scholarly journals Tratment With Folic Acid Increases Paraoxonase 1 Activity Thereby Improving Chronic Kidney Disease

2020 ◽  
Author(s):  
Andressa Matsumoto ◽  
Michael Maes ◽  
Ana Paula Michelin ◽  
Kamila Bonifácio ◽  
Laura Semeão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Folic Acid ◽  
Kidney Disease ◽  
Antioxidant Defenses ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Renal Disease Progression ◽  
Ckd Stage ◽  
Before And After

Introduction: Increased oxidative stress, including elevated homocysteine (Hcy) plasma levels, and lowered levels of antioxidants participate in the pathophysiology and progression of chronic kidney disease (CKD). Paraoxonase (PON)1 activity and folic acid are antioxidants which play a role in Hcy metabolism. However, there are no data whether, in CKD, treatment with folic acid improves glomerular filtration rate (GFR) through effects on PON1 activity and Hcy concentrations. Methods: In the current study, we determined PON1 genotypes and activity, Hcy and estimated GFR (eGFR) both before and after treatment with folic acid (5 mg/d) versus no treatment during three consecutive months in 113 outpatients with CKD classified into stages 4, 3b and 3a. Results: PON1 CMPAase and AREase activities were significantly lower in patients allocated to CKD stage 4 as compared with stages 3b and 3a. Treatment with folic acid significantly improved eGFR and increased levels of CMPAase and AREase in patients allocated to classes 4 and 3b, but not 3a. The improvement of eGFR was associated with increased CMPAase and AREase activities, while the latter were associated with increased levels of folic acid. Treatment with folic acid significantly reduced plasma Hcy levels and the Hcy/PON1 activity ratio. The effects of folic acid increasing PON1 activities were not mediated by changes in Hcy. Discussion: Treatment of CKD patients in early/intermediate stages of CKD patients improves oxidative stress by rebalancing the prooxidant (Hcy) / antioxidant (PON1 activities) ratio. Treatment with folic acid significantly improves eGFR and these effects are mediated via increased PON1 activities. Treatment with folic acid in phase G3b and G4 may reduce renal disease progression by enhancing antioxidant defenses.

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 Thrombomodulin as a New Marker of Endothelial Dysfunction in Chronic Kidney Disease in Children

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Dorota Drożdż ◽  
Monika Łątka ◽  
Tomasz Drożdż ◽  
Krystyna Sztefko ◽  
Przemko Kwinta
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Cystatin C ◽  
Oxidized Ldl ◽  
Left Ventricular ◽  
Intercellular Adhesion Molecule ◽  
Oxidative Stress Biomarkers ◽  
Ckd Stage

Endothelial dysfunction (ED) and oxidative stress are potential new pathomechanisms of cardiovascular diseases in patients with chronic kidney disease (CKD). The aim of the study was to assess the association between endothelial dysfunction, oxidative stress biomarkers, and cardiovascular risk factors in children with CKD. Serum oxidized LDL (oxLDL), protein carbonyl group, urea, creatinine, cystatin C, thrombomodulin, asymmetric dimethylarginine (ADMA), von Willebrand factor, brain natriuretic peptide (BNP), lipids, high sensitivity C-reactive protein, intercellular adhesion molecule-1 levels, and albuminuria were measured. Anthropometric, ambulatory blood pressure (BP) measurements and echocardiography were performed. The studied group consisted of 59 patients aged 0.7–18.6 (mean 11.1) years with stages 1 to 5 CKD. Thrombomodulin strongly correlated with creatinine (R=0.666; p<0.001), cystatin C (R=0.738; p<0.001), BNP (R=0.406; p=0.001), ADMA (R=0.353; p=0.01), oxLDL (R=0.340; p=0.009), 24-hour systolic (R=0.345; p=0.011) and mean (R=0.315; p<0.05) BP values, and left ventricular mass index (LVMI, R=0.293; p=0.024) and negatively with estimated glomerular filtration rate (R=−0.716; p<0.001). In children with CKD, TM strongly depended on kidney function parameters, oxLDL levels, and 24-hour systolic and mean BP values. Thrombomodulin seems to be a valuable marker of ED in CKD patients, correlating with CKD stage as well as oxidative stress, BP values, and LVMI.

scholarly journals ACTI ON OF N- ACETYLCYSTEI NE ON ASYMMETRI C DIMETHYLARGININE AND ALBUMINURIA IN STAGE 1-4 NONDIABETIC CHRONIC KIDNEY DISEASE PATIENTS

