scholarly journals Chronic Kidney Disease as Oxidative Stress- and Inflammatory-Mediated Cardiovascular Disease

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 752 ◽  
Author(s):  
Alina Podkowińska ◽  
Dorota Formanowicz
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Dysfunction ◽  
Acid Base ◽  
Excretory Function ◽  
Activation Of Transcription ◽  
Metabolic Products

Generating reactive oxygen species (ROS) is necessary for both physiology and pathology. An imbalance between endogenous oxidants and antioxidants causes oxidative stress, contributing to vascular dysfunction. The ROS-induced activation of transcription factors and proinflammatory genes increases inflammation. This phenomenon is of crucial importance in patients with chronic kidney disease (CKD), because atherosclerosis is one of the critical factors of their cardiovascular disease (CVD) and increased mortality. The effect of ROS disrupts the excretory function of each section of the nephron. It prevents the maintenance of intra-systemic homeostasis and leads to the accumulation of metabolic products. Renal regulatory mechanisms, such as tubular glomerular feedback, myogenic reflex in the supplying arteriole, and the renin–angiotensin–aldosterone system, are also affected. It makes it impossible for the kidney to compensate for water–electrolyte and acid–base disturbances, which progress further in the mechanism of positive feedback, leading to a further intensification of oxidative stress. As a result, the progression of CKD is observed, with a spectrum of complications such as malnutrition, calcium phosphate abnormalities, atherosclerosis, and anemia. This review aimed to show the role of oxidative stress and inflammation in renal impairment, with a particular emphasis on its influence on the most common disturbances that accompany CKD.

The role of nitric oxide signaling in renoprotective effects of hydrogen sulfide against chronic kidney disease in rats: Involvement of oxidative stress, autophagy and apoptosis

2018 ◽  
Vol 234 (7) ◽  
pp. 11411-11423 ◽  
Author(s):  
Mohammad Khabbaz Shirazi ◽  
Asaad Azarnezhad ◽  
Mohammad Foad Abazari ◽  
Mansour Poorebrahim ◽  
Pegah Ghoraeian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Hydrogen Sulfide ◽  
Kidney Disease ◽  
Nitric Oxide Signaling

scholarly journals New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 529 ◽  
Author(s):  
Hénaut ◽  
Candellier ◽  
Boudot ◽  
Grissi ◽  
Mentaverri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cellular Interactions ◽  
Valvular Interstitial Cells ◽  
Macrophage Subset ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines ◽  
Valvular Cells

Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.

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.

Role of matrix metalloproteinase-9 in chronic kidney disease: a new biomarker of resistant albuminuria

2016 ◽  
Vol 130 (7) ◽  
pp. 525-538 ◽  
Author(s):  
Helena Pulido-Olmo ◽  
Concha F. García-Prieto ◽  
Gloria Álvarez-Llamas ◽  
María G. Barderas ◽  
Fernando Vivanco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Metalloproteinase 9

Resistant albuminuria developed under chronic RAS blockade is strongly associated with increased circulating MMP-9 activity mediated by oxidative stress.

scholarly journals Vascular dysfunction and atherosclerosis in chronic kidney disease; A distinct entity

2019 ◽  
Vol 8 (2) ◽  
pp. 17-17 ◽  
Author(s):  
Eranga Harshani Silva ◽  
Chandima Madhu Wickramatilake ◽  
Sarath Lekamwasam ◽  
Lakmini Kumari Boralugoda Mudduwa ◽  
Ranjuka Arushana Ubayasiri
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Dysfunction ◽  
Therapeutic Interventions ◽  
Cvd Risk ◽  
Unexplored Area ◽  
Calcium And Phosphate Metabolism ◽  
Conventional Risk Factors

Cardiovascular disease (CVD) is prevalent among patients with chronic kidney disease (CKD) and its occurrence and severity cannot be fully defined by the conventional cardiovascular risk factors namely age, hypertension, dyslipidaemia, diabetes mellitus and obesity. Contemporary studies have examined the role of non-conventional risk factors such as anemia, hyperhomocysteinemia, calcium and phosphate metabolism, vascular stiffness due to endothelial dysfunction ( ED), oxidative injury, and inflammation in the causation of CVD in CKD. Therapeutic interventions used in non-CKD patients are found to be less effective on patients with CKD. The purpose of this review was to gather available evidence on the CVD risk among CKD patients. Numerous mechanisms have been postulated to describe the increased atherogenicity in CKD patients. We discuss these mechanisms especially arterial stiffness, ED and inflammation in detail. In conclusion, CVD in CKD is still an unexplored area which needs further studies to uncover the possible mechanisms. Identifying newer therapies to improve health among this group of patients is of paramount importance.

scholarly journals The role of metabolic acidosis in chronic kidney diseases

2010 ◽  
Vol 4 (3) ◽  
pp. 367-372
Author(s):  
James C. M. Chan
Keyword(s):  
Chronic Kidney Disease ◽  
Metabolic Acidosis ◽  
Kidney Disease ◽  
Kidney Diseases ◽  
Original Research ◽  
Due Diligence ◽  
Acid Base ◽  
Chronic Kidney Diseases ◽  
Balance Development

Abstract Background and objectives: This review focuses on three areas, basic acid-base physiology especially concerning hydrogen ion balance, development of acidosis in chronic kidney disease (CKD), and the consequences of acidosis. We highlight what is well established, what is less certain, and what is unknown. Method and results: The literature on acidosis in CKD were searched from 2004 to 2010 utilizing PubMed, Google Scholar, and Ovid to augment the classic work on acid base physiology over the past three decades. The original research in endogenous acid production and net acid excretion were reviewed. Touching upon the development of metabolic acidosis in CKD, we focused on the consequences of chronic metabolic acidosis on growth and other important variables. Finally, we recognize the significant issue of patients’ medical non-compliance and presented treatment strategy to counter this problem. Conclusion: The correction of acidosis in chronic kidney disease needs no advocacy. The case is made conclusively. Patient non-compliance because of the medication that needs to be taken several times a day is a problem, requiring due diligence.

The role of oxidative stress in the development of protein-energy wasting and sarcopenia in patients with stage 5D chronic kidney disease

Nephrology ◽  
2021 ◽  
Vol 2_2021 ◽  
pp. 41-46
Author(s):  
M.Z. Gasanov Gasanov ◽  
V.M. Negoda Negoda ◽  
M.M. Batyushin Batyushin ◽  
◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Protein Energy Wasting ◽  
Protein Energy
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