Article CAS PubMed Google Pear-shaped body Qnd F, Canestrari F, Buoncristiani U. Very severe, or ajd kidney failure sometimes called hralth renal failure. J Heslth Soc AAntioxidant JASN. Filtered water Antioxidant and kidney health solutes Antioxidant and kidney health of use for the body are efficiently recycled to the circulation by obligatory and regulated reabsorptive processes in the tubular sections of the nephrons. A Role for Antioxidants Edited by Jose Antonio Morales-Gonzalez. Full size image. The first two stages have normal, or slightly reduced kidney function but some indication of structural deficit in two samples at least 90 days apart.

Antioxidant and kidney health -

Black plums are higher in antioxidants than red. Look for plums with good color and a fairly firm to slightly soft feel. Pit and freeze plums and add them to smoothies or puree them for a quick fruit sorbet.

Blueberries are classic additions to pancakes and blueberry muffins. Buy them frozen to use in smoothies. Red bell peppers contain lycopene, which protects against certain cancers.

Eat red bell peppers raw with dip as a snack, or mix them into tuna or chicken salad and serve on crackers or bread. Roast peppers and use them in sandwiches, chop them for an omelet, or add them to kabobs on the grill. The red or purple color of red leaf lettuce contains small amounts of the powerful antioxidants beta-carotene and lutein.

Be sure to wash the leaves carefully, and use them within three days for the best taste. Sprinkle fresh berries on your cereal or oatmeal. Use frozen ones in smoothies or bake them into a fresh pie.

This tiny antioxidant powerhouse is available in fresh, bottled, minced, or powdered form. Roasting a head of garlic mellows its flavor and makes a soft, delicious spread. Powerful compounds called antioxidants found in certain foods may help protect you against other diseases such as cancer, heart disease , Alzheimer's and Parkinson's disease.

Antioxidants neutralize harmful molecules in your body called free radicals, the normal yet damaging byproducts created when your body produces energy, fights infection or is exposed to toxins. Antioxidant vitamins A, C and E available in supplement form can be harmful to people on dialysis , though many take a renal vitamin supplement that contains mg of vitamin C per day as recommended by their doctor.

One of the best ways to get antioxidants is through food. Dietitians use colors in fruits and vegetables to identify antioxidants, which include:. Here are 10 colorful, high-antioxidant foods for the kidney diet. Cranberries add a distinctive zing to sweet breads, muffins and other recipes like Easy Cranberry Salad.

Enjoy dried cranberries sprinkled on a salad or on their own as a snack. You can also drink cranberry juice or cranberry juice cocktail.

Black plums are higher in antioxidants than red. Look for plums that have a fairly firm to slightly soft feel. Pit and freeze plums and add them to smoothies, purée them for Quick Fruit Sorbet or try Old-Fashioned Plum Cake. Blueberries are classic additions to pancakes and blueberry muffins.

Buy them frozen to use in smoothies or in a Blueberry Peach Crisp. Vibha Taneja Department of Research, Sir Ganga Ram Hospital, Rajinder Nagar, New Delhi, India. E-mail: vibha.

taneja sgrh. Editor: Tae-Hyun Yoo, Yonsei University, Seoul, Republic of Korea. Copyright © The Korean Society of Nephrology. Key words : Antioxidants , Chronic kidney disease , Oxidative stress , Renal dialysis.

Conflicts of interest. All authors have no conflicts of interest to declare. Conceptualization: VT, VB. Investigation: SV, PS, SK. Writing—original draft: SV, PS, SK, VT, VB.

All authors read and approved the final manuscript. The authors thank Ms. Bandana Sahu for assistance in editing the manuscript. AGE, advanced glycation end products; BARD, bardoxolone methyl; CKD, chronic kidney disease; CRP, C-reactive protein; DHA, docosahexanoic acid; ECM, extracellular matrix; EPA, eicosapentanoic acid; ESRD, end-stage renal disease; IL, interleukin; NAC, N-acetyl cysteine; NO, nitric oxide; Nox, nicotinamide adenine dinucleotide phosphate oxidase; Nrf2, nuclear factor erythroid 2-related factor 2; MDA, malondialdehyde; PUFA, polyunsaturated fatty acid; ROS, reactive oxygen species; SOD, superoxide dismutase; TGF-β, transforming growth factor-β; TNF, tumor necrosis factor.

