scholarly journals Cardiovascular Biomarkers in Chronic Kidney Disease

2010 ◽  
Vol 29 (4) ◽  
pp. 298-303 ◽  
Author(s):  
Mirjana Đerić ◽  
Velibor Čabarkapa
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Disease ◽  
Left Ventricular ◽  
Calcium Phosphorus ◽  
Traditional Risk Factors ◽  
Cardiovascular Biomarkers

Cardiovascular Biomarkers in Chronic Kidney DiseaseCardiovascular morbidity and mortality are markedly increased in chronic renal failure patients. Although it cannot be regarded as a cardiovascular disease risk equivalent, kidney dysfunction is considered an independent predictor of increased cardiovascular risk that increases with deteriorating kidney function. The association is a very complex one, and the term cardiorenal syndrome is now widely used. Cardiovascular disease in chronic kidney disease patients usually manifests as ischemic heart disease (in the form of angina, acute coronary syndrome or sudden cardiac death), cerebrovascular disease, peripheral vascular disease, and congestive heart failure. Vascular disease includes atherosclerosis and vascular calcifications, and cardiomyopathy comprises left ventricular hypertrophy, cardiac fibrosis and left ventricular systolic and diastolic dysfunction. In addition to the well-established traditional risk factors such as hypertension, hyperlipidemia, insulin resistance and diabetes mellitus, the association is supported by synergistic action of non-traditional risk factors such as excessive calcium-phosphorus load, hyperparathyroidism, anemia, hemodynamic overload, malnutrition, inflammation, hyperhomocysteinemia, altered nitric oxide synthase and increased oxidative stress. This paper summarizes the current understanding of the significance of specific uremic retention solutes, natriuretic peptides, biochemical markers of disorders in calcium-phosphorus homeostasis, systemic inflammation, oxidative stress, and dyslipidemia.

scholarly journals Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the Burden?

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
Karolos-Pavlos Rapsomanikis ◽  
Evangelia Dounousi
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Pon1 Activity ◽  
Pathophysiological Mechanism ◽  
Ros Production ◽  
Cardiovascular Damage

Chronic kidney disease (CKD) patients are among the groups at the highest risk for cardiovascular disease and significantly shortened remaining lifespan. CKD enhances oxidative stress in the organism with ensuing cardiovascular damage. Oxidative stress in uremia is the consequence of higher reactive oxygen species (ROS) production, whereas attenuated clearance of pro-oxidant substances and impaired antioxidant defenses play a complementary role. The pathophysiological mechanism underlying the increased ROS production in CKD is at least partly mediated by upregulation of the intrarenal angiotensin system. Enhanced oxidative stress in the setting of the uremic milieu promotes enzymatic modification of circulating lipids and lipoproteins, protein carbamylation, endothelial dysfunction via disruption of nitric oxide (NO) pathways, and activation of inflammation, thus accelerating atherosclerosis. Left ventricular hypertrophy (LVH) and heart failure are hallmarks of CKD. NADPH oxidase activation, xanthine oxidase, mitochondrial dysfunction, and NO-ROS are the main oxidative pathways leading to LVH and the cardiorenal syndrome. Finally, a subset of antioxidant enzymes, the paraoxonases (PON), deserves special attention due to abundant clinical evidence accumulated regarding reduced serum PON1 activity in CKD as a contributor to the increased burden of cardiovascular disease. Future, meticulously designed studies are needed to assess the effects of antioxidant therapy on patients with CKD.

scholarly journals Most exposed: the endothelium in chronic kidney disease

2019 ◽  
Vol 35 (9) ◽  
pp. 1478-1487 ◽  
Author(s):  
Marc Vila Cuenca ◽  
Peter L Hordijk ◽  
Marc G Vervloet
Keyword(s):  
Risk Factors ◽  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Oxygen Species ◽  
Pathological Changes ◽  
Endothelial Lining ◽  
Traditional Risk Factors