2010 ◽  
Vol 1 (3) ◽  
pp. 146
Author(s):  
MOCHAMMAD THAHA ◽  
Widodo Widodo ◽  
Moh. Yogiantoro ◽  
WENNY PUTRI NILAMSARI ◽  
MOCHAMAD YUSUF ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Treatment Group ◽  
Kidney Disease ◽  
Day Treatment ◽  
Oral Treatment ◽  
Control Group ◽  
Adma Level ◽  
Ckd Stage ◽  
Stage 1

Background: Uremic patients are in a pro-oxidant state and show an increased level of asymmetric dimethylarginine (ADMA), which is due to increased PRMT1 activity and reduced dimethylarginine dimethylaminohydrolase (DDAH) as degradation enzymes. Reactive oxidant species may play an important role in increasing the action of PRMT1 and in inhibiting the action of DDAH. Albuminuria and ADMA are closely correlated with progression of cardiovascular disease in chronic kidney disease (CKD) patients as well as indicators for decreasing renal function. Although ACEIs and/or ARBs reduced albuminuria in CKD patients, the results are still conflicting. Several factors in these patients may play important roles in the mechanism of albuminuria such as oxidative stress. The antioxidant N-acetylcysteine may prove to have beneficial therapeutic effect, because it can reduce oxidative stress as shown by evidence in humans, and subsequently increase ADMA. The objective of the present study is to explore the contribution of the antioxidant N-acetylcysteine (NAC) to the decrease of ADMA and albuminuria in non-diabetic CKD patients. Material and Methods: Patients with non-DM CKD stage 1–4 with albuminuria were randomized to receive ACEI and/or ARB alone (control group) or with antioxidant NAC 600 mg orally twice a day (treatment group). Observations were performed for 3 months to measure ADMA and albuminuria before and after-treatment. 80 patients in total 40 in the control group and 40 in the treatment group were used. Results: After oral treatment with NAC, the plasma level of ADMA in the treatment group increased from 0.604 µmol/l to 0.689 µmol/l, whereas ADMA level in the control group exhibited a higher increase from 0.561 µmol/l to 0.743 µmol/l. The increases in these groups were significantly different (p < 0.02). Moreover, the level of albuminuria was reduced from 148.12 µg/mg • cr to 132.7 µg/mg • cr in the treatment group, and from 75.25 µg/mg • cr to 71.85 µg/mg • cr in the control group. The difference was significant (p < 0.001). Conclusion: The anti-oxidant N-acetylcysteine can be used as adjuvant therapy to inhibit the progression of CKD in patients by decreasing the ADMA level and albuminuria.

A randomized trial of short-term treatment with folic acid to reduce the oxidative stress of patients with chronic kidney disease

2021 ◽  
Vol 22 ◽  
Author(s):  
Andressa Keiko Matsumoto ◽  
Ana Paula Michelin ◽  
Laura de Oliveira Semeão ◽  
Walter Sepúlveda-Loyolaa ◽  
João Victor de Lima Pedrão ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Folic Acid ◽  
Kidney Disease ◽  
Acid Treatment ◽  
Nitrosative Stress ◽  
Intervention Group ◽  
Active Intervention ◽  
Stress Biomarkers ◽  
Active Intervention Group

Background: Increased generation of reactive oxygen and nitrogen species in chronic kidney disease (CKD) patients leads to increased oxidative stress. The antioxidant capacity of folic acid has been shown to scavenge radicals efficiently. Objective: The current study was carried out to examine the effects of folic acid treatment on biochemical and oxidative stress biomarkers in patients in different stages of CKD. Methods: This was a randomized, non-blinded, clinical trial that assessed the effects of 3 months of treatment with 5 mg of folic acid daily or no treatment in 113 outpatients within CKD stages 3a and 3b. At the end of the intervention, we analyzed the data of 66 patients treated with folic acid and 47 in the control group. Serum homocysteine levels and biochemical and oxidative/nitrosative stress biomarkers were analyzed in all patients. Results: In most patients, folic acid treatment normalized homocysteine levels and increased antioxidant enzyme activity (paraoxonase 1) and decreased sulfhydryl (SH) groups. In addition, oxidative biomarkers (products of nitric oxide and lipid hydroperoxide) were significantly lower post-treatment compared to baseline in the active intervention group. In the no active intervention group, no statistically significant effects were found on the oxidative and biochemical biomarkers. Conclusion: Folic acid treatment in stages 3a-4 CKD patients effectively ameliorated their hyperhomocysteinemia and increased the activity of antioxidant enzymes, as well as decreased the levels of pro-oxidant biomarkers in stage G3a and G3b CKD patients. Folic acid treatment attenuated oxidative/nitrosative stress and may be considered as a possible strategy to improve redox status and diminish the damages associated with oxidative/nitrosative stress in CKD patients. Further studies are needed to confirm these findings.