Published online: May 26, Moderate levels of endogenous reactive oxygen species ROS are important for various cellular activities, but high levels lead to toxicity and are associated with various diseases. Levels of ROS are maintained as a balance between oxidants and antioxidants.

Accumulating data suggest that oxidative stress is a major factor in deterioration of renal function. In this review, we highlight the possible mechanism by which oxidative stress can lead to chronic kidney disease CKD. This review also describes therapies that counter the effect of oxidative stress in CKD patients.

Numerous factors such as upregulation of genes involved in oxidative phosphorylation and ROS generation, chronic inflammation, vitamin D deficiency, and a compromised antioxidant defense mechanism system cause progressive detrimental effects on renal function that eventually lead to loss of kidney function.

Patients with renal dysfunction are highly susceptible to oxidative stress, as risk factors such as diabetes, renal hypertension, dietary restrictions, hemodialysis, and old age predispose them to increased levels of ROS. Biomolecular adducts DNA, proteins, and lipids formed due to reaction with ROS can be used to determine oxidative stress levels.

Based on the strong correlation between oxidative stress and CKD, reversal of oxidative stress is being explored as a major therapeutic option.

Xanthine oxidase inhibitors, dietary antioxidants, and other agents that scavenge free radicals are gaining interest as treatment modalities in CKD patients.

Living organisms require oxygen to sustain their existence, and oxidative compounds such as reactive oxygen species ROS and reactive nitrogen species in cells are produced from molecular oxygen as a consequence of aerobic metabolism.

Non-radical species include peroxynitrite ONOO — , hydrogen peroxide H 2 O 2 , and hypochlorous acid HOCl [ 1 ]. ROS exhibit both beneficial and harmful effects on the cell.

Oxidative compounds aid in physiological cell processes when produced in low to moderate concentration, but higher concentration causes detrimental effects including damage to molecular components such as DNA, proteins, and lipids; production of pro- and anti-inflammatory cytokines; and activation of several stress-induced transcription factors [ 2 ].

Endogenous sources of ROS include several cellular enzymes such as nicotinamide adenine dinucleotide phosphate NADPH oxidase Nox , xanthine oxidase XO , mitochondrial oxidases, cyclooxygenase, myeloperoxidase, amino acid oxidase, lipoxygenase, and peroxisomes.

Exogenous sources of oxidants include cigarette smoke, ozone exposure, hyperoxia, ionizing radiation, and heavy metal ions. To counterbalance the effects of oxidants, the human body is equipped with enzymatic and nonenzymatic antioxidant defense mechanisms.

Antioxidant enzyme defenses include superoxide dismutase SOD , catalase, glutathione peroxidase, thioredoxin and peroxiredoxin, and glutathione transferase. Nonenzymatic antioxidants include vitamin C, vitamin E, glutathione, and carotenoids.

When the balance between oxidants and antioxidants shifts in favor of oxidants, oxidative stress is produced. Oxidative stress is known to trigger several pathological conditions including neurological disorders [ 3 ], cardiovascular diseases CVDs [ 4 ], diabetes [ 5 ], cancer, and asthma [ 6 ] and has been associated with kidney dysfunction [ 7 ].

In pyelonephritis, renal dysfunction is caused by ROS-mediated lipid peroxidation and DNA damage, leading to structural and functional aberrations in the kidney [ 8 ]. Administration of free radical scavengers such as catalase and dimethyl-sulfoxide neutralizes ROS production, resulting in reversal of oxidative damage and histopathological changes in a chronic pyelonephritis mouse model [ 9 ].

Over the last few decades, a large number of clinical, experimental, and theoretical investigations have been conducted for detection of signs of oxidative stress in renal failure patients [ 10 — 12 ].

