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Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 37912

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Dr. Natalia Di Pietro

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Guest Editor

Department of Medical, Oral and Biotechnological Sciences, University of Chieti-Pescara, Chieti, Italy
Interests: stem cells; biomedical engineering; molecules; extracellular matrix; tissue regeneration; biomaterials
Special Issues, Collections and Topics in MDPI journals

Dr. Mario Bonomini

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Co-Guest Editor

Nephrology and Dialysis Institute, Department of Medicine, G. d’Annunzio University, Chieti-Pescara, SS. Annunziata Hospital, Via dei Vestini, 66013 Chieti, Italy
Interests: chronic kidney disease; dialysis; proteomics; red blood cells; end-stage renal disease; uremic toxins; selenium; nutritional molecules
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

You are cordially invited to submit original research articles and reviews for a new Special Issue entitled "Antioxidants and their Role in the Prevention and Treatment of Chronic Kidney Disease."

Oxidative imbalance is widely recognized as a key component of the pathogenesis of chronic kidney disease (CKD). Indeed, it is recognized as a potential cause and consequence of reduced kidney function. Although increased oxidative stress (OS) is unlikely to be the main event of CKD, it is known as a non-traditional risk factor which, along with other modifiable risk factors (such as drug toxicity, urinary tract infections, autoimmune diseases, hyperuricemia, hypertension, dyslipidemia, diabetes, obesity, and inflammation), contributes to the progression of kidney damage.

For these reasons, trying to counteract the increase in reactive oxygen (ROS) and nitrogen (RNS) species using specific antioxidants represents a contemporary challenge.

In this regard, several recent in vitro (cells), ex vivo (tissues and specimens), in vivo (animals) and clinical studies have shown that the use of dietary antioxidants (the Mediterranean diet, polyphenols, curcumin, sulforaphane, quercetin, probiotics, etc.), antioxidant supplements (vitamins C, E, N-acetylcisteine, L-arginine, etc.) or their combination has potential protective effects for CKD and its main complications such as hypertension, atherosclerosis, inflammation, and anemia.

This Special Issue aims to provide a forum collection of the latest in vitro, in vivo, and clinical studies on antioxidants and their biological activities, with a view to a possible therapeutic application for CKD and its complications. Furthermore, as biomarkers of oxidative stress are critical for the development of novel treatments for CKD, studies on the discovery of novel oxidative stress biomarkers and other innovative biomarkers are also welcome.

Dr. Natalia Di Pietro
Prof. Mario Bonomini
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Antioxidants
Dietary antioxidants
Mediterranean diet
Chronic kidney disease
Dialysis
Diabetic kidney disease
Cardiovascular diseases
Hypertension
Inflammation
Oxidative stress
Biomarkers.

Related Special Issues

Antioxidants and their Role in the Prevention and Treatment of Chronic Kidney Disease-II in Antioxidants (6 articles)
Oxidative Stress in Kidney Disease in Antioxidants (17 articles)

Published Papers (11 papers)

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Research

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12 pages, 1739 KiB

Open AccessEditor’s ChoiceArticle

AGEs and sRAGE Variations at Different Timepoints in Patients with Chronic Kidney Disease

by Paolo Molinari, Lara Caldiroli, Elena Dozio, Roberta Rigolini, Paola Giubbilini, Massimiliano M. Corsi Romanelli, Piergiorgio Messa and Simone Vettoretti

Antioxidants 2021, 10(12), 1994; https://doi.org/10.3390/antiox10121994 - 15 Dec 2021

Cited by 10 | Viewed by 2474

Abstract

Patients with chronic kidney disease (CKD) are affected by enhanced oxidative stress and chronic inflammation, and these factors may contribute to increase advanced glycation end-products (AGEs). In this study we quantified AGEs and soluble receptors for AGE (sRAGE) isoforms and evaluated the association between their variations and eGFR at baseline and after 12 months. We evaluated 64 patients. AGEs were quantified by fluorescence intensity using a fluorescence spectrophotometer, and sRAGE by ELISA. Median age was 81 years, male patients accounted for 70%, 63% were diabetic, and eGFR was 27 ± 10 mL/min/1.73 m². At follow up, sRAGE isoforms underwent a significant decrement (1679 [1393;2038] vs. 1442 [1117;2102], p < 0.0001), while AGEs/sRAGE ratios were increased (1.77 ± 0.92 vs. 2.24 ± 1.34, p = 0.004). Although AGEs and AGEs/sRAGE ratios were inversely related with eGFR, their basal values as well their variations did not show a significant association with eGFR changes. In a cohort of patients with a stable clinical condition at 1 year follow-up, AGEs/sRAGE was associated with renal function. The lack of association with eGFR suggests that other factors can influence its increase. In conclusion, AGEs/sRAGE can be an additional risk factor for CKD progression over a longer time, but its role as a prognostic tool needs further investigation. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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14 pages, 2600 KiB

