Arterial Stiffness: A Nexus between Cardiac and Renal Disease.

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Abstract

Vascular disease is the leading cause of morbidity and mortality in the Western world, and vascular function is determined by structural and functional properties of the arterial vascular wall. Cardiorenal metabolic syndrome such as obesity, diabetes, hypertension, kidney disease, and aging are conditions that predispose to arterial stiffening, which is a pathological alteration of the vascular wall and ultimately results in target organ damage in heart and kidney. In this review, we provide new insights on the interactions between arterial stiffness, vascular resistance and pulse wave velocity as well as final end-organ damage in heart and kidney. Better understanding of the mechanisms of arterial functional and hemodynamic alteration may help in developing more refined therapeutic strategies aimed to reduce cardiovascular and chronic kidney diseases.

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Chronic kidney disease: effects on the cardiovascular system.

Ernesto Schiffrin, Mark L. Lipman, Johannes Mann (2007)

Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.

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Female Mice are Protected against High-Fat Diet Induced Metabolic Syndrome and Increase the Regulatory T Cell Population in Adipose Tissue

Ulrika Pettersson, Tomas B. Waldén, Per-Ola Carlsson … (2012)

Sex differences in obesity-induced complications such as type 2 diabetes have been reported. The aim of the study was to pinpoint the mechanisms resulting in different outcome of female and male mice on a high-fat diet (HFD). Mice fed control or HFD were monitored for weight, blood glucose, and insulin for 14 weeks. Circulating chemokines, islet endocrine function and blood flow, as well as adipose tissue populations of macrophages and regulatory T-lymphocytes (Treg) were thereafter assessed. Despite similar weight (43.8±1.0 and 40.2±1.5 g, respectively), male but not female mice developed hyperinsulinemia on HFD as previously described (2.5±0.7 and 0.5±0.1 pmol/l, respectively) consistent with glucose intolerance. Male mice also exhibited hypertrophic islets with intact function in terms of insulin release and blood perfusion. Low-grade, systemic inflammation was absent in obese female but present in obese male mice (IL-6 and mKC, males: 77.4±17 and 1795±563; females: 14.6±4.9 and 240±22 pg/ml), and the population of inflammatory macrophages was increased in intra-abdominal adipose tissues of high-fat-fed male but not female mice. In contrast, the anti-inflammatory Treg cell population increased in the adipose tissue of female mice in response to weight gain, while the number decreased in high-fat-fed male mice. In conclusion, female mice are protected against HFD-induced metabolic changes while maintaining an anti-inflammatory environment in the intra-abdominal adipose tissue with expanded Treg cell population, whereas HFD-fed male mice develop adipose tissue inflammation, glucose intolerance, hyperinsulinemia, and islet hypertrophy.

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Arterial stiffness and pulse pressure in CKD and ESRD.

Marie Briet, Pierre Boutouyrie, Stephane Laurent … (2012)

We recognize that increased systolic pressure is the most challenging form of hypertension today and that pulse pressure as an independent cardiovascular risk factor has focused attention on arterial stiffness and wave reflections as the most important factors determining these pressures. In recent years, many studies emphasized the role of arterial rigidity in the development of cardiovascular diseases, and it was shown that stiffening of arteries is associated with increased cardiovascular mortality and morbidity. Moreover,arterial stiffening is linked to decreased glomerular filtration rate, and is predictive of kidney disease progression and the patient’s cardiovascular outcome. Premature vascular aging and arterial stiffening are observed with progression of chronic kidney disease (CKD) and in end-stage renal disease(ESRD). This accelerated aging is associated with outward remodeling of large vessels, characterized by increased arterial radius not totally compensated for by artery wall hypertrophy. Arterial stiffening in CKD and ESRD patients is of multifactorial origin with extensive arterial calcifications representing a major covariate. With aging, the rigidity is more pronounced in the aorta than in peripheral conduit arteries, leading to the disappearance or inversion of the arterial stiffness gradient and less protection of the microcirculation from high-pressure transmission. Various non-pharmacological or pharmacological interventions can modestly slow the progression of arterial stiffness,but arterial stiffness is, in part, pressure dependent and treatments able to stop the process mainly include antihypertensive drugs.

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Journal

Journal ID (iso-abbrev): Cardiorenal Med

Title: Cardiorenal medicine

ISSN: 1664-3828

ISSN (Print): 1664-5502

Publication date (Electronic): Apr 2014

Volume: 4

Issue: 1

Affiliations

[1 ] Division of Endocrinology, Diabetes, and Metabolism, Mo., USA ; Diabetes Cardiovascular Center, Mo., USA ; Harry S. Truman Memorial Veterans Hospital, Columbia, Mo., USA.

[2 ] Division of Endocrinology, Diabetes, and Metabolism, Mo., USA ; Diabetes Cardiovascular Center, Mo., USA ; Department of Medical Pharmacology and Physiology, Mo., USA ; Harry S. Truman Memorial Veterans Hospital, Columbia, Mo., USA.

Article

Publisher Item ID: crm-0004-0060

DOI: 10.1159/000360867

PubMed ID: 24847335

SO-VID: 3af37f29-7820-4a2f-a42b-9830a3699c37

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Keywords: Arterial stiffness,Cardiorenal metabolic syndrome,Endothelial cells,Estrogen,Vascular smooth muscle cells

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Keywords: Arterial stiffness, Cardiorenal metabolic syndrome, Endothelial cells, Estrogen, Vascular smooth muscle cells

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Arterial Stiffness: A Nexus between Cardiac and Renal Disease.

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Karger: Nephrology

Most cited references 42

Chronic kidney disease: effects on the cardiovascular system.

Female Mice are Protected against High-Fat Diet Induced Metabolic Syndrome and Increase the Regulatory T Cell Population in Adipose Tissue

Arterial stiffness and pulse pressure in CKD and ESRD.

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