Impact of Serum Bicarbonate Levels on Muscle Mass and Kidney Function in Pre-Dialysis Chronic Kidney Disease Patients

2019 ◽  
Vol 51 (1) ◽  
pp. 24-34 ◽  
Author(s):  
Piyawan Kittiskulnam ◽  
Somrath Srijaruneruang ◽  
Adhisabandh Chulakadabba ◽  
Nintita Sripaiboonkij Thokanit ◽  
Kearkiat Praditpornsilpa ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Muscle Strength ◽  
Sodium Bicarbonate ◽  
Muscle Mass ◽  
Control Group ◽  
Bicarbonate Level ◽  
Serum Bicarbonate ◽  
Serum Bicarbonate Level

Background: Treatment of metabolic acidosis to target the higher serum bicarbonate level than guideline recommendation may downregulate muscle protein degradation and improve renal function among chronic kidney disease (CKD) patients. We conducted a study to test the effects of increased serum bicarbonate level on muscle parameters, nutrition, and renal function in pre-dialysis CKD patients. Methods: This was a randomized, controlled study. CKD stage 3–4 patients with serum HCO3– <22 mEq/L were randomized to either receive oral sodium bicarbonate with high target bicarbonate level of 25 ± 1 or standard level of 22 ± 1 mEq/L as control group using protocol-based titration of dosage adjustment. The changes of muscle mass measured by bioelectrical impedance analysis (BIA), muscle strength by hand grip dynamometer, estimated glomerular filtration rate (eGFR) using CKD-Epidemiology Collaboration equation, nutritional markers, and muscle-related biomarkers were determined. Data at baseline and after 4 months of sodium bicarbonate supplementation were compared between groups using Student t test or chi-square test as appropriate. Results: Forty-two patients completed the study (n = 21 per group). The mean age and eGFR were 61.2 ± 9.8 years and 32.4 ± 14.1 mL/min respectively. Serum bicarbonate levels at baseline were 21.0 ± 2.1 mEq/L. Baseline data including sex, diabetes, serum bicarbonate level, creatinine, and blood pressure were similar. After 4 months of treatment, the average serum bicarbonate levels in both groups were 24.0 ± 1.4 and 20.7 ± 2.3 mEq/L (p < 0.001). Both BIA-derived total-body muscle mass and appendicular lean balance were increased at 4 months in the higher bicarbonate group (26.0 ± 5.3 to 26.7 ± 5.5 kg, p = 0.04 and 19.8 ± 4.1 to 20.7 ± 4.4 kg, p = 0.06, respectively) despite comparable body weight and protein intake. Patients in the high bicarbonate group had a significant reduction of plasma myostatin levels, a surrogate of muscle degradation, at the study exit after adjusting for baseline values (–3,137.8; 95% CI –6,235.3 to –40.4 pg/mL, p= 0.04), but unaltered insulin-like growth factor-1 level, as the mediator of muscle cell growth, (141 [106–156] to 110 [87–144] ng/mL, p = 0.13) compared to the control group. Muscle strength, eGFR as well as serum prealbumin were not significantly different between 2 groups (p > 0.05). Neither worsening hypertension nor congestive heart failure was found throughout the study. Conclusion: Bicarbonate supplementation to achieve the serum level ∼24 mEq/L demonstrates better muscle mass preservation in patients with pre-dialysis CKD. The impact of alkaline therapy on renal function may require a longer period of study.

MO021GALECTIN 3 LEVEL IS REDUCED BY TREATMENT WITH SODIUM BICARBONATE IN PATIENTS WITH CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Mirela Dobre ◽  
Neil Patel ◽  
Hima Sapa ◽  
Edward Horwitz ◽  
Michal Melamed ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Placebo Group ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Myocardial Fibrosis ◽  
Bicarbonate Level ◽  
Serum Bicarbonate ◽  
Galectin 3 ◽  
Serum Bicarbonate Level ◽  
One Year