Open AccessArticle

Sesamol Ameliorates Renal Injury-Mediated Atherosclerosis via Inhibition of Oxidative Stress/IKKα/p53

by Jie-Sian Wang, Ping-Hsuan Tsai, Kuo-Feng Tseng, Fang-Yu Chen, Wen-Chin Yang and Ming-Yi Shen

Antioxidants 2021, 10(10), 1519; https://doi.org/10.3390/antiox10101519 - 24 Sep 2021

Cited by 12 | Viewed by 2584

Abstract

Patients with chronic kidney disease (CKD) are at an increased risk of premature death due to the development of cardiovascular disease (CVD) owing to atherosclerosis-mediated cardiovascular events. However, the mechanisms linking CKD and CVD are clear, and the current treatments for high-risk groups are limited. In this study, we aimed to examine the effects of sesamol, a natural compound extracted from sesame oil, on the development of atherosclerosis in a rodent CKD model, and reactive oxygen species-induced oxidative damage in an endothelial cell model. ApoE^–/– mice were subjected to 5/6 nephrectomy (5/6 Nx) and administered sesamol for 8 weeks. Compared with the sham group, the 5/6 Nx ApoE^–/– mice showed a significant increase in malondialdehyde levels and Oil Red O staining patterns, which significantly decreased following sesamol administration. Sesamol suppressed H₂O₂-induced expression of phospho-IKKα, p53, and caspase-3. Our results highlight the protective role of sesamol in renal injury-associated atherosclerosis and the pathological importance of oxidative stress burden in CKD–CVD interaction. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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16 pages, 2931 KiB

Open AccessArticle

Cytoprotective Effect of Liposomal Puerarin on High Glucose-Induced Injury in Rat Mesangial Cells

by Lassina Barro, Jui-Ting Hsiao, Chu-Yin Chen, Yu-Lung Chang and Ming-Fa Hsieh

Antioxidants 2021, 10(8), 1177; https://doi.org/10.3390/antiox10081177 - 24 Jul 2021

Cited by 6 | Viewed by 2344

Abstract

In diabetic patients, high glucose and high oxidative states activate gene expression of transforming growth factor beta (TGF-β) and further translocate Smad proteins into the nucleus of renal cells. This signal pathway is characterized as the onset of diabetic nephropathy. Puerarin is an active ingredient extracted from Pueraria lobata as an anti-hyperglycemic and anti-oxidative agent. However, the poor oral availability and aqueous solubility limit its pharmaceutical applications. The present paper reports the liposomal puerarin and its protective effect on high glucose-injured rat mesangial cells (RMCs). The purity of puerarin extracted from the root of plant Pueraria lobata was 83.4% as determined by the high-performance liquid chromatography (HPLC) method. The liposomal puerarin was fabricated by membrane hydration followed by ultrasound dispersion and membrane extrusion (pore size of 200 nm). The fabricated liposomes were examined for the loading efficiency and contents of puerarin, the particle characterizations, the radical scavenge and the protective effect in rat mesangial cells, respectively. When the liposomes were subjected to 20 times of membrane extrusion, the particle size of liposomal puerarin can be reduced to less than 200 nm. When liposomal puerarin in RMCs in high glucose concentration (33 mM) was administered, the over-expression of TGF-β and the nuclear translocation of Smad 2/3 proteins was both inhibited. Therefore, this study successfully prepared the liposomal puerarin and showed the cytoprotective effect in RMCs under high glucose condition. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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12 pages, 1339 KiB

Open AccessArticle

TCA Cycle and Fatty Acids Oxidation Reflect Early Cardiorenal Damage in Normoalbuminuric Subjects with Controlled Hypertension

by Aranzazu Santiago-Hernandez, Marta Martin-Lorenzo, Ariadna Martin-Blazquez, Gema Ruiz-Hurtado, Maria G Barderas, Julian Segura, Luis M Ruilope and Gloria Alvarez-Llamas

