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Background: Anaemia is a very common cause of morbidity and mortality in patients with chronic kidney disease (CKD) on chronic haemodialysis7. The main aetiology of anaemia in CKD among patients on chronic haemodialysis is erythropoietin deficiency Aim: To determine the prevalence and associations of anaemia among patients on chronic haemodialysis at the PKDC in Limpopo Province, South Africa. Methods: A retrospective descriptive, cross-sectional quantitative study was performed at a single dialysis centre (PKDC) and included all patients on chronic haemodialysis over a one-year period (01/01/2019 to 31/12/2019). A standardized data collection form created on Epi Info Version 7 was used to collect data from 121 study participants’ hospital files. There was no sampling performed as all patients meeting the inclusion criteria were included in the study. The collected data was analysed using the SPSS Version 25. Results: A total of 121 patients were included in the study. In the final data analysis, 55.5%(n=66) were males and 45.4%(n=55) were females. The overall mean age was 41.9 ± 11.7 years. Using the WHO definition of anaemia (Hb< 13g/dl in males and Hb<12g/dl in females), prevalence of anaemia was 89.3% and 85% in male and female patients, respectively. All 121 (100%) patients were on erythropoietin (EPO). According to the 2012 KDIGO guidelines, the target Hemoglobin (Hb) in haemodialysis patients on EPO is between 10g/dl and 12g/dl. Using a Hb level < 10 g/dl to define anaemia, the overall prevalence of anaemia was 23.1%(n=28). The Chi-square test indicated that there were no associations between anaemia (Hb<10g/dl) and any of the clinical characteristics that were analyzed (all p-values > 0.05). Comparison of the means of two groups (Anaemia: No and Anaemia: Yes) using the t-test it was observed that the p-values were <0.001 and 0.007 for Hb and Albumin respectively. The null hypothesis was rejected, and we concluded that there was a difference between the Hb an

Erythropoietin (Epo) is produced by a subpopulation of resident fibroblasts in the healthy kidney. We have previously demonstrated that, during kidney fibrosis, kidney fibroblasts including Epo-producing cells transdifferentiate into myofibroblasts and lose their Epo-producing ability. However, it remains unclear whether Epo-producing cells survive and transform into myofibroblasts during fibrosis because previous studies did not specifically label Epo-producing cells in pathophysiological conditions. Here, we generated Epo[CreERT2/+] mice, a novel mouse strain that enables labeling of Epo-producing cells at desired time points and examined the behaviors of Epo-producing cells under pathophysiological conditions. Lineage -labeled cells that were producing Epo when labeled were found to be a small subpopulation of fibroblasts located in the interstitium of the kidney, and their number increased during phlebotomy-induced anemia. Around half of lineage-labeled cells expressed Epo mRNA, and this percentage was maintained even 16 weeks after recombination, supporting the idea that a distinct subpopulation of cells with Epo-producing ability makes Epo repeatedly. During fibrosis caused by ureteral obstruction, Epo[CreERT2/+] -labeled cells were found to transdifferentiate into myofibroblasts with concomitant loss of Epo-producing ability, and their numbers and the proportion among resident fibroblasts increased during fibrosis, indicating their high proliferative capacity. Finally, we confirmed that EpoCreERT2/+-labeled cells that lost their Epo-producing ability during fibrosis regained their ability after kidney repair due to relief of the ureteral obstruction. Thus, our analyses have revealed previously unappreciated characteristic behaviors of Epo-producing cells, which had not been clearly distinguished from those of resident fibroblasts.

Aims/Introduction: Clinical studies have shown that treatment with inhibitors of sodium–glucose cotransporter 2 (SGLT2) significantly increases the hematocrit in patients with type 2 diabetes. To investigate whether SGLT2 inhibitors directly promote erythropoietin production independently on blood glucose reduction, the hematopoietic effect of the specific SGLT2 inhibitor, luseogliflozin, was examined in non‐diabetic rats with renal anemia. Materials and Methods: Renal anemia was induced by treatment with adenine (200 or 600 mg/kg/day, orally for 10 days) in non‐diabetic Wistar–Kyoto or Wistar rats, respectively. Luseogliflozin (10 mg/kg bodyweight) or vehicle (0.5% carboxymethyl cellulose) was then administered for 6 weeks. The hematocrit and the hemoglobin (Hb), blood urea nitrogen, plasma creatinine, and plasma erythropoietin levels were monitored. Results: Treatment with adenine decreased the hematocrit and the Hb level, which were associated with increases in the blood urea nitrogen and plasma creatinine levels. In Wistar–Kyoto rats treated with 200 mg/kg/day adenine, administration of luseogliflozin induced glycosuria, but did not change the blood urea nitrogen, plasma creatinine levels, hematocrit, Hb or plasma erythropoietin levels. Similarly, luseogliflozin treatment failed to change the hematocrit or the Hb levels in Wistar rats with renal anemia induced by 600 mg/kg/day of adenine. Plasma erythropoietin concentrations were also not different between luseogliflozin‐ and vehicle‐treated rats. Similarly, in human erythropoietin‐producing cells derived from pluripotent stem cells, luseogliflozin treatment did not change the erythropoietin level in the medium. Conclusions: These data suggest that SGLT2 inhibitor fails to exert hematopoietic effects in non‐diabetic conditions.