Abstract Background and Aims Circulating cardiac biomarkers implicated in the pathogenesis of heart disease are a non-invasive platform to assess the cardiovascular disease (CVD) burden in individuals with chronic kidney disease (CKD). Galectin 3 is a 26 kDa β-galactoside-binding lectin that has a graded and positive association with CKD stages. In animal models, inhibition of galectin-3 prevents myocardial fibrosis. These pre-clinical findings have not been replicated in randomized controlled studies in humans. Metabolic acidosis of CKD has been shown to be associated with adverse CVD outcomes. We sought to examine whether correction of metabolic acidosis of CKD leads to lower circulating levels of Galectin 3, as an expression of myocardial fibrosis. Method A total of 95 participants with stages 3 and 4 CKD and a serum bicarbonate level between 21-25 mEq/L, were randomized to receive sodium bicarbonate at a dose of 0.4 mEq/kg/day once a day or placebo for two years at two clinical sites in US. Galectin 3, was measured at study baseline and after one year. Results Fifty participants were randomized to sodium bicarbonate and 45 to placebo. Mean age (SD) was 61.4 (10.2) years, 48% were women, 57% were non-Hispanic black, and 40% were non-Hispanic white, 61% had diabetes mellitus and 90% had hypertension at baseline. Mean baseline serum bicarbonate level was 23.5 (SD 1.7), mean (SD) baseline eGFR was 38.8 (11.2) ml/min/1.7m2 and mean (SD) baseline systolic BP was 130 (17) mmHg. There were no differences in baseline characteristics between treatment groups. Compared to the placebo group, participants randomized to sodium bicarbonate had statistically significant change in the levels of Galectin 3 after one year of treatment (-7.12% vs 7.76% and -1.25 vs 1.54 ng/ml, p=0.03 in the sodium bicarbonate vs. placebo group, respectively, Figure). In subgroup analyses by CKD stages, participants with stage 3A randomized to sodium bicarbonate observed the highest decrement in Galectin 3 levels (-19.2% vs 14.7%, p=0.01; -3.3% vs -4.8%, p=0.49; and -7.4% vs 29.1%, p=0.09; for CKD 3B, 3B and 4, respectively). Conclusion The level of Galectin 3 was reduced in patients with CKD 3 and 4 treated with sodium bicarbonate. This provides a framework for future therapeutic interventions aimed at reduction of myocardial fibrosis in patients with CKD and metabolic acidosis.

scholarly journals Study of serum homocysteine level in patients with chronic kidney disease and its association with renal function and serum albumin

2020 ◽  
Vol 8 (6) ◽  
pp. 2195
Author(s):  
Vandana Yadav ◽  
Vivek Prakash ◽  
Bushra Fiza ◽  
Maheep Sinha
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Serum Creatinine ◽  
Serum Albumin ◽  
Control Group ◽  
Serum Homocysteine ◽  
The Mean ◽  
Gandhi Medical College ◽  
And Control

 Background: Chronic kidney disease (CKD) includes irreversible destruction of nephrons leading to progressive decline in glomerular filtration rate. A preferential defect in Homocysteine disposal could hypothetically occur in CKD and subsequently lead to hyperhomocysteinemia. Understanding the status of Homocysteine and other parameters in CKD is useful in the management of the disease. Objective of the study is to estimate serum Homocysteine in CKD patients and its association with renal function and serum albumin in patients with CKD.Methods: The study design involves hospital based observational comparative study. The study was conducted in Department of Biochemistry in association with Department of Nephrology of Mahatma Gandhi Medical College and Hospital, Jaipur between May 2017 to June 2018. 100 diagnosed patients of CKD, visiting the Outpatient Department of Nephrology were enrolled as cases for the study. Patients having cardiovascular disease, Chronic liver disease, Age more than 60 years and pregnant females were excluded from study. The control group consists of 100 age and sex matched healthy individuals.Results: The mean serum creatinine levels of case and control group were 7.50±3.74 mg% and 0.83±0.22 mg% respectively. The mean of serum homocysteine levels of subject group was 27.35±12.52 µmol/L while the mean serum homocysteine levels of control group was 11.06±3.52 µmol/L. The serum homocysteine levels were significantly higher in the CKD patient group. The serum level of albumin in CKD patients and control group were 2.86±0.86 g/dl and 4.10±0.58 g/dl respectively. A positive correlation was found between serum creatinine and serum homocysteine levels. A negative correlation between serum homocysteine and serum albumin was found.Conclusions: Findings of the present study exhibit that serum homocysteine levels are elevated in CKD in comparison to healthy controls and it is positively correlated with serum creatinine level.