Antioxidants 2021, 10(7), 1100; https://doi.org/10.3390/antiox10071100 - 09 Jul 2021

Cited by 7 | Viewed by 2357

Abstract

Moderately increased albuminuria, defined by an albumin to creatinine ratio (ACR) > 30 mg/g, is an indicator of subclinical organ damage associated with a higher risk of cardiovascular and renal disease. Normoalbuminuric subjects are considered at no cardiorenal risk in clinical practice, and molecular changes underlying early development are unclear. To decipher subjacent mechanisms, we stratified the normoalbuminuria condition. A total of 37 hypertensive patients under chronic renin–angiotensin system (RAS) suppression with ACR values in the normoalbuminuria range were included and classified as control (C) (ACR < 10 mg/g) and high-normal (HN) (ACR = 10–30 mg/g). Target metabolomic analysis was carried out by liquid chromatography and mass spectrometry to investigate the role of the cardiorenal risk urinary metabolites previously identified. Besides this, urinary free fatty acids (FFAs), fatty acid binding protein 1 (FABP1) and nephrin were analyzed by colorimetric and ELISA assays. A Mann–Whitney test was applied, ROC curves were calculated and Spearman correlation analysis was carried out. Nine metabolites showed significantly altered abundance in HN versus C, and urinary FFAs and FABP1 increased in HN group, pointing to dysregulation in the tricarboxylic acid cycle (TCA) cycle and fatty acids β-oxidation. We showed here how cardiorenal metabolites associate with albuminuria, already in the normoalbuminuric range, evidencing early renal damage at a tubular level and suggesting increased β-oxidation to potentially counteract fatty acids overload in the HN range. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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18 pages, 8743 KiB

Open AccessArticle

Protective Effect of Curcumin against Sodium Salicylate-Induced Oxidative Kidney Damage, Nuclear Factor-Kappa Dysregulation, and Apoptotic Consequences in Rats

by Yasmina M. Abd-Elhakim, Attia A. A. Moselhy, Adil Aldhahrani, Rasha R. Beheiry, Wafaa A. M. Mohamed, Mohamed Mohamed Soliman, Bayan A. Saffaf and Maha M. El Deib

Antioxidants 2021, 10(6), 826; https://doi.org/10.3390/antiox10060826 - 21 May 2021

Cited by 13 | Viewed by 2896

Abstract

This study examined the effect of sodium salicylates (SS), alone and in combination with curcumin (CUR), on kidney function and architecture in rats. Five rat groups were given 1 mL physiological saline/rat orally, 1 mL olive oil/rat orally, 50 mg CUR/kg bwt orally, 300 mg SS/kg bwt intraperitoneally, or CUR+SS for 15 days. The hematological indices, serum protein profile, serum electrolytes balance, oxidative stress, and lipid peroxidation of kidney tissues were assessed. The histopathological examination and immune expression of Caspase-3 and nuclear factor kappa (NF-κB) were conducted. The findings showed that SS injection induced nephrotoxic activity, including increased serum urea, creatinine, and uric acid levels. It also caused apparent pathological alterations with increased Caspase-3 and NF-κB immuno-expression. In addition, thrombocytopenia, leukocytosis, neutrophilia, hyponatremia, hypochloremia, hypocalcemia, and hypomagnesemia but not hyperkalemia and hyperphosphatemia were evident in SS-injected rats. Moreover, SS exposure increased serum α1 globulin, renal tissue malondialdehyde, and Caspase-3 levels but superoxide dismutase, glutathione peroxidase, and Bcl-2 levels declined. Meanwhile, CUR significantly counteracted the SS harmful impacts on kidneys but SS+CUR co-administration induced an anemic condition. Overall, CUR has an evident protective role against SS-induced renal damage, but the disturbed hematological alterations should be carefully taken into consideration in their combined use. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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13 pages, 1034 KiB

Open AccessArticle

Plasma Vitamin C and Risk of Late Graft Failure in Kidney Transplant Recipients: Results of the TransplantLines Biobank and Cohort Study

by Camilo G. Sotomayor, Nicolas I. Bustos, Manuela Yepes-Calderon, Diego Arauna, Martin H. de Borst, Stefan P. Berger, Ramón Rodrigo, Robin P. F. Dullaart, Gerjan J. Navis and Stephan J. L. Bakker

