Özet:

Introduction: Hypoxia-inducible factor-1 (HIF-1) is the protein product of the gene with the same name that is induced by hypoxia and induces a series of reactions that act in the adaptive response of the cell. HIF-1 activation is a primary defense mechanism against the hypoxia of the tissue. In general, it is activated when tissue oxygenation is disrupted. Tissue hypoxia in kidney disease provides adaptation to the current situation by activating the HIF-1 alpha level. In this report, it was aimed to measure HIF-1 alpha levels in early stage renal failure patients, compare them with healthy volunteers, and evaluate the relationship between HIF-1 alpha and other biochemical and inflammatory parameters. Methods: This study included 22 healthy subjects (male/ female; 8/14) as the control group and 25 patients (male/ female; 11/14) who are followed up in the outpatient clinic with the diagnosis of early stage renal failure (glomerular filtration rate 60-90 mL/min/1.73m²). HIF-1 alpha level, biochemical parameters [glucose, creatinine, uric acid, aspartate aminotransferase (AST), alanine aminotransferase (ALT)], hemoglobin and inflammatory parameters [C-reactive protein (CRP), neutrophil/lymphocyte ratio], platelet count (PLT), platelet parameters [mean platelet volume (MPV), plateletcrit (PCT) and platelet distribution width (PDW)] were viewed in venous blood samples in both groups, and results were compared using descriptive statistical methods as well as Mann-Whitney U, chi-square, student t-test. Results: HIF-1 alpha, glucose, AST, ALT, gamma-glutamyl transpeptidase (GGT), PLT, MPV, PCT and PDW values were not statistically significantly different (p>0.05) among the case and control groups. There was no statistically significant correlation (p>0.05) between HIF-1 alpha and glucose, urea, creatinine, AST, GGT, CRP, neutrophile/lymphocyte ratio, PLT, MPV, PCT, PDW values. Conclusion: It is known that chronic hypoxia is an important factor in the progression of chronic renal diseases regardless of the underlying cause. It was assumed that the factors including normotension, normal hemoglobin level and the presence of medical therapy reducing oxidative stress (angiotensin converting enzyme inhibitors and angiotensin receptor blockers) in the patientsimproved renal hypoxia and therefore affected the results of this study.

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