P0739PANEL OF SENSITIVE BIOMARKERS OF THE PRIMARY RESPONSE TO RENAL INJURY FOR AN EARLY DIAGNOSIS OF CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Maria João Valente ◽  
Susana Rocha ◽  
Irina Lousa ◽  
Flávio Reis ◽  
Sara Nunes ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Renal Injury ◽  
Primary Response ◽  
Control Group ◽  
Tubulointerstitial Injury ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Ckd Stage

Abstract Background and Aims The identification of early kidney injury biomarkers is of utmost importance, since most widely used markers of kidney function vary only after several biological changes. Biomarkers allowing an earlier diagnosis of chronic kidney disease (CKD) would avoid delays in the treatment of patients. It is unlikely that a single marker is sufficient to detect the onset of CKD considering the multiple pathophysiological changes underlying primary renal response to renal injury. Several markers of inflammation, endothelial (dys)function, glomerular and tubulointerstitial injuries have been proposed and could be used combined as a panel of markers with different specificities, allowing an early detection of renal injury. Our aim was to study a panel of biomarkers proposed as early markers of renal injury, with different specificities, to evaluate and compare their sensitivities at different CKD stages. Method In this preliminary study, we enrolled 22 healthy individuals and 27 CKD patients separated into 3 groups, according to the CKD stage: 9 in stages 1 and 2; 9 in stage 3, and 9 in stages 4 and 5. None of the patients presented inflammatory, infectious or neoplastic diseases. Diagnosis and CKD stage assignment were performed according to KDIGO guidelines. We evaluated circulating levels of cystatin C (CystC), creatinine (Cr), beta trace protein (BTP) as markers of renal function; tissue inhibitor metalloproteinase 1 (TIMP-1), neutrophil gelatinase-associated lipocalin (NGAL) and transforming growth factor-β (TGF-β) as markers of interstitial tubulointerstitial injury; asymmetric dimethylarginine (ADMA) and tissue plasminogen activator (t-PA), as markers of endothelial (dys)function; pentraxin 3 (PTX3), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), as markers of inflammation; and, pro B-type natriuretic peptides (proBNP), as a marker of cardiac (dys)function. Results In early stages of CKD (1 and 2), we found significant changes in markers of renal function (BTP, but not Cr and CystC), of tubular interstitial injury (TIMP-1 and TGF-β), of inflammation (TNF-α), of endothelial (ADMA) and cardiac (proBNP) dysfunction (vs. controls). In stage 3, we found significant changes (vs. stages 1-2) in markers of renal function (Cr and CystC), inflammation (TNF-α, IL-6), endothelial dysfunction (t-PA) and tubulointerstitial injury (TIMP-1); in stages 4-5 (vs. stage 3), we found significant changes only in the classic marker, Cr, and a trend towards increased CystC. Moreover, we found that at stages 1-2 all patients showed higher levels of BTP and proBNP when compared to the median value in the control group; TIMP-1 and ADMA were increased in 7/9 patients; TNF-α was increased in 7/9 patients; and 7/9 patients had lower values of TGF-β compared to the median value of controls. For the classical markers, Cr and CystC, we found that 5/9 and 4/9 patients, respectively, had lower values than the median value of controls; however, only 2/9 patients showed abnormal creatinine values (vs. reference values). Conclusion Our data suggest that a panel including classic (Cr and CystC) and more sensitive blood markers of the primary response to renal injury (BTP, TIMP-1 or TGF-β, ADMA, TNF-α and proBNP) would allow an earlier diagnosis of CKD, avoiding a delay in diagnosis and management of CKD patients.

