Role of Neurohormonal Activation in the Pathogenesis of Cardiovascular Complications in Chronic Kidney Disease

2010 ◽  
pp. 279-290
Author(s):  
Andrea Stella ◽  
Giovanna Castoldi
2021 ◽  
Vol 25 (6) ◽  
pp. 63-70
Author(s):  
F. U. Dzgoeva ◽  
O. V. Remizov ◽  
V. Kh. Botsieva ◽  
N. G. Malakhova ◽  
Z. R. Ikoeva ◽  
...  

BACKGROUND. Cardiovascular complications caused by vascular calcification in chronic kidney disease (CKD) are closely related to disorders of bone and mineral metabolism, the mechanisms of which require further study.THE AIM: to clarify the role of the regulatory proteins of bone metabolism of sclerostin and osteoprotegerin in the processes of vascular calcification and the development of cardiovascular complications in CKD.PATIENTS AND METHODS. 110 patients with stage 3-5D CKD (67 men) were examined. Median age is 47.0 (23.0-68.0) years. Osteoprotegerin (OPG), sclerostin, intact parathyroid hormone (IPTG), troponin I in blood serum were determined using commercial kits "Enzyme-linked Immunosorbent Assay Kit for Sclerostin" ("Cloud-Clone Corp.", USA) and commercial kits "ELISA kit" ("Biomedica" (Austria) by enzyme immunoassay (ELISA). Echocardiography with Dopplerography was performed on the device "ALOKA 4000" ("Toshiba", Japan). The left ventricular myocardial mass index (LVMI) and peak systolic blood flow velocity in the aortic arch (Vps, peak systolic velocity) were determined to quantify hemodynamic changes indirectly indicating the state of the aortic vascular wall.RESULTS. Analysis of the ratios of the calculated glomerular filtration rate (EGFR), IMLJ, Vps, OPG, and sclerostin showed that a decrease in excretory kidney function is accompanied by an increase in the concentrations of OPG and sclerostin in the blood serum. At the same time, there is an increase in IMLJ and Vps. During the correlation analysis, it was shown that the level of OPG was positively correlated with the level of sclerostin and negatively with the level of iPTG.CONCLUSION. In our study, we obtained data confirming the interactive interaction between the vascular and bone systems. Morphogenetic proteins-inhibitors of bone metabolism (sclerostin and OPG) play a significant role in the defeat of the cardiovascular system in patients with CKD, as they promotes the development of vascular calcification.


The Clinician ◽  
2021 ◽  
Vol 14 (3-4) ◽  
pp. 78-85
Author(s):  
I. T. Murkamilov

In the development of renocardial relationships in chronic kidney disease, an important role is given to the activation of the renin-angiotensin-aldosterone system (RAAS), as the main component of the progression and development of cardiovascular complications..The presented review is devoted to the analysis of modern scientific data on the effect of high RAAS activity in chronic kidney disease on the course and prognosis of cardiovascular complications, as well as the protective capabilities of angiotensin-converting enzyme inhibitors, in particular perindopril. The results of scientific research on the role of the RAAS in the progression of chronic kidney disease are summarized. Data on chronic kidney disease as a risk factor for cardiovascular and cerebral complications are presented. Attention is focused on the possibilities of prolonging the pre-dialysis period of chronic kidney disease when using angiotensin-converting enzyme inhibitors. The role of perindopril as a lipophilic angiotensin-converting enzyme inhibitor with a high affinity for tissue RAAS was emphasized in reducing cardiovascular and cerebral risk in chronic kidney disease.


