The evaluation of renin, aldosterone, angiotensin and lipid metabolism genes in pathogenesis of primary childhood hypertension and relation between genotype and fenotype

Primary hypertansion growth in children parallels the growth of children's obesity prevelans. Childhood hypertansion is known to cause hypertansion in adulthood. Epigenetic alterations also have an effect on the cause of hypertansion. In this article the etiological factors of hypertansion and the genetic polymorphism are investigated. In this study which consists of 100 children from whom 50 are sick and the other 50 shape the control group, we investigated their age, gender, BMI, family history, blood glucose and lipids levels, their weight and height measurements and perantiles on hypertansion diagnosis, medications, weight and height controls after receiving therapy and target- organ damage. ACE, renine, angiotensin, aldosterone, FABP2, ApoB100 polymorphisms were evaluated. The average BMI of the sick children was 28.6 and the control group's was 19.2. It was established that the BMI of the children with elevated blood pressure is significantly higher (p<0.001) compared to that of the control group. Upon family history investigation we found that %40 of the patients had a member with hypertansion in their families whereas no family member of the childen in control group had elevated blood pressure. There was a significant difference in hypertansion existence in the families of the patients and the healthy children's(p<0.001). 14 (%70) of the 20 patients had a first- degree relative with hypertansion. In the biochemical examinations which were conducted in both groups, only the average HDL levels of the patients were found significantly lower of those of the control group (p<0.001). When investigated in the patients' group target- organ damage, the clinical outcome of most significance in hypertansion, was detected in 8 children (%16). 7 of those had shown only cardiac damage while one had also renal damage. When ACE, renine, angiotensin, aldosterone, FABP2, ApoB100 polymorphism distribution range was investigated (with 1 homozygous dominant, 1 homozygous recessive and heterozygous grouping) there were reported nostatistical differences of value. The trinary grouping of genotypes, the high rate of homozygosity in patients and the other ways of grouping when the differences between the sick and healthy were evaluated, there were also reported no significant statistical differences. The genetic polymorphisms detected in hypertansion and related diseases reported by other studies there were found no relativity to the outcomes of our research or there were reported results that were in contrast to ours. In cases where opposing outcomes due to epigenetic interference are reported, studies associated with the etiology of primary hypertansion should be conducted on a larger group of patients and would require patient and control groups representative of various populations.