Efeitos do Tratamento Crônico com Sinvastatina na Função Renal de Ratos Submetidos a um Modelo Experimental de Doença Renal Crônica/ Effects of Chronic Treatment with Sinvastatin on Renal Function in Rats Subjected to an Experimental Model of Chronic Ki

1970 ◽  
Vol 4 (2) ◽  
pp. 64-73
Author(s):  
André Luiz Rios Dos Santos ◽  
Nilo César do Vale Baracho
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Experimental Model ◽  
Chronic Treatment ◽  
Chronic Renal Disease ◽  
Male Rats ◽  
Control Group ◽  
Group 2 ◽  
Moderate Chronic Kidney Disease

Objetivos: Avaliar os efeitos do tratamento crônico com sinvastatina na função renal de ratos submetidos a um modelo experimental de doença renal crônica. Metodologia: Foram utilizados 30 ratos, machos, adultos jovens, da linhagem Wistar, com peso entre 200 e 250 g e idade entre 60 e 90 dias. Os animais foram divididos aleatoriamente em 3 grupos com 10 ratos cada. Foi realizada a cirurgia seguindo o modelo experimental de doença renal crônica moderada (DRC-M) baseado na metodologia descrita por Ormrod & Miller, 1980. Após os procedimentos cirúrgicos, os animais receberam os referidos tratamentos, por um período de duas semanas: Grupo 1 - Animais com DRC-M tratados com água destilada VO (Gavagem) (n=10). Grupo 2 - Animais com DRC-M tratados com 5mg/Kg de sinvastatina VO (n=10). Grupo 3 - Animais com DRC-M tratados com 10mg/Kg de sinvastatina VO (n=10). Resultados: A indução de DRC-M não produziu alterações significativas sobre o débito urinário, ingesta hídrica, ingesta alimentar e parâmetros da função renal estudados, quando comparados o grupo controle com sinvastatina 5mg/Kg ou com sinvastatina 10mg/Kg ou quando comparados os grupos sinvastatinas entre si. Conclusão: Esses dados demonstram que o tratamento com sinvastatina, independente da dosagem do trabalho, não produziu melhora da função renal de ratos submetidos a um modelo experimental de Doença Renal Crônica Moderada (DRC-M).  Palavras-chave: doença renal crônica, sinvastatina, experimentos com ratos ABSTRACT Objectives: To evaluate the effects of chronic treatment with sinvastatin on renal function in rats subjected to an experimental model of chronic renal disease. Methods: 30 male rats were young adults, the Wistar strain, weighing between 200 and 250 g and aged between 60 and 90 days were used. The animals were randomly divided into 3 groups with 10 rats in each. Surgery was performed following the experimental moderate chronic (CKD-M) model of kidney disease based on the methodology described by Miller & Ormrod, 1980. After the surgical procedures, animals receive these treatments for a period of two weeks: Group 1 - animals with CKD-M with distilled water and treated orally (gavage) (n = 10). Group 2 - animals with CKD-M and treated with sinvastatin 5mg/kg orally (n = 10). Group 3- animals with CKD-M and sinvastatin treated with 10mg/kg orally (n = 10). Results: Induction of CKD-M produced no significant change on urine output, fluid intake, food intake and renal function parameters studied when comparing the control group with sinvastatin or sinvastatin 5mg/kg or 10mg/kg when comparing groups sinvastatin to each other. Conclusion: These data demonstrate that treatment with sinvastatin dosage independent from the work produced no improvement in renal function in rats subjected to an experimental model of Moderate Chronic Kidney Disease (CKD-M). Keywords: Chronic Kidney Disease, sinvastatin, experiments with rats. 

scholarly journals Sodium bicarbonate to improve physical function in patients over 60 years with advanced chronic kidney disease: the BiCARB RCT

2020 ◽  
Vol 24 (27) ◽  
pp. 1-90 ◽  
Author(s):  
Miles D Witham ◽  
Margaret Band ◽  
Huey Chong ◽  
Peter T Donnan ◽  
Geeta Hampson ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Confidence Interval ◽  
Sodium Bicarbonate ◽  
Serum Bicarbonate ◽  
Advanced Chronic Kidney Disease ◽  
Bicarbonate Therapy ◽  
Oral Sodium

