000360867

Cited by 57 publications

(54 citation statements)

References 116 publications

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“…Beyond promoting glucose uptake and utilization, insulin-dependent PI3K/Akt activation also phosphorylates/activates endothelial nitric oxide (NO) synthase which in turn increases bioavailable NO in the vascular endothelium [22,23,24]. Thus, under conditions of tissue resistance to insulin, the alterations in insulin-dependent responses of the PI3K/Akt pathway lead to reductions in bioavailable NO, impaired NO-dependent vascular relaxation, and increased tissue inflammation and fibrosis.…”

Section: Mechanisms Of Insulin Resistance and Impact Of Insulin On Thmentioning

confidence: 99%

Insulin Resistance in Kidney Disease: Is There a Distinct Role Separate from That of Diabetes or Obesity

Whaley‐Connell¹,

Sowers

2017

Cardiorenal Med

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Insulin resistance is a central component of the metabolic dysregulation observed in obesity, which puts one at risk for the development of type 2 diabetes and complications related to diabetes such as chronic kidney disease. Insulin resistance and compensatory hyperinsulinemia place one at risk for other risk factors such as dyslipidemia, hypertension, and proteinuria, e.g., development of kidney disease. Our traditional view of insulin actions focuses on insulin-sensitive tissues such as skeletal muscle, liver, adipose tissue, and the pancreas. However, insulin also has distinct actions in kidney tissue that regulate growth, hypertrophy, as well as microcirculatory and fibrotic pathways which, in turn, impact glomerular filtration, including that governed by tubuloglomerular feedback. However, it is often difficult to discern the distinct effects of excess circulating insulin and impaired insulin actions, as exist in the insulin resistance individual, from the associated effects of obesity or elevated systolic blood pressure on the development and progression of kidney disease over time. Therefore, we review the experimental and clinical evidence for the distinct impact of insulin resistance on kidney function and disease.

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Section: Mechanisms Of Insulin Resistance and Impact Of Insulin On Thmentioning

confidence: 99%

Insulin Resistance in Kidney Disease: Is There a Distinct Role Separate from That of Diabetes or Obesity

Whaley‐Connell¹,

Sowers

2017

Cardiorenal Med

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“…11 Arterial stiffness not only relates to HT but also left ventricular hypertrophy (LVH), a manifestation of hypertensive target organ damage. 12 Several noninvasive assessments of subclinical CVD have been established in adults, including pulse wave velocity (PWV), augmentation index (AI), and ABPM-derived arterial stiffness index (AASI). 13 With limited pediatric data, the use of these assessments in children and adolescents awaits further validation.…”

Section: Cardiovascular Assessmentsmentioning

confidence: 99%

Homocysteine and Arginine-to-Asymmetric Dimethylarginine Ratio Associated With Blood Pressure Abnormalities in Children With Early Chronic Kidney Disease

Chien

Lin

Hsu

et al. 2015

Circ J

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Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp (NO), a vasodilator, regulates endothelial function and blood pressure (BP). Our previous review indicated emerging evidence supporting that a deficiency of NO links endothelial dysfunction to CVD in pediatric CKD. 3 Because asymmetric dimethylarginine (ADMA) is an analog of L-arginine (ARG), the substrate for NO synthase (NOS), the ARG-to-ADMA ratio (AAR) represents NO bioavailability and maintains NO homeostasis. 4 Elevated plasma ADMA levels are observed in patients with hypertension (HT) as well as CKD. 5,6 Ambulatory BP monitoring (ABPM) has proven to be the best method of detecting abnormal BP and cardiovascular outcome in CKD. 7 Our recent reports showed that ARG metabolites in the NO pathway are interrelated and involved in abnormal ABPM profiles in children with CKD. 8,9 ADMA is synthesized by the ardiovascular disease (CVD) is a major cause of morbidity and mortality in children and adults with chronic kidney disease (CKD). 1 Unlike adults, young CKD patients rarely present with CV events. Thus assessment of CVD in childhood mainly relies on the characteristics of vascular phenotype. Less attention has been paid to evaluating subclinical CVD in the early stage of CKD in the pediatric population. It is noteworthy that CKD children with subclinical CVD are at risk of subsequent development of CVD in adulthood. Thus, identification of surrogate markers to detect subclinical CVD in early CKD children may aid in reducing the global burden of CKD.Deterioration in endothelial function and arterial stiffness are early events in the development of CVD. Background: Less attention has been paid to evaluating subclinical cardiovascular disease (CVD) in the early stage of pediatric chronic kidney disease (CKD). Ambulatory blood pressure monitoring (ABPM) and arterial stiffness are the earliest detectable assessments of subclinical CVD. Asymmetric dimethylarginine (ADMA) is an analog of L-arginine (ARG) that inhibits nitric oxide (NO) production; thus the ARG-to-ADMA ratio (AAR) is an index of NO. Homocysteine (HCY) is a risk factor for CVD and it can be metabolized to L-cysteine (CYS). Given that HCY and ADMA/NO are closely linked and related to hypertension, we therefore investigated whether ARG and HCY metabolites, arterial stiffness parameters, ABPM profile, and left ventricular hypertrophy (LVH) are interrelated in children and adolescents with early CKD.

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“…However, in addition to hypertension, a number of other cardiovascular, renal, and metabolic diseases were found to be associated with increased serum uric acid concentration. Thus, several studies published recently in Cardiorenal Medicine and elsewhere clearly indicated that hyperuricemia may be involved in the pathogenesis of cardiovascular and renal diseases, insulin resistance, and metabolic disorders [56,57,58,59,60,61]. Apparently, an increased serum uric acid level may contribute to increased oxidative stress, endothelial dysfunction, increased vascular stiffness, and inappropriate reaction of the renin-angiotensin system [56].…”

Section: Clinical and Epidemiological Studiesmentioning

confidence: 99%

Hyperuricemia: A Biomarker of Renal Hemodynamic Impairment

Sušić

Fröhlich²

2015

Cardiorenal Med

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Background: Many epidemiological, clinical, and experimental reports have demonstrated an association between serum uric acid concentration and a variety of cardiovascular and renal diseases, particularly in hypertension. At present, there seems to be no resolution to the question whether this relationship is causal or coincidental. Summary: This discussion examines a number of biological, pathophysiological, fundamental, and clinical relationships between serum uric acid concentration and several of these disorders. To this end, discussion and review provide some specific insight conclusions and recommendations related to their clinical relevance. Key Messages: We suggest that, in most instances (especially in patients with essential hypertension), the increase in serum uric acid concentration is coincidental, serving as a useful biomarker that relates the magnitude of circulating plasma uric acid concentration with the extent of impaired cardiovascular and renal function. Moreover, the value of certain pharmaceutical agents affecting the serum uric acid level should be considered carefully by taking into consideration the associated pathophysiological derangements.

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Arterial Stiffness: A Nexus between Cardiac and Renal Disease

Cited by 57 publications

References 116 publications

Insulin Resistance in Kidney Disease: Is There a Distinct Role Separate from That of Diabetes or Obesity

Insulin Resistance in Kidney Disease: Is There a Distinct Role Separate from That of Diabetes or Obesity

Homocysteine and Arginine-to-Asymmetric Dimethylarginine Ratio Associated With Blood Pressure Abnormalities in Children With Early Chronic Kidney Disease

Hyperuricemia: A Biomarker of Renal Hemodynamic Impairment

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