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Association of genetic variants of pentraxin 3 rs3816527 with hypertension in Chronic kidney disease patients

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Abstract

Hypertension is a nearly constant feature and both a cause and a consequence of chronic kidney disease (CKD). Atherosclerotic lesions showed a marked expression of pentraxin 3 on the surface of lumen and in the plaque. The aim was to assess the correlation of exon 2 of pentraxin 3 gene SNP rs3816527 with hypertension with CKD. The study was conducted on 110 CKD patients (60 patients with and 50 patients without hypertension) and 40 healthy subjects as control. Laboratory investigations including the measurement of fasting blood glucose, lipid profile, and indices of oxidative stress, liver function tests, and renal function tests were done. Genotyping of pentraxin 3 gene SNP rs3816527 was done by real-time PCR. There was a significant difference between CKD patients with hypertension and the subjects in the control group regarding systolic and diastolic BP, urea, creatinine, GFR, TG, cholesterol, LDL, HDL, and total antioxidant levels (p < 0.001). There is a statistically significant difference between CKD patients with hypertension and the other studied groups regarding the frequencies of AA genotype and A allele of exon 2 SNP of pentraxin 3 gene compared to CC genotype and C allele (wild type) (p < 0.001), while there was significant difference between CKD patients without hypertension and control (p > 0.05). Pentraxin 3 AA genotype SNP rs3816527 can be considered as a potential biomarker and a risk factor for CKD patients, especially hypertensive patients, and specifically as an independent predictor of hypertension in CKD.

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Correspondence to Safaa I. Tayel.

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The study was conducted in accordance with the Declaration of Helsinki. All participants provided written informed consent, and the Ethics Committee of Faculty of Medicine, Menoufia University approved the study protocol.

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Badr, E.A.E., Hamoda, G.E., Tayel, S.I. et al. Association of genetic variants of pentraxin 3 rs3816527 with hypertension in Chronic kidney disease patients. Mol Cell Biochem 425, 203–212 (2017). https://doi.org/10.1007/s11010-016-2874-z

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  • DOI: https://doi.org/10.1007/s11010-016-2874-z

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