Background Advanced chronic kidney disease is common in older people and is frequently accompanied by metabolic acidosis. Oral sodium bicarbonate is used to treat this acidosis, but evidence is lacking on whether or not this provides a net gain in health or quality of life for older people. Objectives The objectives were to determine whether or not oral bicarbonate therapy improves physical function, quality of life, markers of renal function, bone turnover and vascular health compared with placebo in older people with chronic kidney disease and mild acidosis; to assess the safety of oral bicarbonate; and to establish whether or not oral bicarbonate therapy is cost-effective in this setting. Design A parallel-group, double-blind, placebo-controlled randomised trial. Setting The setting was nephrology and geriatric medicine outpatient departments in 27 UK hospitals. Participants Participants were adults aged ≥ 60 years with advanced chronic kidney disease (glomerular filtration rate category 4 or 5, not on dialysis) with a serum bicarbonate concentration of < 22 mmol/l. Interventions Eligible participants were randomised 1 : 1 to oral sodium bicarbonate or matching placebo. Dosing started at 500 mg three times daily, increasing to 1 g three times daily if the serum bicarbonate concentration was < 22 mmol/l at 3 months. Main outcome measures The primary outcome was the between-group difference in the Short Physical Performance Battery score at 12 months, adjusted for baseline. Other outcome measures included generic and disease-specific health-related quality of life, anthropometry, 6-minute walk speed, grip strength, renal function, markers of bone turnover, blood pressure and brain natriuretic peptide. All adverse events were recorded, including commencement of renal replacement therapy. For the health economic analysis, the incremental cost per quality-adjusted life-year was the main outcome. Results In total, 300 participants were randomised, 152 to bicarbonate and 148 to placebo. The mean age of participants was 74 years and 86 (29%) were female. Adherence to study medication was 73% in both groups. A total of 220 (73%) participants were assessed at the 12-month visit. No significant treatment effect was evident for the primary outcome of the between-group difference in the Short Physical Performance Battery score at 12 months (–0.4 points, 95% confidence interval –0.9 to 0.1 points; p = 0.15). No significant treatment benefit was seen for any of the secondary outcomes. Adverse events were more frequent in the bicarbonate arm (457 vs. 400). Time to commencement of renal replacement therapy was similar in both groups (hazard ratio 1.22, 95% confidence interval 0.74 to 2.02; p = 0.43). Health economic analysis showed higher costs and lower quality of life in the bicarbonate arm at 1 year, with additional costs of £564 (95% confidence interval £88 to £1154) and a quality-adjusted life-year difference of –0.05 (95% confidence interval –0.08 to –0.01); placebo dominated bicarbonate under all sensitivity analyses for incremental cost-effectiveness. Limitations The trial population was predominantly white and male, limiting generalisability. The increment in serum bicarbonate concentrations achieved was small and a benefit from larger doses of bicarbonate cannot be excluded. Conclusions Oral sodium bicarbonate did not improve a range of health measures in people aged ≥ 60 years with chronic kidney disease category 4 or 5 and mild acidosis, and is unlikely to be cost-effective for use in the NHS in this patient group. Once other current trials of bicarbonate therapy in chronic kidney disease are complete, an individual participant meta-analysis would be helpful to determine which subgroups, if any, are more likely to benefit and which treatment regimens are more beneficial. Trial registration Current Controlled Trials ISRCTN09486651 and EudraCT 2011-005271-16. The systematic review is registered as PROSPERO CRD42018112908. Funding This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment; Vol. 24, No. 27. See the NIHR Journals Library website for further project information.