Antioxidants 2021, 10(5), 631; https://doi.org/10.3390/antiox10050631 - 21 Apr 2021

Cited by 2 | Viewed by 2855

Abstract

Recent studies have shown that depletion of vitamin C is frequent in outpatient kidney transplant recipients (KTR) and that vitamin C is inversely associated with risk of death. Whether plasma vitamin C is associated with death-censored kidney graft failure remains unknown. We investigated KTR who participated in the TransplantLines Insulin Resistance and Inflammation Biobank and Cohort Study. The primary outcome was graft failure (restart of dialysis or re-transplantation). Overall and stratified (p_interaction < 0.1) multivariable-adjusted Cox regression analyses are presented here. Among 598 KTR (age 51 ± 12 years-old; 55% males), baseline median (IQR) plasma vitamin C was 44.0 (31.0–55.3) µmol/L. Through a median follow-up of 9.5 (IQR, 6.3‒10.2) years, 75 KTR developed graft failure (34, 26, and 15 events over increasing tertiles of vitamin C, log-rank p < 0.001). Plasma vitamin C was inversely associated with risk of graft failure (HR per 1–SD increment, 0.69; 95% CI 0.54–0.89; p = 0.004), particularly among KTR with triglycerides ≥1.9 mmol/L (HR 0.46; 95% CI 0.30–0.70; p < 0.001; p_interaction = 0.01) and among KTR with HDL cholesterol ≥0.91 mmol/L (HR 0.56; 95% CI 0.38–0.84; p = 0.01; p_interaction = 0.04). These findings remained materially unchanged in multivariable-adjusted analyses (donor, recipient, and transplant characteristics, including estimated glomerular filtration rate and proteinuria), were consistent in categorical analyses according to tertiles of plasma vitamin C, and robust after exclusion of outliers. Plasma vitamin C in outpatient KTR is inversely associated with risk of late graft failure. Whether plasma vitamin C‒targeted therapeutic strategies represent novel opportunities to ease important burden of graft failure necessitates further studies. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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18 pages, 1401 KiB

Open AccessArticle

The Role of Oxidative Stress Markers in Predicting Acute Thrombotic Occlusion of Haemodialysis Vascular Access and Progressive Stenotic Dysfunction Demanding Angioplasty

by Jenq-Shyong Chan, Po-Jen Hsiao, Wen-Fang Chiang and Prabir Roy-Chaudhury

Antioxidants 2021, 10(4), 569; https://doi.org/10.3390/antiox10040569 - 08 Apr 2021

Cited by 5 | Viewed by 2183

Abstract

Haemodialysis vascular access (VA) dysfunction is a major cause of morbidity in haemodialysis (HD) patients. Primary venous outflow occlusion and restenosis after percutaneous transluminal angioplasty (PTA) are two major obstacles for the long-term use of dialysis VA. It remains unclear whether oxidative stress markers can be used as predictors for thrombotic occlusion of VA and progressive stenosis dysfunction demanding PTA. All routine HD patients at one teaching hospital participated in this study including ankle-brachial index (ABI) examinations and serum oxidative stress markers. The serum oxidative stress markers (high-sensitivity C-reactive protein (hs-CRP), matrix metalloproteinase-2 (MMP-2), MMP-9, homocysteine, asymmetrical dimethylarginine (ADMA), nitrate oxidase (NO), tumour necrosis factor-α (TNF-α), monocyte chemotactic protein 1 (MCP-1), interleukin-1β (IL-1β), and transforming growth factor-β (TGF-β)) were measured using immunosorbent assays in 159 HD patients (83 men and 76 women; mean age: 65 ± 12 years). The participants met the following criteria: (1) received regular HD treatment for at least 6 months, without clinical evidence of acute or chronic inflammation, recent myocardial infarction, unstable angina or circulatory congestion; and (2) received an arteriovenous fistula (AVF)/arteriovenous graft (AVG: polytetrafluoroethylene, PTFE) as the current VA for more than 6 months, without interventions within the last 6 months. All the participants were followed up clinically for up to 12 months to estimate the amount of primary thrombotic occlusion and VA dysfunction demanding PTA. During the 12-month observation, 24 patients (15.1%) had primary thrombotic occlusion of VAs. Another 24 patients (15.1%) required PTA because of clinical dysfunction of access. Additionally, during the follow-up period, restenosis occurred in 12 patients (50% of 24 patients). The access types of arteriovenous grafts (AVGs) and a diagnosis of peripheral arterial occlusive disease (PAOD) were two strong predictors for acute thrombotic events of VA (hazard ratio (HR): 16.93 vs. 2.35; p < 0.001 vs. 0.047). Comparing dysfunctional with non-dysfunctional VAs, up to 27.7% of patients with high levels of ADMA (>0.6207 μM, N = 65) received required PTA compared with 4.4% of those with low levels (≤0.6207 μM; N = 90; p < 0.001). In multivariate analysis, the plasma baseline levels of ADMA independently conferred nearly 4.55 times the risk of primary stenotic dysfunction of HD VA (HR: 4.55; 95% confidence interval: 1.20 to 17.26; p = 0.026). In conclusion, our findings suggest the role of ADMA in the development of symptomatic VA dysfunction. Additionally, PAOD severity can be used in clinical practice to predict whether acute thrombotic occlusion of VA will easily occur in HD patients. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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15 pages, 25079 KiB

