Oxidative Stress in Hemodialysis Patients: A Review of the Literature

Liakopoulos, Vassilios; Roumeliotis, Stefanos; Gorny, Xenia; Dounousi, Evangelia; Mertens, Peter R.

doi:10.1155/2017/3081856

Cited by 212 publications

(255 citation statements)

References 210 publications

(222 reference statements)

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“…Oxidative stress represents the imbalance between antioxidant systems and oxidative products [20]. Phosphate up-regulates the expression of NOX4 and CYBA , two critical components of the superoxide-generating NADH/NADPH oxidase system [48, 49] and reduces total antioxidant capacity of VSMCs.…”

Section: Discussionmentioning

confidence: 99%

“…Excessive oxidative stress is involved in the pathogenesis of vascular calcification [20, 28-30]. Reactive oxygen species are mediators of CKD-related vascular calcification [48, 50].…”

Section: Discussionmentioning

confidence: 99%

“…In these patients, oxidative stress is further associated with increased cardiovascular and all-cause mortality [18-20] and thus, Fibulin-3 may have overall protective effects in systemic changes during disease progression. However, Fibulin-3 may promote neoplastic growth in some tumors [69, 70].…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress is commonly associated with cardiovascular disease [18, 19] and all-cause mortality in patients with chronic kidney disease (CKD) [20]. The high cardiovascular morbidity and mortality of CKD patients is associated with medial vascular calcification [21].…”

Section: Introductionmentioning

confidence: 99%

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Fibulin-3 Attenuates Phosphate-Induced Vascular Smooth Muscle Cell Calcification by Inhibition of Oxidative Stress

Luong

Schelski

Boehme

et al. 2018

Cell Physiol Biochem

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Background/Aims: Fibulin-3, an extracellular matrix glycoprotein, inhibits vascular oxidative stress and remodeling in hypertension. Oxidative stress is prevalent in chronic kidney disease (CKD) patients and is an important mediator of osteo-/chondrogenic transdifferentiation and calcification of vascular smooth muscle cells (VSMCs) during hyperphosphatemia. Therefore, the present study explored the effects of Fibulin-3 on phosphate-induced vascular calcification. Methods: Experiments were performed in primary human aortic smooth muscle cells (HAoSMCs) treated with control or with phosphate without or with additional treatment with recombinant human Fibulin-3 protein or with hydrogen peroxide as an exogenous source of oxidative stress. Results: Treatment with calcification medium significantly increased calcium deposition in HAoSMCs, an effect significantly blunted by additional treatment with Fibulin-3. Moreover, phosphate-induced alkaline phosphatase activity and mRNA expression of osteogenic and chondrogenic markers MSX2, CBFA1, SOX9 and ALPL were all significantly reduced by addition of Fibulin-3. These effects were paralleled by similar regulation of oxidative stress in HAoSMCs. Phosphate treatment significantly up-regulated mRNA expression of the oxidative stress markers NOX4 and CYBA, down-regulated total antioxidant capacity and increased the expression of downstream effectors of oxidative stress PAI-1, MMP2 and MMP9 as well as BAX/BLC2 ratio in HAoSMCs, all effects blocked by additional treatment with Fibulin-3. Furthermore, the protective effects of Fibulin-3 on phosphate-induced osteogenic and chondrogenic markers expression in HAoSMCs were reversed by additional treatment with hydrogen peroxide. Conclusions: Fibulin-3 attenuates phosphate-induced osteo-/ chondrogenic transdifferentiation and calcification of VSMCs, effects involving inhibition of oxidative stress. Up-regulation or supplementation of Fibulin-3 may be beneficial in reducing the progression of vascular calcification during hyperphosphatemic conditions such as CKD.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Excessive oxidative stress is involved in the pathogenesis of vascular calcification [20, 28-30]. Reactive oxygen species are mediators of CKD-related vascular calcification [48, 50].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Fibulin-3 Attenuates Phosphate-Induced Vascular Smooth Muscle Cell Calcification by Inhibition of Oxidative Stress

Luong

Schelski

Boehme

et al. 2018

Cell Physiol Biochem

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“…The activation of the AT1 receptor by angiotensin II leads to the increase of superoxide production [23][24][25]. On the other hand, CaSR expression has been documented in the juxtaglomerular cells, and its activation has been shown to decrease the renin release and thus decrease of plasma renin activity [26][27][28].…”

