scholarly journals Cardiac Remodeling in Chronic Kidney Disease

Toxins ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 161 ◽  
Author(s):  
Nadine Kaesler ◽  
Anne Babler ◽  
Jürgen Floege ◽  
Rafael Kramann
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiac Remodeling ◽  
Mineral Metabolism ◽  
Treatment Options ◽  
Renin Angiotensin System ◽  
Cell Types ◽  
Current Treatment ◽  
Left Ventricular ◽  
Heart Functions

Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.

A new role for vitamin D receptor activation in chronic kidney disease

2009 ◽  
Vol 297 (6) ◽  
pp. F1502-F1509 ◽  
Author(s):  
José M. Valdivielso ◽  
Jorge Cannata-Andía ◽  
Blai Coll ◽  
Elvira Fernández
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Receptor ◽  
Mineral Metabolism ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Traditional Use ◽  
Transplant Patients ◽  
Therapeutic Uses

Vitamin D has proven to be much more than a simple “calcium hormone.” The fact that the vitamin D receptor has been found in cells not related to mineral metabolism supports that statement. The interest of nephrologists in vitamin D and its effects beyond mineral metabolism has increased over the last few years, evidencing the importance of this so-called “sunshine hormone.” In the present review, we highlight the most recent developments in the traditional use of vitamin D in chronic kidney disease (CKD) patients, namely, the control of secondary hyperparathyroidism (sHPT). Furthermore, we also explore the data available regarding the new possible therapeutic uses of vitamin D for the treatment of other complications present in CKD patients, such as vascular calcification, left ventricular hypertrophy, or proteinuria. Finally, some still scarce but very promising data regarding a possible role of vitamin D in kidney transplant patients also are reviewed. The available data point to a potential beneficial effect of vitamin D in CKD patients beyond the control of mineral metabolism.

scholarly journals Chronic Kidney Disease: Current Scenario of diagnosis and treatment in India

2021 ◽  
Author(s):  
Bhavya V
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Low Income ◽  
Conventional Treatment ◽  
Treatment Options ◽  
Current Treatment ◽  
Low Income Countries ◽  
Specific Marker ◽  
Treatment Scenario ◽  
Current Scenario

Chronic Kidney Disease (CKD) is one of the most burdensome disease with high mortality rate globally. Even though there are diagnostically accepted markers for the detection of CKD, the unreliability of the non-specific marker is a lacuna in the clinical world for an early prognosis and prevention of this chronic disease. Further, the economically challenging conventional treatment options available currently are a burden for many low-income countries to overcome this disease. This article discusses the current treatment scenario for CKD, and limitations of the diagnostic and treatment options available for CKD.

Vascular calcification in chronic kidney disease

2010 ◽  
Vol 119 (3) ◽  
pp. 111-121 ◽  
Author(s):  
Adrian Covic ◽  
Mehmet Kanbay ◽  
Luminita Voroneanu ◽  
Faruk Turgut ◽  
Dragomir N. Serban ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Left Ventricular ◽  
Arterial Calcification ◽  
Pathophysiological Mechanism ◽  
Cardiovascular Morbidity And Mortality

VC (vascular calcification) is highly prevalent in patients with CKD (chronic kidney disease), but its mechanism is multifactorial and incompletely understood. In addition to increased traditional risk factors, CKD patients also have a number of non-traditional cardiovascular risk factors, which may play a prominent role in the pathogenesis of arterial calcification, such as duration of dialysis and disorders of mineral metabolism. The transformation of vascular smooth muscle cells into chondrocytes or osteoblast-like cells seems to be a key element in VC pathogenesis, in the context of passive calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. The process may be favoured by the low levels of circulating and locally produced VC inhibitors. VC determines increased arterial stiffness, left ventricular hypertrophy, a decrease in coronary artery perfusion, myocardial ischaemia and increased cardiovascular morbidity and mortality. Although current therapeutic strategies focus on the correction of phosphate, calcium, parathyroid hormone or vitamin D, a better understanding of the mechanisms of abnormal tissue calcification may lead to development of new therapeutic agents, which could reduce VC and improve cardiovascular outcome in CKD patients. The present review summarizes the following aspects: (i) the pathophysiological mechanism responsible for VC and its promoters and inhibitors, (ii) the methods for detection of VC in patients with CKD, including evaluation of arterial stiffness, and (iii) the management of VC in CKD patients.

Chronic kidney disease and vascular remodelling: molecular mechanisms and clinical implications

2012 ◽  
Vol 123 (7) ◽  
pp. 399-416 ◽  
Author(s):  
Marie Briet ◽  
Kevin D. Burns
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Mineral Metabolism ◽  
Renin Angiotensin System ◽  
Cardiovascular Complications ◽  
Arterial Calcification ◽  
Clinical Consequences ◽  
Cv Disease

CKD (chronic kidney disease) is a severe and complex disease with a very high prevalence of CV (cardiovascular) complications. CKD patients are exposed to haemodynamic disturbances in addition to severe metabolic abnormalities that lead to a specific form of arterial remodelling, which contributes to the development of CV disease. Arterial calcification is a major event in the arterial remodelling process and is strongly linked to mineral metabolism abnormalities associated with CKD. Arterial remodelling is not limited to arterial calcification and modifications in arterial wall composition are also observed. Activation of the RAS (renin–angiotensin system), ET-1 (endothelin-1), endothelial dysfunction, oxidative stress and ADMA (asymmetric ω-NG,NG-dimethylarginine), as well as the anti-aging molecule Klotho, are implicated in this process. The present review details the mechanisms involved in arterial calcification and arterial remodelling associated with CKD, and provides the clinical consequences of large and small artery stiffness and remodelling in CKD patients.

