Abstract
This study designed to examine association between-174G/C polymorphism of interleukin-6 gene and phosphate, calcium, vitamin D3, and parathyroid hormone levels in Iraqi patient with chronic kidney disease on maintenance hemodialysis. Seventy chronic renal failure patients (patients group) and 20 healthy subjects (control group) were genotyped for interleukin-6 polymorphism and genotyping was performed by conventional polymerase chain reaction-restriction fragment length polymorphism. No significant differences in phosphate levels were observed in patients and control with different interleukin-6 genotypes. Control had non-significant differences in calcium levels, while patients with GG and CG genotypes displayed significant elevation with time. Conversely, control and patients with GG and CC genotypes had significant elevation in vitamin D3 levels with time. Regarding parathyroid hormone, control had non-significant differences, while patients with GG and CC genotypes displayed significant elevation with time.
 Patients with GG genotype displayed significant changes in calcium, vitamin D3 and parathyroid hormone levels with time.
Highlights
The effect of genetic variation in renal failure development is becoming clearer and highlights the necessity to demonstrate the genetic basis for renal diseases as well as their complications [1]
The major complications related to chronic kidney disease (CKD) include cardiovascular disease, neuropathy, infectious complications, anemia, and abnormalities related to mineral bone metabolism [2]
Marckmann et al [24] reported that cholecalciferol supplementation in CKD patients caused a significant elevation in 1,25(OH)2 vitamin D3. This increment was statistically significant in nonhemodialysis patients, while in patients on hemodialysis, the increase was smaller and nonsignificant. These findings indicate that circulating concentrations of -25-(OH) -vitamin- -D are necessary for -the- production of -1,25(OH)2- vitamin D3 in CKD patients who have limited renal 1-α-hydroxylase activity [24]
Summary
The effect of genetic variation in renal failure development is becoming clearer and highlights the necessity to demonstrate the genetic basis for renal diseases as well as their complications [1]. The major complications related to chronic kidney disease (CKD) include cardiovascular disease, neuropathy, infectious complications, anemia, and abnormalities related to mineral bone metabolism [2]. Chronic kidney disease-mineral and bone disorder (CKD-MBD) is a systemic disorder of bone and mineral metabolism because of CKD usually explained by either one or a combination of the following: Abnormalities of biochemical parameters of phosphorus, calcium, parathyroid hormone (PTH), or vitamin D metabolism. Abnormalities of bone mineralization, volume, strength, turnover, or linear growth. Bone and mineral metabolism in end stage renal disease (ESRD) patients appears to be under the influence of genetic control, with various genes playing a critical role. Gene polymorphism association studies to date have revealed conflicting results with low reproducibility [6]
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