Section: Discussionmentioning

confidence: 99%

Treatment Based on Cinacalcet Reduces Oxidative Stress in Hemodialysis Patients with Secondary Hyperparathyroidism

Kuczera

Adamczak

Machnik³

et al. 2018

Nephron

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Background/Aims: Oxidative stress is one of the leading factors contributing to increased mortality in patients with chronic kidney disease (CKD) and secondary hyperparathyroidism (sHPT). Cinacalcet is now commonly used in the treatment of sHPT in patients with CKD. The aim of this study was to assess the influence of treatment with cinacalcet on the oxidative stress markers in patients on hemodialysis with sHPT. Methods: In 58 hemodialysed patients with sHPT (parathyroid hormone [PTH] > 300 pg/mL) plasma Advanced Oxidation Protein Products (AOPP), serum total antioxidant capacity – ImAnOx (TAS/TAC), serum PTH, calcium and phosphate concentrations were assessed before the first dose of cinacalcet and after 6 months of treatment. Results: Serum PTH concentration decreased significantly from 895 (748–1,070) to 384 (289–510) pg/mL after 6 months of treatment; p < 0.0001. Mean serum concentrations of calcium and phosphate remained stable. Plasma AOPP concentration decreased significantly from 152 (126–185) to 49 (43–57) µmol/L after 6 months of treatment; p < 0.0001. ImAnOx significantly increased from 260 (251–270) to 272 (264–280) µmol/L; p = 0.04. After 6 months of treatment, a significant, positive correlation was found between ImAnOx and the daily dose of cinacalcet (r = 0.30; p = 0.02). Also, the change of serum ImAnOx during treatment with cinacalcet significantly correlated with the daily dose of cinacalcet r = 0.35; p = 0.01. No significant correlations were found between plasma AOPP concentration or ImAnOx and PTH, or their changes in time. Conclusions: (1) Six-month treatment based on cinacalcet seems to reduce oxidative stress markers in maintenance hemodialysis patients with sHPT. (2) This benefit may be related rather to the direct action of cinacalcet than to the serum PTH concentration decrease.

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Effects of mussel‐inspired co‐deposition of 2‐hydroxymethyl methacrylate and poly (2‐methoxyethyl acrylate) on the hydrophilicity and binding tendency of common hemodialysis membranes: Molecular dynamics simulations and molecular docking studies

2021

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Despite advances in the field, hemoincompatibility remains a critical issue for hemodialysis (HD) as interactions between various human blood constituents and the polymeric structure of HD membranes results in complications such as activation of immune system cascades. Adding hydrophilic polymer structures to the membranes is one modification approach that can decrease the extent of protein adsorption. This study conducted molecular dynamics (MD) simulations to understand the interactions between three human serum proteins (fibrinogen [FB], human serum albumin, and transferrin) and common HD membranes in untreated and modified forms. Poly(aryl ether sulfone) (PAES) and cellulose triacetate were used as the common dialyzer polymers, and membrane modifications were performed with 2-hydroxymethyl methacrylate (HEMA) and poly (2-methoxyethyl acrylate) (PMEA), using polydopamine-assisted co-deposition. The MD simulations were used as the framework for binding energy simulations, and molecular docking simulations were also performed to conduct molecular-level investigations between the two modifying polymers (HEMA and PMEA) and FB. Each of the three proteins acted differently with the membranes due to their unique nature and surface chemistry. The simulations show PMEA binds less intensively to FB with a higher number of hydrogen bonds, which reflects PMEA's superior performance compared to HEMA. The simulations suggest PAES membranes could be used in modified forms for blood-contact applications as they reflect the lowest binding energy to blood proteins.

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Oxidative Stress in Hemodialysis Patients: A Review of the Literature

Cited by 212 publications

References 210 publications

Fibulin-3 Attenuates Phosphate-Induced Vascular Smooth Muscle Cell Calcification by Inhibition of Oxidative Stress

Fibulin-3 Attenuates Phosphate-Induced Vascular Smooth Muscle Cell Calcification by Inhibition of Oxidative Stress

Treatment Based on Cinacalcet Reduces Oxidative Stress in Hemodialysis Patients with Secondary Hyperparathyroidism

Effects of mussel‐inspired co‐deposition of 2‐hydroxymethyl methacrylate and poly (2‐methoxyethyl acrylate) on the hydrophilicity and binding tendency of common hemodialysis membranes: Molecular dynamics simulations and molecular docking studies

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