2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Kerstin Benz ◽  
Karl-Friedrich Hilgers ◽  
Christoph Daniel ◽  
Kerstin Amann

Cardiovascular complications are extremely frequent in patients with chronic kidney disease (CKD) and death from cardiac causes is the most common cause of death in this particular population. Cardiovascular disease is approximately 3 times more frequent in patients with CKD than in other known cardiovascular risk groups and cardiovascular mortality is approximately 10-fold more frequent in patients on dialysis compared to the age- and sex-matched segments of the nonrenal population. Among other structural and functional factors advanced calcification of atherosclerotic plaques as well as of the arterial and venous media has been described as potentially relevant for this high cardiovascular morbidity and mortality. One potential explanation for this exceedingly high vascular calcification in animal models as well as in patients with CKD increased systemic and most importantly local (micro)inflammation that has been shown to favor the development of calcifying particles by multiple ways. Of note, local vascular upregulation of proinflammatory and proosteogenic molecules is already present at early stages of CKD and may thus be operative for vascular calcification. In addition, increased expression of costimulatory molecules and mast cells has also been documented in patients with CKD pointing to a more inflammatory and potentially less stable phenotype of coronary atherosclerotic plaques in CKD.


2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Bojana Kisic ◽  
Dijana Miric ◽  
Ilija Dragojevic ◽  
Julijana Rasic ◽  
Ljiljana Popovic

Chronic kidney disease (CKD) is a worldwide public health problem. Patients with CKD have a number of disorders in the organism, and the presence of oxidative stress and systemic inflammation in these patients is the subject of numerous studies. Chronic inflammation joined with oxidative stress contributes to the development of numerous complications: accelerated atherosclerosis process and cardiovascular disease, emergence of Type 2 diabetes mellitus, development of malnutrition, anaemia, hyperparathyroidism, and so forth, affecting the prognosis and quality of life of patients with CKD. In this review we presented the potential role of the myeloperoxidase enzyme in the production of reactive/chlorinating intermediates and their role in oxidative damage to biomolecules in the body of patients with chronic kidney disease and end-stage renal disease. In addition, we discussed the role of modified lipoprotein particles under the influence of prooxidant MPO intermediates in the development of endothelial changes and cardiovascular complications in renal failure.


2020 ◽  
Vol 21 (7) ◽  
pp. 2483 ◽  
Author(s):  
Camélia Makhloufi ◽  
Fanny Nicolas ◽  
Nathalie McKay ◽  
Samantha Fernandez ◽  
Guillaume Hache ◽  
...  

Cardiovascular complications observed in chronic kidney disease (CKD) are associated with aryl hydrocarbon receptor (AhR) activation by tryptophan-derived uremic toxins—mainly indoxyl sulfate (IS). AhR is a ligand-activated transcription factor originally characterized as a receptor of xenobiotics involved in detoxification. The aim of this study was to determine the role of AhR in a CKD mouse model based on an adenine diet. Wild-type (WT) and AhR−/− mice were fed by alternating an adenine-enriched diet and a regular diet for 6 weeks. Our results showed an increased mortality rate of AhR−/− males. AhR−/− females survived and developed a less severe renal insufficiency that WT mice, reflected by urea, creatinine, and IS measurement in serum. The protective effect was related to a decrease of pro-inflammatory and pro-fibrotic gene expression, an attenuation of tubular injury, and a decrease of 2,8-dihydroxyadenine crystal deposition in the kidneys of AhR−/− mice. These mice expressed low levels of xanthine dehydrogenase, which oxidizes adenine into 2,8-dihydroxyadenine, and low levels of the IS metabolism enzymes. In conclusion, the CKD model of adenine diet is not suitable for AhR knockout mice when studying the role of this transcription factor in cardiovascular complications, as observed in human CKD.


2017 ◽  
Vol 71 (0) ◽  
pp. 0-0
Author(s):  
Emilia Mierzwińska ◽  
Tomasz Hryszko ◽  
Emilia Szablak-Uliszewska ◽  
Beata Naumnik

Chronic kidney disease (CKD) leads to the development of mineral and skeletal disturbances. They increase the risk of fractures, cardiovascular complications and, in consequence, decrease patients’ lifespan. Wnt/β-catenin pathway plays an important role in the development and homeostasis of the skeleton. The system is tightly regulated by group of inhibitors, such as sclerostin. Sclerostin inhibits bone formation and increases its resorption. There is mounting evidence that sclerostin may take part in the progress of bone and cardiovascular complications among patients with CKD. This review presents the current state of knowledge on the role of sclerostin in bone and cardiovascular disturbances in CKD patients.


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