Abstract 409: Effects of Angiotensin II Receptor Blocker (ARB) and PPAR-gamma Agonist on Vascular Failure in Patients with Hypertension, Diabetic Mellitus and Chronic Kidney Disease

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideki Watanabe ◽  
Kunio Nakagawa ◽  
Masaaki Kakihana
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
High Sensitivity ◽  
Ppar Gamma ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Ppar Γ ◽  
Ckd Stage ◽  
Measured Flow

Background: Hypertension (HT), diabetes mellitus (DM), and chronic kidney disease (CKD) are known to be associated with “vascular failure”, which is defined as the integration of endothelial dysfunction and metabolic abnormalities of the vessel wall including inflammation, oxidative stress. We evaluated effects of ARB, calcium channel blocker (CCB), and PPAR-γ agonist on vascular failure in patients with HT, DM and CKD. Methods: Forty eight patients with untreated HT, type 2 DM (HbA1c 6.0 – 6.5%), and CKD (stage 3 or 4) were randomized to receive telmisartan ( Tel. group , n=12), telmisartan and pioglitazone ( Tel. and Pio. group , n=12), amlodipine ( Aml. group , n=12), or amlodipine and pioglitazone ( Aml. and Pio. group , n=12). We measured flow-mediated dilatation (FMD) and nitroglycerin-induced dilatation (NID) of brachial artery, and pulse wave velocity (PWV). We also measured high sensitivity C-reactive peptide (hsCRP) and TBARS levels as indexes of inflammation and oxidative stress. Measurements were performed at baseline, and then at every 6 months after the treatments. Results: Blood pressure was significantly decreased in these groups, and there was no difference among four groups at baseline and during the study. FMD was significantly increased, and PWV, hsCRP, and TBARS were significantly decreased in four groups. However, these improvements were much better in the Tel. and Pio. group than the other groups. NID did not change during the study. Conclusion: Combination therapy with ARB and PPAR-γ agonist was much better in the improvement of vascular failure in patients with HT, DM and CKD as compared with the therapy with ARB alone, CCB alone, or CCB and PPAR-γ agonist.

scholarly journals Red Blood Cell Lifespan Shortening in Patients with Early-Stage Chronic Kidney Disease

2019 ◽  
Vol 44 (5) ◽  
pp. 1158-1165 ◽  
Author(s):  
Jiu-Hong Li ◽  
Jun-Feng Luo ◽  
Ying Jiang ◽  
Yong-Jian Ma ◽  
Yong-Qiang Ji ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Folic Acid ◽  
Kidney Disease ◽  
Blood Cell ◽  
Vitamin B12 ◽  
Red Blood Cell ◽  
Early Stage ◽  
Renal Anemia ◽  
Ckd Stage ◽  
Stage 1

Background: Although reduced red blood cell (RBC) lifespan has been reported to be a contributory factor to anemia in patients with end-stage chronic kidney disease (CKD), there are limited data regarding RBC lifespan in early-stage CKD. Serum erythropoietin (EPO) is considered a primary causative factor of renal anemia. The aims of this study were to compare the RBC lifespan, serum EPO levels, and other renal anemia indicators across CKD-stage groups of patients and to analyze the impacts of etiological factors on renal anemia. Methods: A cohort of 74 non-smoking patients with CKD were enrolled, including 15 in stage 1, 18 in stage 2, 15 in stage 3, 15 in stage 4, and 11 in stage 5. RBC lifespan was determined by CO breath tests. Potential correlations of hemoglobin (Hb) concentration with RBC lifespan, reticulocyte count (Ret), and levels of EPO, ferritin, folic acid, and vitamin B12 were analyzed. Results: CKD progression was associated with decreases in (Hb) and RBC lifespan. RBC lifespan durations in CKD stages 1–5 were 122 ± 50, 112 ± 26, 90 ± 32, 88 ± 28, and 60 ± 24 days, respectively. RBC lifespan means for the stage 3, 4 and 5 groups were significantly shorter than those for the stage 1 and 2 groups. Serum EPO did not differ significantly between the CKD stage groups. (Hb) correlated directly with RBC lifespan (r = 0.372, p = 0.002) and Ret (r = 0.308, p = 0.011), but did not correlate with serum EPO, ferritin, folic acid, or vitamin B12 levels. Conclusions: Reduced RBC lifespan in early-stage CKD, demonstrated in this study, suggests that increased RBC destruction may play a more important etiological role in renal anemia than other indicators in patients with CKD.

scholarly journals MO474PCSK9 LEVELS AND MARKERS OF INFLAMMATION, OXIDATIVE STRESS AND ENDOTHELIAL DYSFUNCTION IN A POPULATION OF NON-DIALYSIS CHRONIC KIDNEY DISEASE PATIENTS: IS THERE AN ASSOCIATION?