scholarly journals Impact of Homoarginine on Myocardial Function and Remodeling in a Rat Model of Chronic Renal Failure

2022 ◽  
Vol 27 ◽  
pp. 107424842110546
Author(s):  
Vitali Koch ◽  
Christophe Weber ◽  
Johannes H. Riffel ◽  
Kristina Buchner ◽  
Sebastian J. Buss ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Myocardial Fibrosis ◽  
Cardiac Remodeling ◽  
Heart Function ◽  
Plasma Concentrations ◽  
Left Ventricular ◽  
Cross Sectional

Purpose: Low plasma concentrations of the amino acid homoarginine (HA) have been shown to correlate with adverse cardiovascular outcome, particularly in patients with chronic kidney disease. The present study sought to investigate the effect of HA treatment on cardiac remodeling in rats undergoing artificially induced renal insufficiency by 5/6 nephrectomy (5/6 Nx). Methods: A total of 33 male Wistar rats were randomly divided into sham and 5/6 Nx groups, receiving either placebo treatment or 400 mg·kg−1·day−1 HA over a 4-week period. Results: 5/6 Nx per se resulted in adverse myocardial remodeling with aggravated cardiac function and associated cardiac overload as the most obvious alteration (−23% ejection fraction, P < 0.0001), as well as increased myocardial fibrosis (+80%, P = 0.0005) compared to placebo treated sham animals. HA treatment of 5/6 Nx rats has led to an improvement of ejection fraction (+24%, P = 0.0003) and fractional shortening (+21%, P = 0.0126), as well as a decrease of collagen deposition (−32%, P = 0.0041), left ventricular weight (−14%, P = 0.0468), and myocyte cross-sectional area (−12%, P < 0.0001). These changes were accompanied by a downregulation of atrial natriuretic factor (−65% P < 0.0001) and collagen type V alpha 1 chain (−44%, P = 0.0006). Sham animals revealed no significant changes in cardiac function, myocardial fibrosis, or any of the aforementioned molecular changes after drug treatment. Conclusion: Dietary HA supplementation appears to have the potential of preventing cardiac remodeling and improving heart function in the setting of chronic kidney disease. Our findings shed new light on HA as a possible new therapeutic agent for patients at high cardiovascular risk.

scholarly journals Chronic Kidney Disease –Mineral Bone Disorder (CKD- MBD) – Further Insight at the Indian patients.

JMS SKIMS ◽  
2019 ◽  
Vol 22 (3) ◽  
Author(s):  
Muzaffar Maqsood Wani ◽  
Imtiyaz Ahmad Wani
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Left Ventricular ◽  
Normal Serum ◽  
Vitamin D Metabolism ◽  
Mineral Bone Disorder ◽  
Bone Disorder ◽  
Normal Serum Calcium

The kidneys play an important role in maintaining normal serum calcium (Ca) and phosphorous (P) concentrations. Chronic kidney disease (CKD) is associated with significant disturbances in bone and mineral metabolism, leading to altered serum concentrations of Ca, P, vitamin D and parathyroid hormone (PTH)1,2,3. These changes are initially detected when the glomerular filtration rate (GFR) falls to ≤60 mL/min and are nearly uniform as GFR drops to <30ml/min2,3. This leads to a number of bone abnormalities previously called “renal osteodystrophy”, renamed as CKD-Mineral Bone Disorder (CKD-MBD) by National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) consensus group4 . CKD-MBD is a systemic disorder manifested by either one or a combination of a) abnormalities of Ca, P, PTH or vitamin D metabolism, b) abnormalities in bone turnover, mineralization, volume, linear growth or strength c) vascular or soft tissue calcification. This has over time been expanded to include left ventricular hypertrophy, hypertension, immune dysfunction and inflammation5,6. 

scholarly journals Changes of FGF23 and the Renin-Angiotensin-System in Male Mouse Models of Chronic Kidney Disease and Cardiac Hypertrophy

2021 ◽  
Author(s):  
Kohei Okamoto ◽  
Hideki Fujii ◽  
Kentaro Watanabe ◽  
Shunsuke Goto ◽  
Keiji Kono ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Renin Angiotensin System ◽  
Close Correlation ◽  
Left Ventricular ◽  
Heart Weight ◽  
Related Factors ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin

Abstract Serum fibroblast growth factor 23 (FGF23) levels and the renin-angiotensin-aldosterone system (RAAS) are elevated in chronic kidney disease (CKD) patients, and their association with left ventricular hypertrophy (LVH) has been reported. However, whether the FGF23 elevation is the cause or result of LVH remains unclear. At 10 weeks, male C57BL/6J mice were divided into four groups: Sham, CKD (5/6 nephrectomy), LVH (transaortic constriction), and CKD/LVH group. At 16 weeks, the mice were sacrificed, and blood and urine, cardiac expressions of FGF23 and RAAS-related factors, and cardiac histological analyses were performed. Heart weight, serum FGF23 levels, and cardiac expression of FGF23 and RAAS-related factors, except for angiotensin-converting enzyme 2, more increased in the CKD/LVH group compared to the other groups. A significant correlation between LVH and cardiac expressions of FGF23 and RAAS-related factors was observed. Furthermore, there was a significantly close correlation of the cardiac expression of FGF23 with LVH and RAAS-related factors. The coexisting CKD and LVH increased serum and cardiac FGF23 and RAAS-related factors, and there was a significant correlation between them. A close correlation of cardiac, but not serum FGF23, with LVH and RAAS suggested that local FGF23 levels may be associated with LVH and RAAS activation.

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