Oxidative stress is widely considered a biochemical hallmark of chronic kidney disease CKD influencing progression of renal function deterioration [ 13 ] and onset of major systemic comorbidities including CVD. Kidneys are responsible for homeostasis of extracellular fluids.

Progressive decline in kidney function causes CKD, which leads to accumulation of toxic waste uremia. CKD has become a global health concern, with more than one million annual deaths from end-stage renal disease ESRD [ 14 ].

Onset and progression of CKD are associated with various components of metabolic syndrome MetS including hypertension, diabetes, obesity, and dyslipidemia. The relationship between MetS and CKD is complex and bidirectional.

However, it is difficult to define the etiological role of MetS in CKD as the individual components of MetS are sensitive to lifestyle modifications, medications, and other factors.

Some of the additional risk factors for CKD include exposure to nephrotoxins, acute kidney disease, smoking, and aging [ 16 ]. All these risk factors significantly disturb the redox balance in the body. Increased oxidative species and decreased antioxidant capacity have been documented in various renal insufficiencies including CKD Fig.

In kidney diseases, cellular oxidative stress induces apoptosis and senescence, reduced regenerative capability of cells, and fibrosis in the kidney cells.

Oxidative stress leads to accumulation of extracellular matrix proteins, podocyte damage, mesangial expansion, renal hypertrophy, endothelial dysfunction, tubulointerstitial fibrosis, and glomerulosclerosis [ 1 ].

Thus, oxidative stress further contributes to deterioration of renal function and disease progression. The mitochondrial electron transport complex is major source of ROS production via oxidative phosphorylation system OXPHOS in the cell. In CKD patients, mitochondrial deregulation causes overproduction of ROS and enhances oxidative stress.

Several genes involved in OXPHOS have been found to be upregulated in CKD patients [ 17 ]. Other enzymes including Nox, XO, and lipoxygenases, which initiate ROS production, are upregulated in CKD [ 18 ].

Several isoforms of Nox have been implicated in renal diseases including nephrolithiasis, hypertension, membranous nephropathy, renal transplantation, and acute kidney injury [ 19 ]. Nox4, the predominant Nox isoform in kidney, acts as a major source of ROS and plays a central role in chronic renal diseases such as diabetic nephropathy [ 20 ].

Increased Nox-dependent superoxide generation has been reported in patients at an early stage of chronic renal failure [ 21 ] and has been shown to contribute to microvascular dysfunction in CKD [ 22 ]. XO is the oxidative radical-producing isoform of xanthine oxidoreductase XOR , also known as urate-producing enzyme.

The XO enzyme catalyzes oxidation of hypoxanthine to xanthine and then xanthine to uric acid together with ROS release. XO activity is higher in plasma of CKD patients and has been suggested to be an independent predictor of cardiovascular events in CKD patients [ 23 ].

Recently, Terawaki et al. Further, these researchers showed higher XOR redox, the ratio of XO to total XOR, in the plasma of advanced CKD patients, indicating its role in elevated ROS production.

Nitric oxide NO influences kidney function and aids in maintaining normal blood pressure by promoting natriuresis and diuresis, aiding in adaptation to variations in dietary salt intake. NO also acts as a powerful anti-oxidative agent that minimizes the adverse effects of O 2 -. Studies have reported reduced NO production in CKD patients [ 25 ].

Multiple factors are responsible for the diminished levels of NO including decreased availability of L-arginine, the substrate for NO synthesis, and increased levels of NO synthase inhibitors such as asymmetric dimethylarginine [ 26 ]. The decreased NO activity and further deactivation by superoxide anion radical increase vascular resistance in renal arteries and manifest as hypertensive nephropathy and CVD [ 27 ].

CKD patients have severe vitamin D deficiency that is further decreased by reduced activity of the enzyme 1-α hydroxylase CYP27B1 , which converts hydroxyvitamin D to its more active form, 1,dihydroxyvitamin D. Deficiency of vitamin D causes oxidative stress, inflammation, hypertension, and hypocalcemia, which lead to progression of CKD and CVD [ 28 ].