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Evangelia Ntounousi ◽  
Konstantinos Tellis ◽  
Paraskevi Pavlakou ◽  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Renal Function ◽  
Lipid Metabolism ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Endothelial Damage ◽  
Apo B ◽  
Markers Of Inflammation ◽  
Ckd Stage

Abstract Background and Aims Proprotein convertase subtilisin / kexin 9 (PCSK9) plays an important role in lipid metabolism while available literature regarding its involvement in the pathogenesis of atherosclerosis and in the expression of genes associated with apoptosis and inflammation is constantly increasing. Patients with chronic kidney disease (CKD) experience disproportionately increased cardiovascular morbidity and mortality due to dyslipidemia, accelerated atherosclerosis, inflammation, oxidative stress and other risk factors. In the present cross-sectional study, we investigated the possible association of serum PCSK9 levels with markers of inflammation, oxidative stress and endothelial damage in patients with CKD. Method Ninety-two patients with CKD stage II-ΙV (eGRF CKD-EPI 47.3 ±25.7ml/min/1,73m2, mean age 66 years, 51 men) were included. Plasma PCSK9 levels were correlated with comorbidities (arterial hypertension; diabetes mellitus, history of cardiovascular disease), renal function indices (eGFR, proteinuria – UPR/24h), lipid parameters (LDL-cholesterol, HDL-cholesterol, triglycerides, Lp (a), APO-A1, APO-B), as well as soluble biomarkers of inflammation, oxidative stress and endothelial damage (hs-CRP, fibrinogen, 8-epiPGF2a, ox-LDL, IL-6, TNF-α, sICAM-1, sVCAM-1). Results The mean plasma value of PCSK9 was 278.1ng/ml. PCSK9 levels showed direct correlation with serum triglycerides (p = 0.03), Lp(a) (p = 0.01), and sICAM-1 levels (p = 0.03). There was no significant correlation between PCSK9 levels and indices of renal function, other lipid profile parameters, inflammatory markers or co-morbidities. Multiple regression analysis showed a significant effect of the Lp(a) on PCSK9 levels, for each unit of higher Lp(a), an increase by 3.082 is expected (95% CI: 0.935 - 5.228, p=0.006). At the same time, patients receiving statins are expected to have on average 63.8ng/ml higher PCSK9 values compared to patients not receiving statins (95% CI: 14.6 - 113.5 p=0.012). Conclusion Plasma levels of PCSK9 in non-dialysis CKD patients are correlated with endothelial dysfunction and lipid metabolism parameters. Statin intake increases PCSK9 levels significantly in this patient population. PCSK9 levels are not correlated with the severity of kidney disease. Major prospective studies are necessary to investigate the role of PCSK9 in the atherosclerotic cardiovascular outcome in CKD

scholarly journals The Role of Vitamin D and Oxidative Stress in Chronic Kidney Disease

2018 ◽  
Vol 15 (12) ◽  
pp. 2701 ◽  
Author(s):  
Keith Norris ◽  
Opeyemi Olabisi ◽  
M. Barnett ◽  
Yuan-Xiang Meng ◽  
David Martins ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ethnic Minorities ◽  
Communicable Disease ◽  
Hypovitaminosis D ◽  
Ckd Stage ◽  
Poor Outcomes ◽  
Racial Ethnic

Chronic kidney disease (CKD) is a major non-communicable disease associated with high rates of premature morbidity and mortality. The prevalence of hypovitaminosis D (deficiency of 25(OH)D or 25D) is greater in racial/ethnic minorities and in patients with CKD than the general population. Low 25D is associated with bone and mineral disorders as well as immune, cardiometabolic and cardiovascular (CV) diseases. Thus, it has been suggested that low 25D contributes to the poor outcomes in patients with CKD. The prevalence of hypovitaminosis D rises progressively with advancing severity of kidney disease with over 30% of patients with CKD stage 3 and 70% patients with CKD stage 5 estimated to have low levels of 25D. This report describes several of the abnormal physiologic and counter-regulatory actions related to low 25D in CKD such as those in oxidative stress and inflammatory systems, and some of the preclinical and clinical evidence, or lack thereof, of normalizing serum 25D levels to improve outcomes in patients with CKD, and especially for the high risk subset of racial/ethnic minorities who suffer from higher rates of advanced CKD and hypovitaminosis D.

