الفهرس 
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Abstract
Anaemia is a commonly diagnosed complication among patients suffering from chronic kidney disease. If left untreated, it may affect the patient’s quality of life. ESAs and iron supplementation are the cornerstones in the management of anaemia in CKD and dialysis. Emerging concepts about the RAS indicate that ACE is a critical regulator of angiotensin peptide metabolism and the pathogenesis of renal disease. There is a genetic variation within the ACE gene, a 278 base pair insertion/deletion (I/D) polymorphism, resulting in three different ACE genotypes: I/I, I/D, and D/D.
This study was performed at Sohag University Hospital from June 2021 to January 2022, with a population of 50 patients analyzed in a prospective way compared with 40 control cases. After the approval of the ethical committee of Sohag Faculty of Medicine, informed written consent was obtained from all individuals included in the study. All individuals were informed regarding the tests and their clinical meanings before the study.
Inclusion criteria:
1. Patients treated with haemodialysis for three months or more.
2. Age 18 years or above.
3. Sub cutaneous injection of either alpha or beta epoetin for renal anaemia.
Exclusion criteria are:
1. Recent symptoms and signs of bleeding that required a blood transfusion.
2. Acute renal failure.
3. Malignant disease.
4. Haematologic disease.
5. Acute infectious disease.
It was designed to:
1. Evaluate the association of ACE gene polymorphism rs1797552 with chronic kidney disease on maintenance hemodialyzed patients in Sohag.
2. Examine the association between this polymorphism, serum EPO, and haemoglobin (HB) levels.
3. Assess how hemodialyzed patients with varied ACE genotypes respond to alphaerythropoietin.
4. Clarify factors affecting erythropoietin resistance.
In the present study, we found significant differences between the three genotypes, with DD being the most common. There was a significant difference in the distribution of D and I alleles, with D being the most prevalent. The D allele was associated with an increased risk of chronic glomerulonephritis but not with an increased risk of diabetic nephropathy type 2 with hypertension.
There were significant differences in laboratory markers such as plasma urea, creatinine, HB, Hct, platelets count, and WBCs between HD patients and healthy controls.
We found a significant boost in serum EPO levels in patients with CKD with DD and ID genotypes comparable to II genotype using quantitative analysis of serum EPO, HB, and ACE gene polymorphism. Patients with the ID genotype had higher EPO and HB levels, followed by the DD and II genotypes.
The correlation between EPO and HB in the control group was insignificant both overall and according to different ACE genotypes. The overall correlation between EPO and HB in the patients’ group was insignificant, however, only ID genotype had high negative significant correlation.
Non significant difference between different ACE genotypes and Erythropoietin resistance index, with ID being the least resistant and II being the most resistant. Non significant correlation between Para thyroid hormone and Erythropoietin resistance index. Non significant correlation between duration of dialysis and EPO level. Significant correlation between ferritin and Erythropoietin resistance index.
Conclusion:
The polymorphism in the angiotensin-converting enzyme gene had a considerable effect on serum erythropoietin and haemoglobin levels. Genotypes of the Angiotensin-converting enzyme played a role in chronic kidney disease. The D allele was found to be a substantial risk factor for chronic glomerulonephritis. In patients on frequent haemodialysis who received alphaerythropoietin, ACE genotypes played no significant role in the Erythropoietin resistance index. There was a significant variation in the allele distribution (D and I alleles) between the patients and the controls, with DD being the most common.
Recommendation:
1. The present study needs to be done over a wider scale of patients.
2. Screening for ACE (rs1799752) gene polymorphism before rHuEpo injection in patients on frequent haemodialysis may assist predict patient response.
3. Atrial of holding ACE inhibitor therapy could potentially increase the erythropoietin response in some patients on frequent haemodialysis.
4. We propose that our Egyptian community, which is predominantly DD, avoid risk factors for chronic Glomerulonephritis, Hypertension, and Diabetes Mellitus.
5. We advocate capturing numerous potential confounders, such as iron status, previous kidney transplantation, immunosuppressive medication use, and para thyroid hormone level, all of which are likely to impact erythropoiesis in individuals undergoing recurrent haemodialysis.