Elevated levels of lipid-associated oxidation markers such as F2-isoprostanes and malondialdehyde MDA ; protein-associated oxidation markers including oxidized low-density lipoproteins, carbonyls, and glycations; and DNA-associated oxidation markers such as 8-oxo-2'-deoxyguanosine reflect the status of oxidative stress in CKD and can be correlated to disease severity Fig.

The free radicals generated due to oxidative stress have high reactivity and short half-lives seconds and are difficult to quantitate in clinical settings. Therefore, biomolecular adducts having longer half-lives hours to weeks have become an important tool to measure the levels of oxidative stress.

Oxidative stress is an important contributor to chronic inflammation in CKD. Long-term low-grade inflammation has been implicated in the pathophysiology of CKD.

Accumulation of ROS triggers an inflammatory chain reaction by recruiting macrophages and secreting cytokines, chemokines, and eicosanoids.

Cytokines and inflammatory mediators such as tumor necrosis factor TNF -α, transforming growth factor β, and interleukins ILs have been shown to modulate GFR, renal blood flow, and sodium excretion [ 29 ].

In addition, oxidative stress activates nuclear factor NF -κB, a transcription factor responsible for expression of inflammatory mediator genes [ 30 ]. Oxidative stress affects the phosphorylation and degradation of I-κB, an inhibitory protein that maintains NF-κB in an inactivated state, and leads to activation of NF-κB.

The presence of antioxidants inhibits activation of NF-κB by ROS [ 31 ]. Patients with advanced-stage CKD have high levels of inflammation markers such as C-reactive protein, TNF-α, and IL-6 as well as oxidative stress markers such as plasma protein carbonyls and F2-isoprostanes, supporting the link between inflammation and oxidative stress in disease pathogenesis [ 32 , 33 ].

Antioxidant defense mechanisms have been shown to be compromised in patients with renal dysfunction. The free radical scavenger SOD is down-regulated in renal patients [ 34 ]. Genetic polymorphism in glutathione-S transferase, another antioxidant enzyme, contributes to elevated oxidative stress in ESRD patients [ 35 ].

In addition, reduced plasma levels of antioxidant enzymes including catalase, glutathione peroxidase, intracellular glutathione, and thiol have been reported in patients with CKD [ 36 ].

Increased susceptibility to oxidative stress in patients with renal dysfunction can be attributed to various mechanisms Figure 1. Risk factors such as diabetes, renal hypertension, and old age predispose these patients to increased levels of oxidative stress compared to the normal population.

Normal potassium level is critical to maintain normal heart function; in hyperkalemia, the reduced ability of the kidney to excrete potassium from blood can disrupt potassium hemostasis and lead to abnormal heart rhythms. Severe hyperkalemic condition results in mortality.

Renal dysfunction leads to accumulation of several uremic toxins such as indoxyl sulfate, p-cresol, and p-cresyl sulfate, which trigger progression of CKD and increase the risk of CVD [ 37 — 39 ]. Indoxyl sulfate stimulates oxidative stress to contribute to atherosclerotic vascular disease, arrhythmia, and chronic heart failure, indicating its role in the high prevalence of CVD that accelerates progression of CKD [ 40 ].

In addition, accumulation of uremic toxins in CKD causes uremic sarcopenia and uremic osteoporosis [ 41 , 42 ]. Similarly, p-cresyl sulfate increases oxidative stress and is involved in various mechanisms associated with cardiovascular and renal dysfunction [ 43 ].

Hemodialysis HD , which is currently one of the major renal replacement therapies, is associated with increased oxidative stress [ 44 ]. HD is a nonselective procedure that removes solutes and results in loss of antioxidant molecules including water-soluble vitamins [ 45 — 48 ] and trace elements [ 49 ].

Furthermore, the bioincompatible dialyzer membranes used in HD cause ROS production via activation of polymorphonuclear neutrophils PMNs.

Activated PMNs generate myeloperoxidase, which is a key trigger for ROS activation and inactivation of nitrogen oxide.

Studies have shown that increased serum myeloperoxidase is associated with markers of both inflammation and mortality in HD patients [ 50 ].