Abstract Accumulating evidence indicates that the pathological changes of the endothelium may contribute to the development of cardiovascular complications in chronic kidney disease (CKD). Non-traditional risk factors related to CKD are associated with the incidence of cardiovascular disease, but their role in uraemic endothelial dysfunction has often been disregarded. In this context, soluble α-Klotho and vitamin D are of importance to maintain endothelial integrity, but their concentrations decline in CKD, thereby contributing to the dysfunction of the endothelial lining. These hormonal disturbances are accompanied by an increment of circulating fibroblast growth factor-23 and phosphate, both exacerbating endothelial toxicities. Furthermore, impaired renal function leads to an increment of inflammatory mediators, reactive oxygen species and uraemic toxins that further aggravate the endothelial abnormalities and in turn also inhibit the regeneration of disrupted endothelial lining. Here, we highlight the distinct endothelial alterations mediated by the abovementioned non-traditional risk factors as demonstrated in experimental studies and connect these to pathological changes in CKD patients, which are driven by endothelial disturbances, other than atherosclerosis. In addition, we describe therapeutic strategies that may promote restoration of endothelial abnormalities by modulating imbalanced mineral homoeostasis and attenuate the impact of uraemic retention molecules, inflammatory mediators and reactive oxygen species. A clinical perspective on endothelial dysfunction in CKD may translate into reduced structural and functional abnormalities of the vessel wall in CKD, and ultimately improved cardiovascular disease.

scholarly journals Uremic Toxins, Oxidative Stress, Atherosclerosis in Chronic Kidney Disease, and Kidney Transplantation

2021 ◽  
Vol 2021 ◽  
pp. 1-15 ◽  
Author(s):  
Ewa Wojtaszek ◽  
Urszula Oldakowska-Jedynak ◽  
Marlena Kwiatkowska ◽  
Tomasz Glogowski ◽  
Jolanta Malyszko
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Transplantation ◽  
Kidney Disease ◽  
Uremic Toxins ◽  
Transplant Recipients ◽  
Risk Of Death ◽  
The Impact

Patients with chronic kidney disease (CKD) are at a high risk for cardiovascular disease (CVD), and approximately half of all deaths among patients with CKD are a direct result of CVD. The premature cardiovascular disease extends from mild to moderate CKD stages, and the severity of CVD and the risk of death increase with a decline in kidney function. Successful kidney transplantation significantly decreases the risk of death relative to long-term dialysis treatment; nevertheless, the prevalence of CVD remains high and is responsible for approximately 20-35% of mortality in renal transplant recipients. The prevalence of traditional and nontraditional risk factors for CVD is higher in patients with CKD and transplant recipients compared with the general population; however, it can only partly explain the highly increased cardiovascular burden in CKD patients. Nontraditional risk factors, unique to CKD patients, include proteinuria, disturbed calcium, and phosphate metabolism, anemia, fluid overload, and accumulation of uremic toxins. This accumulation of uremic toxins is associated with systemic alterations including inflammation and oxidative stress which are considered crucial in CKD progression and CKD-related CVD. Kidney transplantation can mitigate the impact of some of these nontraditional factors, but they typically persist to some degree following transplantation. Taking into consideration the scarcity of data on uremic waste products, oxidative stress, and their relation to atherosclerosis in renal transplantation, in the review, we discussed the impact of uremic toxins on vascular dysfunction in CKD patients and kidney transplant recipients. Special attention was paid to the role of native and transplanted kidney function.

