Main Article Content
The study aimed at optimization of diagnosis and evaluation of chronic kidney disease (CKD) in hypertensive patients by studying the role of adipokines (leptin, omentin, visfatin, resistin) in patients with hypertension combined with chronic kidney disease. Materials and methods. The study enrolled 100 patients with hypertension of II and III degrees of Stage 2, of which 51 patients were diagnosed with chronic kidney disease. The control group consisted of 20 apparently healthy people. Results. Our study showed that leptin, omentin, resistin, and visfatin levels were significantly higher in patients with essential hypertension (EH) combined with CKD, in contrast to patients with EH without CKD and in the control group. The results of the Kraskel-Wallis dispersion analysis demonstrated that in patients with EH combined with CKD, adipokines significantly correlated with systolic blood pressure (BP), diastolic blood pressure, hypertension degree, body mass index, low-density lipoproteins, thyroglobulin, glomerular filtration rate, creatinine, end-diastolic size, relative wall thickness index, left ventricular myocardial mass, left ventricular myocardial mass index, presence of diastolic dysfunction, type of diastolic function. Conclusions. Hypertensive patients with CKD presented with a significant increase in adipokine levels (leptin, omentin, resistin, visfatin) in the blood compared to patients with EH without CKD (p < 0.05) and apparently healthy individuals (p < 0.05). The data obtained indicate that adipokines (leptin, omentin, resistin, visfatin) have a significant pathogenetic role in patients with hypertension combined with chronic kidney disease.
This work is licensed under a Creative Commons Attribution 4.0 International License.
Our edition uses the copyright terms of Creative Commons for open access journals.
Authors, who are published in this journal, agree with the following terms:
- The authors retain rights for authorship of their article and grant to the edition the right of first publication of the article on a Creative Commons Attribution 4.0 International License, which allows others to freely distribute the published article, with the obligatory reference to the authors of original works and original publication in this journal.
- Directing the article for the publication to the editorial board (publisher), the author agrees with transmitting of rights for the protection and using the article, including parts of the article, which are protected by the copyrights, such as the author’s photo, pictures, charts, tables, etc., including the reproduction in the media and the Internet; for distributing; for the translation of the manuscript in all languages; for export and import of the publications copies of the writers’ article to spread, bringing to the general information.
- The rights mentioned above authors transfer to the edition (publisher) for the unlimited period of validity and on the territory of all countries of the world.
- The authors guarantee that they have exclusive rights for using of the article, which they have sent to the edition (publisher). The edition (the publisher) is not responsible for the violation of given guarantees by the authors to the third parties.
- The authors have the right to conclude separate supplement agreements that relate to non-exclusive distribution of their article in the form in which it had been published in the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.
- The policy of the journal permits and encourages the publication of the article in the Internet (in institutional repository or on a personal website) by the authors, because it contributes to productive scientific discussion and a positive effect on efficiency and dynamics of the citation of the article.
- The rights to the article are deemed transferred by the authors to the edition (the publisher) since the moment of the publication of the article in the printed or electronic version of journal.
GBD 2015 Mortality and Causes of Death Collaborators. Global, regional, and national life expectancy, all-cause mortality, and cause-specifi c mortality for 249 causes of death, 1980-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016 Oct 8;388(10053):1459-1544. doi:10.1016/S0140-6736(16)31012-1.
Solini A, Ferrannini E. Pathophysiology, prevention and management of chronic kidney disease in the hypertensive patient with diabetes mellitus. J Clin Hypertens (Greenwich). 2011 Apr;13(4):252-257. doi:10.1111/j.1751-7176.2011.00446.x.
Axelsson J, Bergsten A, Qureshi AR, et al. Elevated resistin levels in chronic kidney disease are associated with decreased glomerular filtration rate and inflammation, but not with insulin resistance. Kidney Int. 2006 Feb;69(3):596-604. doi:10.1038/sj.ki.5000089.
Malyszko J, Malyszko JS, Mysliwiec M. Visfatin, a new adipocytokine, is predominantly related to inflammation/endothelial damage in kidney allograft recipients. Transplant Proc. Jan-Feb 2009;41(1):150-153. doi:10.1016/j.transproceed.2008.10.086.
Doumatey AP, Zhou J, Huang H, et al. Circulating adiponectin is associated with renal function independent of age and serum lipids in west africans. Int J Nephrol. 2012;2012:730920. doi:10.1155/2012/730920.
Kidney Disease: Improving Global Outcomes (KDIGO) Hepatitis C Work Group. KDIGO 2018 Clinical Practice Guideline for the Prevention, Diagnosis, Evaluation, and Treatment of Hepatitis C in Chronic Kidney Disease. Kidney Int Suppl (2011). 2018 Oct;8(3):91-165. doi:10.1016/j.kisu.2018.06.001.
Inker LA, Heerspink HJL, Tighiouart H, et al. GFR Slope as a Surrogate End Point for Kidney Disease Progression in Clinical Trials: A Meta-Analysis of Treatment Effects of Randomized Controlled Trials. J Am Soc Nephrol. 2019 Sep;30(9):1735-1745. doi:10.1681/ASN.2019010007.
Tekce H, Tekce BK, Aktas G, Alcelik A, Sengul E. Serum omentin-1 levels in diabetic and nondiabetic patients with chronic kidney disease. Exp Clin Endocrinol Diabetes. 2014 Sep;122(8):451-456. doi:10.1055/s-0034-1375674.
Gansevoort RT, Correa-Rotter R, Hemmelgarn BR, et al. Chronic kidney disease and cardiovascular risk: epidemiology, mechanisms, and prevention. Lancet. 2013 Jul 27;382(9889):339-352. doi:10.1016/S0140-6736(13)60595-4.
Tomey MI, Winston JA. Cardiovascular pathophysiology in chronic kidney disease: opportunities to transition from disease to health. Ann Glob Health. 2014 Jan-Feb;80(1):69-76. doi:10.1016/j.aogh.2013.12.007.
Hsueh YM, Chen WJ, Lin YC, et al. Adiponectin gene polymorphisms and obesity increase the susceptibility to arsenic-related renal cell carcinoma. Toxicol Appl Pharmacol. 2018 Jul 1;350:11-20. doi:10.1016/j.taap.2018.04.034.