Low fat adiponectin expression is associated with oxidative stress in nondiabetic humans with chronic kidney disease—impact on plasma adiponectin concentration

2007 ◽  
Vol 293 (1) ◽  
pp. R47-R54 ◽  
Author(s):  
Rocco Barazzoni ◽  
Annamaria Bernardi ◽  
Franco Biasia ◽  
Annamaria Semolic ◽  
Alessandra Bosutti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Adipose Tissue ◽  
Plasma Concentration ◽  
Kidney Disease ◽  
Maintenance Hemodialysis ◽  
Renal Transplant Recipients ◽  
Plasma Adiponectin ◽  
Ckd Stage ◽  
Adiponectin Mrna

In spite of association between high plasma adiponectin and high metabolic and cardiovascular (CV) risk, highest adiponectin increments retain CV and metabolic protective effects in advanced chronic kidney disease (CKD). Passive accumulation can favor CKD-associated hyperadiponectinemia but potential additional regulation by adipose tissue remains undefined. Oxidative stress (OS) is associated with metabolic and CV disease and with CKD [increasing from conservative treatment (CT) to maintenance hemodialysis (MHD)], and OS can reduce adiponectin expression in experimental models. OS (in the form of plasma thiobarbituric acid-reactive substances: TBARS), subcutaneous adipose adiponectin mRNA, and plasma adiponectin were studied in CKD patients ( stages 4 and 5) on CT ( n = 7) or MHD ( n = 11). Compared with CT and controls (C: n = 6) MHD had highest TBARS and lowest adiponectin mRNA ( P < 0.05) with lower adipose adiponectin protein ( P < 0.05 vs. CT). MHD also had lower plasma adiponectin than CT, although both had higher adiponectin than C ( P < 0.05). In renal transplant recipients (RT: CKD stage 3; n = 5) normal TBARS were, in turn, associated with normal adiponectin mRNA ( P < 0.05 vs. MHD). In all CKD ( n = 23), adiponectin mRNA was associated positively with adiponectin plasma concentration ( P < 0.01). In all subjects ( n = 29), adiponectin mRNA was related ( P < 0.05) negatively with TBARS after adjusting for plasma C-reactive protein (CRP) or CRP and creatinine. Thus altered OS, adiponectin expression, and plasma concentration represent a novel cluster of metabolic and CV risk factors in MHD that are normalized in RT. The data suggest novel roles of 1) MHD-associated OS in modulating adiponectin expression and 2) adipose tissue in contributing to circulating adiponectin in advanced CKD.

scholarly journals The Role of Vitamin D and Oxidative Stress in Chronic Kidney Disease

2018 ◽  
Author(s):  
Keith C. Norris ◽  
Opeyemi Olabisi ◽  
M. Edwina Barnett ◽  
Yuan-Xiang Meng ◽  
David Martins ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ethnic Minorities ◽  
Communicable Disease ◽  
Hypovitaminosis D ◽  
Ckd Stage ◽  
Poor Outcomes ◽  
Racial Ethnic

Chronic kidney disease (CKD) is a major non-communicable disease associated with high rates of premature morbidity and mortality. The prevalence of hypovitaminosis D (deficiency of 25(OH)D or 25D) is greater in racial/ethnic minorities and in patients with CKD than the general population. Low 25D is associated with bone and mineral disorders as well as immune, cardiometabolic and cardiovascular (CV) diseases. Thus, it has been suggested low 25D contributes to the poor outcomes in patients with CKD. The prevalence of hypovitaminosis D rises progressively with advancing severity of kidney disease with over 30% of patients with CKD stage 3 and 70% patients with CKD stage 5 estimated to have low levels of 25D. This report describes several of the abnormal physiologic and counter-regulatory actions related to low 25D in CKD such as those in oxidative stress and inflammatory systems, and some of the preclinical and clinical evidence or lack of thereof of normalizing serum 25D levels to improve outcomes in patients with CKD, and especially for the high risk subset of racial/ethnic minorities who suffer from higher rates of advanced CKD and hypovitaminosis D.

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