The presence of bacterial endotoxins such as lipopolysaccharide or anticoagulants in the dialysate triggers formation of oxidative species [ 51 — 53 ]. A growing body of evidence clearly suggests a role of oxidative stress in the pathogenesis of CKD and has prompted researchers worldwide to explore the possibility of reversing oxidative stress.

Oxidative stress is enhanced in patients undergoing HD. Studies indicate that supplementation of antioxidants is beneficial in treating and preventing progression of CKD in predialysis as well as dialysis patients [ 54 ].

Several clinical trials have been performed to examine the therapeutic potential of various antioxidants in slowing progression of CKD. XO inhibitors XOi have been the primary choice for treatment of hyperuremia associated with various diseases including CKD.

The first-generation XOi allopurinol has been shown to exert a moderate nephroprotective effect by reducing ROS generation and inflammation and improving endothelial function [ 55 , 56 ]. Recently, new randomized clinical trials with second-generation XOi febuxostat and topiroxostat have been initiated [ 57 ].

N-acetylcysteine NAC , a precursor of glutathione, has also emerged as a potential molecule for slowing CKD progression to ESRD by attenuating systemic oxidative stress [ 58 ]. NAC has been shown to improve endothelial dysfunction in CKD patients on HD [ 59 ].

Noxs are a major source of ROS in the kidney; therefore, Nox inhibitors are emerging as potential therapeutics for CKD [ 60 ]. Preclinical studies have shown that GKT setanaxib , a dual inhibitor of Nox1 and Nox4, exhibits renoprotective effects by attenuating glomerular structural changes, podocyte loss, extracellular matrix accumulation, and albuminuria in a mouse model of diabetic nephropathy [ 61 , 62 ].

Owing to the crucial role of setanaxib in attenuating renal pathology, it has now been enrolled in a Phase 2 clinical trial for type I diabetes and kidney disease. Recently, Cha et al.

Moreover, APX decreased albuminuria and preserved creatinine level [ 63 ]. Another study showed that APX effectively prevented kidney injury such as oxidative stress, inflammation, and fibrosis in diabetic mice [ 64 ].

Moreover, APX treatment effectively inhibited mitochondrial and peroxisomal dysfunction, suggesting pan-Nox inhibition as an effective therapy. Nuclear factor erythroid 2-related factor 2 Nrf2 is another emerging treatment target to counteract oxidative stress and inflammation in CKD [ 65 ]. Nrf2 is a transcription factor responsible for regulation of various antioxidant genes.

Enhancing Nrf2 activity in renal tubules decreases oxidative stress and prevents kidney disease progression [ 66 ].

Bardoxolone methyl BARD , a semisynthetic triterpenoid, is one of the most potent activators of Nrf2. BARD has been shown to increase estimated GFR and preserve kidney function in stage 4 CKD patients.

This strongly suggests that restoring Nrf2 activity could potentially retard CKD progression [ 67 ]. The protective effect of dietary antioxidant micronutrients in various diseases associated with oxidative stress has been well documented.

Antioxidant therapy reduces serum creatinine level and improves kidney function which contributes to reduced risk of progression to ESRD. Vitamins E and C are strong and powerful antioxidants that have been considered for CKD therapy [ 68 - 70 ].

Alpha-tocopherol, the biologically active form of vitamin E, counteracts oxidative stress by protecting against peroxidation of lipids and increasing low-density lipoprotein resistance [ 71 ].

Vitamin E is a strong scavenger of peroxyl radical and also regulates the expression of inflammatory genes. Supplementation with vitamin E in HD patients causes significant decrease in serum MDA and induces SOD1 and catalase activity [ 68 ].

In addition, vitamin E-modified cellulose membrane use in HD has been shown to suppress oxidative stress and inflammation and improves endothelial function. Furthermore, hemolipodialysis has been shown to reduce oxidative stress caused during HD using vitamin C and liposomes containing vitamin E in the dialysate [ 72 ].

However, daily administration of vitamin E in ESRD patients significantly reduces cardiovascular complications but does not affect mortality [ 73 ].

