scholarly journals Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jeanie Park
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Nervous System ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Renal Disease ◽  
Left Ventricular ◽  
Sympathetic Nervous

Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.

scholarly journals Cardiovascular Risk Factors and Chronic Kidney Disease—FGF23: A Key Molecule in the Cardiovascular Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Rika Jimbo ◽  
Tatsuo Shimosawa
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Cardiovascular Risks ◽  
Mineral And Bone Disorder ◽  
Promising Target ◽  
Increased Risk

Patients with chronic kidney disease (CKD) are at increased risk of mortality, mainly from cardiovascular disease. Moreover, abnormal mineral and bone metabolism, the so-called CKD-mineral and bone disorder (MBD), occurs from early stages of CKD. This CKD-MBD presents a strong cardiovascular risk for CKD patients. Discovery of fibroblast growth factor 23 (FGF23) has altered our understanding of CKD-MBD and has revealed more complex cross-talk and endocrine feedback loops between the kidney, parathyroid gland, intestines, and bone. During the past decade, reports of clinical studies have described the association between FGF23 and cardiovascular risks, left ventricular hypertrophy, and vascular calcification. Recent translational reports have described the existence of FGF23-Klotho axis in the vasculature and the causative effect of FGF23 on cardiovascular disease. These findings suggest FGF23 as a promising target for novel therapeutic approaches to improve clinical outcomes of CKD patients.

scholarly journals Contribution of Selected Vasoactive Systems to Blood Pressure Regulation in Two Models of Chronic Kidney Disease

2020 ◽  
pp. 405-414
Author(s):  
N DRÁBKOVÁ ◽  
S HOJNÁ ◽  
J ZICHA ◽  
I VANĚČKOVÁ
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Nervous System ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Renal Artery ◽  
Partial Nephrectomy ◽  
Wistar Rats ◽  
Sympathetic Nervous

It is generally accepted that angiotensin II plays an important role in high blood pressure (BP) development in both 2-kidney-1-clip (2K1C) Goldblatt hypertension and in partial nephrectomy (NX) model of chronic kidney disease (CKD). The contribution of sympathetic nervous system and nitric oxide to BP control in these models is less clear. Partial nephrectomy or stenosis of the renal artery was performed in adult (10-week-old) male hypertensive heterozygous Ren-2 transgenic rats (TGR) and normotensive control Hannover Sprague Dawley (HanSD) rats and in Wistar rats. One and four weeks after the surgery, basal blood pressure (BP) and acute BP responses to the consecutive blockade of renin-angiotensin (RAS), sympathetic nervous (SNS), and nitric oxide (NO) systems were determined in conscious rats. Both surgical procedures increased plasma urea, a marker of renal damage; the effect being more pronounced following partial nephrectomy in hypertensive TGR than in normotensive HanSD rats with a substantially smaller effect in Wistar rats after renal artery stenosis. We demonstrated that the renin-angiotensin system does not play so fundamental role in blood pressure maintenance during hypertension development in either CKD model. By contrast, a more important role is exerted by the sympathetic nervous system, the activity of which is increased in hypertensive TGR-NX in the developmental phase of hypertension, while in HanSD-NX or Wistar-2K1C it is postponed to the established phase. The contribution of the vasoconstrictor systems (RAS and SNS) was increased following hypertension induction. The role of NO-dependent vasodilation was unchanged in 5/6 NX HanSD and in 2K1C Wistar rats, while it gradually decreased in 5/6 NX TGR rats.

scholarly journals SYMPATHETIC HYPERACTIVITY IN CHRONIC KIDNEY DISEASE PATIENTS: FROM PATHOGENESIS TO TREATMENT

2017 ◽  
pp. 141-160
Author(s):  
N. Stepanova
Keyword(s):  
Chronic Kidney Disease ◽  
Nervous System ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Crucial Role ◽  
Clinical Relevance ◽  
Cardiovascular Complications ◽  
Current Treatment ◽  
Sympathetic Hyperactivity ◽  
Sympathetic Nervous

Sympathetic nervous system plays a crucial role in the development of cardiovascular complications in chronic kidney disease (CKD) patients. The aim of this review is to summarize up-to-date knowledge of the sympathetic hyperactivity in the pathogenesis of CKD, its clinical relevance, and as the options of current treatment.

The Sympathetic Nervous System in Chronic Kidney Disease

2013 ◽  
Vol 15 (4) ◽  
pp. 370-376 ◽  
Author(s):  
Sebastian Ewen ◽  
Christian Ukena ◽  
Dominik Linz ◽  
Roland E. Schmieder ◽  
Michael Böhm ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Nervous System ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous

The Role of Sympathetic Nervous System in the Progression of Chronic Kidney Disease in the Era of Catheter Based Sympathetic Renal Denervation

2013 ◽  
Vol 8 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Dimitrios Petras ◽  
Konstantinos Koutroutsos ◽  
Athanasios Kordalis ◽  
Costas Tsioufis ◽  
Christodoulos Stefanadis
Keyword(s):  
Chronic Kidney Disease ◽  
Nervous System ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Renal Denervation ◽  
Sympathetic Nervous

scholarly journals Comparison of the Modification of Diet in Renal Disease Study and Chronic Kidney Disease Epidemiology Collaboration Equations for Detection of Cardiovascular Risk: Tehran Lipid and Glucose Study