V̇In this study the effects of renal anemia on exercise tolerance and cardiac function were evaluated in maintenance hemodialysis patients. Twenty-seven patients were classified into two groups according to hemoglobin concentration (Hb) level (Group A1 : patients with Hb 7.0 g/dl or more ; Group A2 : patients with Hb 7.0 g/dl or less). Peak oxygen consumption (⩒o₂ peak) and anaerobic threshold (AT) were measured by cardiopulmonary exercise test, echocardiography was carried out and arterial blood oxygen transport capacity (O₂ transport capacity) was calculated. Further, the fourteen patients of Group A2 were re-examined after correction of anemia by recombinant human erythropoietin (EPO). (1) The exercise tolerance of maintenance hemodialysis patients was significantly reduced, about 50 per cent compared with the control group, and Group A2 showed lower ⩒o₂ peak and AT level than Group A1. (2) There was a significant correlation between Hb and exercise tolerance, and a closer correlation was shown between O₂ transport capacity and exercise tolerance. (3) There were significant elevations in ⩒o₂ peak (17.6±4.9 to 22.5±4.5 ml/min/kg) and AT (9.8±3.6 to 13.4±3.3 ml/min/kg) after improvement of renal anemia by EPO. (4) Because of improvement of anemia by EPO, left atrial dimension, left ventricular end-diastolic dimension and left ventricular mass were decreased. (5) Because of improvement of anemia by EPO, each significant decrease was shown in heart rate, pressure rate product, blood lactate concentration and plasma norepinephrine concentration during steady-state exercise. These findings suggest that patients with anemia who are undergoing maintenance hemodialysis show remarkably decreased exercise tolerance, and correction of anemia by EPO improves cardiac function, exercise tolerance and neurohumoral response to exercise.

V̇In this study the effects of renal anemia on exercise tolerance and cardiac function were evaluated in maintenance hemodialysis patients. Twenty-seven patients were classified into two groups according to hemoglobin concentration (Hb) level (Group A1 : patients with Hb 7.0 g/dl or more ; Group A2 : patients with Hb 7.0 g/dl or less). Peak oxygen consumption (⩒o₂ peak) and anaerobic threshold (AT) were measured by cardiopulmonary exercise test, echocardiography was carried out and arterial blood oxygen transport capacity (O₂ transport capacity) was calculated. Further, the fourteen patients of Group A2 were re-examined after correction of anemia by recombinant human erythropoietin (EPO). (1) The exercise tolerance of maintenance hemodialysis patients was significantly reduced, about 50 per cent compared with the control group, and Group A2 showed lower ⩒o₂ peak and AT level than Group A1. (2) There was a significant correlation between Hb and exercise tolerance, and a closer correlation was shown between O₂ transport capacity and exercise tolerance. (3) There were significant elevations in ⩒o₂ peak (17.6±4.9 to 22.5±4.5 ml/min/kg) and AT (9.8±3.6 to 13.4±3.3 ml/min/kg) after improvement of renal anemia by EPO. (4) Because of improvement of anemia by EPO, left atrial dimension, left ventricular end-diastolic dimension and left ventricular mass were decreased. (5) Because of improvement of anemia by EPO, each significant decrease was shown in heart rate, pressure rate product, blood lactate concentration and plasma norepinephrine concentration during steady-state exercise. These findings suggest that patients with anemia who are undergoing maintenance hemodialysis show remarkably decreased exercise tolerance, and correction of anemia by EPO improves cardiac function, exercise tolerance and neurohumoral response to exercise.

Background : Renal anemia is a very serious problem in hemodialysis patients. In this regard, the investigation was focused on whether ultrapure dialysate could improve renal anemia and the mechanism of renal anemia. / Methods : Ultrapure dialysate was used over a 2 years period for 61 patients on maintenance hemodialysis. During this period, the changes in renal anemia and red blood cell life span were investigated. The changes in the latter were evaluated using the creatine concentration in red blood cell....

Background : Renal anemia is a very serious problem in hemodialysis patients. In this regard, the investigation was focused on whether ultrapure dialysate could improve renal anemia and the mechanism of renal anemia. / Methods : Ultrapure dialysate was used over a 2 years period for 61 patients on maintenance hemodialysis. During this period, the changes in renal anemia and red blood cell life span were investigated. The changes in the latter were evaluated using the creatine concentration in red blood cell....

The oxidative injury to erythrocytes, red blood cell (RBC) rigidity and splenic hemolysis was assayed in 17 chronically hemodialyzed patients before and during recombinant erythropoietin (EPO) treatment. When a stable hematocrit between 30 and 35% had been established for at least 4 months, a statistically significant increase in RBC volume, hemoglobin concentration, hematocrit, reticulocyte count, and several RBC enzymes (2,3-diphosphoglycerate, glucose 6-phosphate dehydrogenase, pyruvate kinase, hexokinase) was noted. This indicated significant RBC rejuvenation under the influence of EPO. However, no significant improvement in the RBC oxidative sensitivity, RBC deformability, splenic RBC volume, slow mixing splenic RBC volume, and the intrasplenic RBC transit time could be disclosed. These data confirm the existence of an extraerythrocytic factor in uremic plasma, which is partly responsible for a reduced RBC life span in hemodialysis patients despite EPO treatment.