Reduced vitamin C level has been observed in CKD patients undergoing HD. Vitamin C prevents oxidative damage by directly scavenging superoxide anion and hydroxyl radical.

A moderate dose of vitamin C has been suggested as a corrective measure in CKD. Coadministration of vitamin C and vitamin E decreases the formation of carbonyl compounds and MDA concentration and increases total antioxidant capacity levels in peritoneal dialysis patients [ 74 ].

CKD patients are also supplemented with 1, vitamin D, the active form of vitamin D, as these patients have very a high rate of vitamin D deficiency [ 28 ].

Numerous studies have reported a beneficial effect of vitamin D supplementation, including reduced proteinuria, improvement in endothelial cardiovascular markers, increased serum level of 1,vitamin D, and decreased inflammation markers and serum parathyroid hormone levels in CKD and dialysis patients [ 75 — 79 ].

A recent meta-analysis demonstrated that vitamin D supplementation modulates various parameters of oxidative stress including total antioxidant capacity, glutathione, and MDA [ 80 ]. Experimental evidence suggests that vitamin D supplementation reduces oxidative stress and inflammation by increasing Nrf2 and up-regulating antioxidant enzymes [ 81 ].

Along with lifestyle changes such as exercise, smoking cessation, and dietary measures, treatment of CKD is focused on controlling albuminuria, blood pressure, blood glucose, and lipids. Agents such as beta blockers, angiotensin-converting enzyme ACE inhibitors, angiotensin II receptor blockers ARBs , and direct renin inhibitors DRI suppress the renin-angiotensin-aldosterone-system RAAS , a regulator of blood pressure.

These agents have been demonstrated to attenuate oxidative stress and therefore play a protective role in early as well as end stages of kidney disease [ 82 , 83 ]. A meta-analysis of randomized trials showed that ACE inhibitors were effective in decreasing blood pressure and excretion of urinary protein and in slowing progression of renal disease [ 84 ].

Monotherapy with ARBs or ACE inhibitors has been shown to reduce proteinuria. Similarly, a combination of ACE inhibitors and ARBs maximizes RAAS inhibition and normalizes proteinuria and GFR. Based on experimental evidence, a combination of RAAS inhibitors was suggested to be more effective than monotherapy in attenuating the progression of renal dysfunction.

However, this regimen was linked with higher occurrence of adverse events such as hypotension and hyperkalemia [ 85 ]. Aliskiren, the first orally bioactive DRI, has been predicted to have greater potential for suppression of RAAS than any other class of drug. Additionally, aliskiren attenuates oxidative stress and provides protection of renal tubules in patients with CKD [ 81 , 87 ].

Natural compounds that target mitochondria, alone or in combination with conventional therapies and lifestyle modifications, are gaining worldwide interest as treatment modalities in CKD patients undergoing both conservative and dialysis treatment because of the low prevalence of adverse effects associated with their use.

Although these antioxidant therapies seem promising, their use is controversial. Most studies demonstrating a benefit are either in vivo , isolated, or non-holistic studies.

Large-scale randomized controlled trials RCTs are lacking for most of these compounds. Currently, there are ongoing trials for various antioxidants including resveratrol, NAC, coenzyme Q10, tocopherols, and curcumin.

There is an abundance of crosstalk between pathways of inflammation and oxidative stress.

Open Professional head lice removal peer-reviewed snd. Submitted: 21 September Dance fueling essentials 13 April Published: 26 October ehalth customercare cbspd. Chronic Kidneyy disease CKD is defined as the atrophy of the kidney or progressive decline of renal function mainly caused by chronic diseases such as diabetes mellitus and hypertension. Moreover, there is no single treatment to improve kidney function in CKD patients. This kirney is Antioxidant and kidney health intended to diagnose, treat, helath, Pear-shaped body prevent any disease. Anitoxidant consult with a qualified healthcare professional prior Antiviral immunity-boosting supplements beginning Antioxidaant diet or exercise program or taking any dietary supplement. The content on our website is for informational and educational purposes only. Written By: Steve L. Belcher, RN, MSN, MS, DN-CM. One of the best ways to get antioxidants is by eating a variety of colorful foods daily.