2020 ◽  
Vol 18 (4) ◽  
Author(s):  
Pouria Mousapour ◽  
Maryam Barzin ◽  
Majid Valizadeh ◽  
Maryam Mahdavi ◽  
Fereidoun Azizi ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Renal Disease ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Atherosclerotic Cardiovascular Disease ◽  
Disease Study

Objectives: The study aimed to compare the Modification of Diet in Renal Disease Study (MDRD) and the Epidemiology Collaboration (CKD-EPI) equations for the detection of cardiovascular risk. Methods: Data of 9,970 Tehranian participants aged ≥ 20 years were analyzed. The prevalence of cardiovascular disease (CVD), its risk factors, and 10-year atherosclerotic cardiovascular disease (ASCVD) risk were compared across the categories of glomerular filtration rate based on the MDRD and CKD-EPI equations. Chronic kidney disease (CKD) was defined as the estimated Glomerular Filtration Rate (eGFR) < 60 mL/min/1.73 m2 according to each equation. Results: The prevalence of CKD weighted to the 2016 Tehranian urban population was 11.0% (95% confidence interval: 10.3 - 11.6) and 9.7% (9.1 - 10.2) according to the MDRD and CKD-EPI equations, respectively. Besides, 8.3% and 1.5% of the participants with CKDMDRD and non-CKDMDRD were reclassified to non-CKDCKD-EPI and CKDCKD-EPI categories, respectively. Participants with CKDCKD-EPI but without CKDMDRD were more likely to be male and older, and more frequently had diabetes, hypertension, dyslipidemia, and CVD, when compared to those without CKD according to both equations; they were also more likely to be male, older, and smokers, and had less dyslipidemia and more CVD, when compared to those with CKD by using both equations. In multivariate logistic regression analysis, compared to CKDMDRD, the odds of CKDCKD-EPI were significantly higher for older age and lower for the female gender. Conclusions: Compared to MDRD, the CKD-EPI equation provides more appropriate detection of cardiovascular risk, which is caused by the reclassification of older individuals and fewer females into lower eGFR categories.

scholarly journals Increased fibroblast growth factor-21 in chronic kidney disease is a trade-off between survival benefit and blood pressure dysregulation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Toshihiro Nakano ◽  
Kazuhiro Shiizaki ◽  
Yutaka Miura ◽  
Masahiro Matsui ◽  
Keisei Kosaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Nervous System ◽  
Growth Factor ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Fibroblast Growth Factor 21 ◽  
Fibroblast Growth ◽  
Wild Type ◽  
Sympathetic Nervous

AbstractCirculating levels of fibroblast growth factor-21 (FGF21) start increasing in patients with chronic kidney disease (CKD) since early stages during the cause of disease progression. FGF21 is a liver-derived hormone that induces responses to stress through acting on hypothalamus to activate the sympathetic nervous system and the hypothalamus-pituitary-adrenal endocrine axis. However, roles that FGF21 plays in pathophysiology of CKD remains elusive. Here we show in mice that FGF21 is required to survive CKD but responsible for blood pressure dysregulation. When introduced with CKD, Fgf21−/− mice died earlier than wild-type mice. Paradoxically, these Fgf21−/− CKD mice escaped several complications observed in wild-type mice, including augmentation of blood pressure elevating response and activation of the sympathetic nervous system during physical activity and increase in serum noradrenalin and corticosterone levels. Supplementation of FGF21 by administration of an FGF21-expressing adeno-associated virus vector recapitulated these complications in wild-type mice and restored the survival period in Fgf21−/− CKD mice. In CKD patients, high serum FGF21 levels are independently associated with decreased baroreceptor sensitivity. Thus, increased FGF21 in CKD can be viewed as a survival response at the sacrifice of blood pressure homeostasis.

Biochemical and Paraclinical Evaluation of Organ Damage in Arterial Hypertension with Associated Chronic Kidney Disease

2020 ◽  
Vol 71 (6) ◽  
pp. 194-204
Author(s):  
Teim Baaj ◽  
Ahmed Abu-Awwad ◽  
Mircea Botoca ◽  
Octavian Marius Cretu ◽  
Elena Ardeleanu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Ventricular Hypertrophy ◽  
Ankle Brachial Index ◽  
Intima Media Thickness ◽  
Organ Damage ◽  
Left Ventricular ◽  
Study Group ◽  
Group A

Organ damages, which contribute to the overall cardiovascular risk of hypertensive patients, should be early detected, prevented and treated. The study evaluated organ damage in a hypertensive study group with chronic kidney disease (CKD), compared with a study group of hypertension without CKD. Albuminuria was present in 41.2% and reduced estimated glomerular filtration rate [60 ml/min/m2 was present in 72.5% of hypertensive with CKD. The comparison of organ damage revealed in the CKD group a statistical significant higher prevalence of organ damage as follows: intima-media thickness ]0.9 mm in 39.9% vs 10.5%, carotid plaques in 28.2% vs 12.6%, left ventricular hypertrophy in 39.9% vs 31%, ankle brachial index in 6.2% vs 3.5%. Early detection and treatment of additional cardiovascular risk factors as dyslipidaemia and hyperglycaemia, that have significant role in the pathogenesis of organ damage, contribute to the better prevention of cardiovascular and renal complications in hypertension with CKD.

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