Potential protective effect of leptin and uncoupling protein-2 genes polymorphism in Egyptian patients with chronic kidn
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NEPHROLOGY - ORIGINAL PAPER
Potential protective effect of leptin and uncoupling protein‑2 genes polymorphism in Egyptian patients with chronic kidney disease Esraa A. Ghazaly1 · Afaf M. EL‑Saeed2 · Mostafa Abdelsalam3 · Dina M. Seoudi1 Received: 12 March 2020 / Accepted: 7 July 2020 © Springer Nature B.V. 2020
Abstract Background Kidney disease is a serious public health problem worldwide. It is the fifth top-ranking cause of death in Egypt, causing approximately 3.98% of all deaths. This study’s objective was to examine whether an association exists between leptin (− 2548G/A) and uncoupling protein-2 45 bp I/D genes, individually and collectively, in CKD and progression to ESRD. Methods One hundred patients (69 males, 31 females) aged (47.1 ± 16.11 years) with ESRD, 40 patients (19 males, 21 females) aged (43.15 ± 10.00 years with CKD, and 50 healthy controls (23 males, 27 females) aged (37.84 ± 1.95 years) were enrolled. Polymerase chain reaction (PCR) was employed to measure variation in gene expression among the study groups. The frequency of single nucleotide polymorphisms (SNP) genotypes were identified in controls, CKD and ESRD patients. Results Leptin genotypes were associated with lower CKD incidence in control versus study subjects (95% CI = (0.08–0.63), P = 0.01) with risk value equal to 0.22 90 ml/min/1.73 m2, with no abnormal ultrasound findings and within normal urine analysis values were included. Patients with active infection, heart failure, thyroid disorders, suprarenal diseases, dehydration, anemia, elevated liver enzymes, chronic hepatitis B virus, human immunodeficiency virus, patients with drug-induced, genetic or metabolic
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International Urology and Nephrology
induced nephropathy, overlap syndrome, and those with neoplastic disorders were excluded. An 8 ml venous blood sample was withdrawn from each participant and divided as follows: 5 ml was placed in a plain tube and allowed to clot for 10–15 min, centrifuged for 10 min at 5000 g. Separated serum was used to calculate hemoglobin, serum creatinine, calcium, phosphate, parathormone hormone (PTH), albumin, total bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and fasting blood sugar (FBS) concentrations using commercially available kits supplied for human samples (Spinreact, Co., Spain). The remaining 3 ml was placed in an EDTA-coated tube for detection of gene polymorphisms.
DNA extraction from blood DNA was extracted from the blood samples were using QIAamp DNA Blood Mini Kit (Qiagen, Hilden, Germany) according to the manufacturers’ protocol.
Genotyping of the leptin − 2548G/A and UCP‑2 genes polymorphism Leptin G/A polymorphisms were determined according to the method of Catherine et al. [13]. The sequences of the forward and reverse primers were (5′-TTT CCT GTA ATT TTC CCG TGA G-3′) and (5′-AAA GCA AAG ACA GGC ATA AAA A-3′), respectively. PCR determined the UCP-2 genotypes (DD, ID, and II) according to the method of Hashemi et al. [14]. The sequences of the forward and reverse primers were (5′
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