Iron-based phosphorus chelator: Risk of iron deposition and action on bone metabolism in uremic rats

2021 ◽  
pp. 153537022110572
Author(s):  
Wander Barros do Carmo ◽  
Bárbara Bruna Abreu Castro ◽  
Luísa Cardoso Manso ◽  
Priscylla Aparecida Vieira do Carmo ◽  
Clóvis Antônio Rodrigues ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Parathyroid Hormone ◽  
Calcium Carbonate ◽  
Kidney Disease ◽  
Therapeutic Option ◽  
Fractional Excretion ◽  
Control Group ◽  
Clinical Settings ◽  
Iron Based

Phosphate chelators are frequently used in patients with chronic kidney disease (CKD). New iron-based chelators remain understudied and offer a promising therapeutic option for the control of bone and mineral disorders of chronic kidney disease (BMD-CKD). We assessed the effect of the phosphorus chelator, chitosan-iron III (CH-FeCl), compared to calcium carbonate (CaCO3) in BMD-CKD and the potential iron overload in uremic rats. Thirty-two animals were divided into four groups, namely the control, CKD, CKD/CH-FeCl, and CKD/CaCO3 groups. CKD was induced by adding 0.75% (4 weeks) and 0.1% (3 weeks) adenine to the diet. The chelators were administered from week 3 through week 7. The renal function, BMD-CKD markers, and histomorphometry of the femur were assessed at week 7. The CKD group showed a significant increase in creatinine (83.9 ± 18.6 vs. 41.5 ± 22.1 µmol/L; P = 0.001), phosphate (3.5 ± 0.8 vs. 2.2 ± 0.2 mmol/L; P = 0.001), fractional excretion of phosphorus (FEP) (0.71 ± 0.2 vs. 0.2 ± 0.17; P = 0.0001), and FGF23 (81.36 ± 37.16 pg/mL vs. 7.42 ± 1.96; P = 0.011) compared to the control group. There was no accumulation of serum or bone iron after the use of CH-FeCl. The use of chelators reduced the FEP (control: 0.71 ± 0.20; CKD/CH-FeCl: 0.40 ± 0.16; CKD/CaCO3 0.34 ± 0.15; P = 0.001), without changes in the serum FGF23 and parathyroid hormone levels. Histomorphometry revealed the presence of bone disease with high remodeling in the uremic animals without changes with the use of chelators. The CH-FeCl chelator was efficient in reducing the FEP without iron accumulation, thereby paving the way for the use of this class of chelators in clinical settings in the future.

scholarly journals Recombinant Erythropoietin Provides Protection against Renal Fibrosis in Adenine-Induced Chronic Kidney Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Estefanía Vázquez-Méndez ◽  
Yanet Gutiérrez-Mercado ◽  
Edgar Mendieta-Condado ◽  
Francisco Javier Gálvez-Gastélum ◽  
Hugo Esquivel-Solís ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Renal Fibrosis ◽  
Inflammatory Cells ◽  
Erythropoietin Receptor ◽  
Control Group ◽  
Recombinant Erythropoietin ◽  
Tubular Atrophy ◽  
Human Recombinant Erythropoietin

Chronic kidney disease (CKD) causes anemia by renal damage. In CKD, the kidney is submitted to hypoxia, persistent inflammation, leading to fibrosis and permanent loss of renal function. Human recombinant erythropoietin (rEPO) has been widely used to treat CKD-associated anemia and is known to possess organ-protective properties that are independent from its well-established hematopoietic effects. Nonhematopoietic effects of EPO are mediated by an alternative receptor that is proposed to consist of a heterocomplex between the erythropoietin receptor (EPOR) and the beta common receptor (βcR). The present study explored the effects of rEPO to prevent renal fibrosis in adenine-induced chronic kidney disease (Ad-CKD) and their association with the expression of the heterodimer EPOR/βcR. Male Wistar rats were randomized to control group (CTL), adenine-fed rats (Ad-CKD), and Ad-CKD with treatment of rEPO (1050 IU/kg, once weekly for 4 weeks). Ad-CKD rats exhibited anemia, uremia, decreased renal function, increased infiltration of inflammatory cells, tubular atrophy, and fibrosis. rEPO treatment not only corrected anemia but reduced uremia and partially improved renal function as well. In addition, we observed that rEPO diminishes tubular injury, prevents fibrosis deposition, and induces the EPOR/βcR heteroreceptor. The findings may explain the extrahematopoietic effects of rEPO in CKD and provide new strategies for the treatment of renal fibrosis in CKD.

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