Cardiovascular Protection With Sodium-Glucose Cotransporter-2 Inhibitors and Mineralocorticoid Receptor Antagonists in Chronic Kidney Disease

Hypertension ◽  
2021 ◽  
Vol 77 (5) ◽  
pp. 1442-1455
Author(s):  
Pantelis Sarafidis ◽  
Christodoulos E. Papadopoulos ◽  
Vasilios Kamperidis ◽  
George Giannakoulas ◽  
Michael Doumas
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Mineralocorticoid Receptor ◽  
Mineralocorticoid Receptor Antagonists ◽  
Receptor Antagonists ◽  
Cardiovascular Protection ◽  
Sodium Glucose Cotransporter

Chronic kidney disease (CKD) and cardiovascular disease are intimately linked. They share major risk factors, including age, hypertension, and diabetes, and common pathogenetic mechanisms. Furthermore, reduced renal function and kidney injury documented with albuminuria are independent risk factors for cardiovascular events and mortality. In major renal outcome trials and subsequent meta-analyses in patients with CKD, ACE (angiotensin-converting enzyme) inhibitors and ARBs (angiotensin II receptor blockers) were shown to effectively retard CKD progression but not to significantly reduce cardiovascular events or mortality. Thus, a high residual risk for cardiovascular disease progression under standard-of-care treatment is still present for patients with CKD. In contrast to the above, several outcome trials with SGLT-2 (sodium-glucose cotransporter-2) inhibitors and MRAs (mineralocorticoid receptor antagonists) clearly suggest that these agents, apart from nephroprotection, offer important cardioprotection in this population. This article discusses existing evidence on the effects of SGLT-2 inhibitors and MRAs on cardiovascular outcomes in patients with CKD that open new roads in cardiovascular protection of this heavily burdened population.

scholarly journals SAT-LB96 Chronic Kidney Disease Incidence and Cardiorespiratory Fitness Association in Patients With Diabetes And/Or Hypertension

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Joseph Powell ◽  
Eric S Nylen ◽  
Jonathan Myers ◽  
Pamela Karasik ◽  
Hans Moore ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiorespiratory Fitness ◽  
Cox Regression ◽  
Disease Incidence ◽  
Metabolic Equivalents ◽  
Patients With Diabetes ◽  
Exercise Treadmill ◽  
Traditional Risk Factors

Abstract Introduction: Type 2 diabetes mellitus (T2DM) and hypertension (HTN) are considered strong risk factors for developing chronic kidney disease (CKD). Increased cardiorespiratory fitness (CRF) is associated with lower CKD risk. However, the CRF-CKD association in patients with T2DM and/or HTN has not been assessed.Methods: We identified 9,751 patients (age 58.6 + 10.1 years) with T2DM (N=1,444) or HTN (n=5,031) or both (n=3,276) prior to a maximal standardized exercise treadmill test (ETT) and no evidence of ischemia as indicated by the ETT. We established four CRF categories based on age-adjusted peak metabolic equivalents (METs) achieved: Least-Fit (4.6±1.2 METs; n=2,231); Low-Fit Fit (6.4±1.1 METs; n=2,693); Moderate-Fit (8.0±1.0 METs; n=2,432); and High-Fit (10.8±2.1 METs; n=2,395). We performed multivariable Cox Regression analyses to access the risk of CKD according to fitness. The models were adjusted for age, body mass index (BMI), traditional risk factors and medications. Results: During the median follow-up of 12.4 years, 1,118 patients developed CKD, accounting for 9.1 events/ 1,000 person-years of observation. The association between CRF and CKD was inverse and graded. The risk of CKD was 21% lower (Hazard Ratio [HR] 0.79; 95% confidence interval [CI] 0.77-0.81). When CRF categories were considered, the CKD risk was 44% lower for Moderate-Fit patients (HR 0.56; 95% CI 0.48-0.67) and 80% lower for High-Fit (HR 0.20; 95% CI 0.15-0.25). Similar findings were noted in patients with both T2DM and HTN. Conclusions: We noted an inverse and dose-response association between CRF and CKD incidence. The risk was attenuated significantly beyond a mean peak MET level of 8.0±1.0, suggesting that moderate increases in exercise capacity confers favorable health benefits in patients at high risk of developing CKD.

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.

Sign in / Sign up

Export Citation Format

Share Document