Open AccessArticle

NQO1 Deficiency Aggravates Renal Injury by Dysregulating Vps34/ATG14L Complex during Autophagy Initiation in Diabetic Nephropathy

by Geum-Lan Hong, Kyung-Hyun Kim, Chul-Ho Lee, Tae-Won Kim and Ju-Young Jung

Antioxidants 2021, 10(2), 333; https://doi.org/10.3390/antiox10020333 - 23 Feb 2021

Cited by 9 | Viewed by 2694

Abstract

Diabetic nephropathy (DN) is one of the causes of end-stage renal failure, featuring renal fibrosis. However, autophagy, a vital process for intracellular homeostasis, can counteract renal fibrosis. Moreover, NAD(P)H: quinone dehydrogenase 1 (NQO1) modulates the ratios of reduced/oxidized nicotinamide nucleotides, exerting a cytoprotective function. Here, to examine the role of NQO1 genes in DN progression, the levels of autophagy-related proteins and pro-fibrotic markers were assessed in silencing or overexpression of NQO1 in human proximal tubular cells (HK2), and C57BL/6 (wild-type) and Nqo1 knockout (KO) mice injected to streptozotocin (50 mg/kg). NQO1 deficiency impaired the autophagy process by suppressing basal expression of ClassⅢ PI 3-kinase (Vps34) and autophagy-related (ATG)14L and inducing the expressions of transforming growth factor beta (TGF-β1), Smad3, and matrix metallopeptidase9 (MMP9) in high-glucose (HG) -treated HK2 cells. Meanwhile, NQO1 overexpression increased the expression of Vps34 and ATG14L, while, reducing TGF-β1, Smad3 and MMP9 expression. In vivo, the expression of Vps34 and ATG14L were suppressed in Nqo1 KO mice indicating aggravated glomerular changes and interstitial fibrosis. Therefore, NQO1 deficiency dysregulated autophagy initiation in HK2 cells, with consequent worsened renal cell damage under HG condition. Moreover, STZ-treated Nqo1 KO mice showed that NQO1 deficiency aggravated renal fibrosis by dysregulating autophagy. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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Review

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19 pages, 1116 KiB

Open AccessReview

Vitamin E (Alpha-Tocopherol) Metabolism and Nutrition in Chronic Kidney Disease

by Francesco Galli, Mario Bonomini, Desirée Bartolini, Linda Zatini, Gianpaolo Reboldi, Giada Marcantonini, Giorgio Gentile, Vittorio Sirolli and Natalia Di Pietro

Antioxidants 2022, 11(5), 989; https://doi.org/10.3390/antiox11050989 - 18 May 2022

Cited by 26 | Viewed by 10142

Abstract

Vitamin E (alpha-tocopherol) is an essential micronutrient and fat-soluble antioxidant with proposed role in protecting tissues from uncontrolled lipid peroxidation. This vitamin has also important protein function and gene modulation effects. The metabolism of vitamin E depends on hepatic binding proteins that selectively retain food alpha-tocopherol for incorporation into nascent VLDL and tissue distribution together with esterified cholesterol and triglycerides. Chronic kidney disease (CKD) is a condition of oxidative stress and increased lipid peroxidation, that are associated with alterations of alpha-tocopherol metabolism and function. Specific changes have been reported for the levels of its enzymatic metabolites, including both short-chain and long-chain metabolites, the latter being endowed with regulatory functions on enzymatic and gene expression processes important for the metabolism of lipids and xenobiotics detoxification, as well as for the control of immune and inflammatory processes. Vitamin E therapy has been investigated in CKD using both oral vitamin E protocols and vitamin E-coated hemodialyzers, showing promising results in the secondary prevention of cardiovascular disease, as well as of immune and hematological complications. These therapeutic approaches are reviewed in the present article, together with a narrative excursus on the main findings indicating CKD as a condition of relative deficiency and impaired metabolism of vitamin E. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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33 pages, 3686 KiB

Open AccessReview

Molecular Mechanistic Pathways Targeted by Natural Antioxidants in the Prevention and Treatment of Chronic Kidney Disease

by Mohamed Mohany, Mohammed M. Ahmed and Salim S. Al-Rejaie

Antioxidants 2022, 11(1), 15; https://doi.org/10.3390/antiox11010015 - 22 Dec 2021

Cited by 13 | Viewed by 4103

Abstract

Chronic kidney disease (CKD) is the progressive loss of renal function and the leading cause of end-stage renal disease (ESRD). Despite optimal therapy, many patients progress to ESRD and require dialysis or transplantation. The pathogenesis of CKD involves inflammation, kidney fibrosis, and blunted renal cellular antioxidant capacity. In this review, we have focused on in vitro and in vivo experimental and clinical studies undertaken to investigate the mechanistic pathways by which these compounds exert their effects against the progression of CKD, particularly diabetic nephropathy and kidney fibrosis. The accumulated and collected data from preclinical and clinical studies revealed that these plants/bioactive compounds could activate autophagy, increase mitochondrial bioenergetics and prevent mitochondrial dysfunction, act as modulators of signaling pathways involved in inflammation, oxidative stress, and renal fibrosis. The main pathways targeted by these compounds include the canonical nuclear factor kappa B (NF-κB), canonical transforming growth factor-beta (TGF-β), autophagy, and Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor erythroid factor 2-related factor 2 (Nrf2)/antioxidant response element (ARE). This review presented an updated overview of the potential benefits of these antioxidants and new strategies to treat or reduce CKD progression, although the limitations related to the traditional formulation, lack of standardization, side effects, and safety. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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15 pages, 1843 KiB

Open AccessReview

Are Antioxidants Useful in Preventing the Progression of Chronic Kidney Disease?

by Alfredo G. Casanova, Francisco J. López-Hernández, Laura Vicente-Vicente and Ana I. Morales

Antioxidants 2021, 10(11), 1669; https://doi.org/10.3390/antiox10111669 - 23 Oct 2021

Cited by 8 | Viewed by 1960

Abstract

Chronic kidney disease (CKD) is a progressive impairment of renal function for more than three months that affects 15% of the adult population. Because oxidative stress is involved in its pathogenesis, antioxidants are under study for the prophylaxis of CKD progression. The objective of this work was to meta-analyze the efficacy of antioxidant therapy in CKD patients and to identify the most effective candidate antioxidants. Our meta-analysis showed that, despite being quite heterogeneous, overall antioxidant therapy apparently reduced CKD progression. Pentoxifylline and bardoxolone methyl demonstrated a robust and statistically significant protection, while other products showed a favorable but non-significant tendency, due to a high interindividual variability. Off-target (i.e., antioxidant-independent) effects, such as body weight reduction and heart failure-associated blood dilution, might totally or partially explain the protection provided by effective antioxidants. This potential pleiotropy introduces uncertainty on the role of oxidative stress in CKD progression and on antioxidant therapy in its prevention, which needs to be further investigated. Independently, identification of factors determining the nephroprotective effect of each candidate on each patient is thus necessary for a prospectively personalized antioxidant therapy. Finally, pentoxifylline should be further explored for the prophylaxis of CKD progression. Full article

(This article belongs to the Special Issue Antioxidants and Their Role in the Prevention and Treatment of Chronic Kidney Disease)

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