Маркери запалення у хворих на хронічну хворобу нирок з артерійною гіпертензією

Abstract

Aim. To make a comparative description of concentrations of markers of inflammation (CRP, IL-1β, IL-4, TNF-α) in patients with chronic kidney disease with and without hypertension in order to determine the possible mechanisms of progressive inflammation in patients. Material and Methods. The conventional clinical, laboratory (serum concentration of cytokines was performed by ELISA) and instrumental methods of examination were used in the study. The work is based on the results of the survey of 56 patients with chronic kidney disease (CKD) in stages II and-III (chronic glomerulonephritis and pyelonephritis) with and without hypertension of ²² degree. Results and Discussion. The results of our study show the dynamics of changes in rates of CRP, TNF-α, IL-lβ, IL-4 in CKD patients with hypertension background and with normal blood pressure. The CRP content was within 6,56-8,5 mg/L, with an average 7,53±0,92 mg/l in the main group of patients with CKD and hypertension. In the second comparison group of patients who were not hypertensive, range of CRP content in blood was within 4.78-6.46 mg/l (with an average of 5,62±0,84 mg/l). Comparison of the obtained changes in CRP in patients of both groups with controls showed a significant (p<0.01) increase of CRP. In patients with chronic kidney disease with hypertension this increase was higher and significantly different from that of the comparison group (p<0.05). The significant decreasing of anti-inflammatory cytokine IL-4 in serum of patients along with activation of proinflammatory mechanisms was observed. Conclusions. Development of CKD with the background of essential hypertension is associated with increased activity of cytokine component of the immune system. The principles of impact of hypertension on inflammation processes in renal patients profile are established. The assessment of the content of the inflammatory markers in patients with chronic kidney disease in dependence of blood pressure level, allowed us to assert their participation in the development of CKD, both in terms of direct effects of hypertension on cytokine profile in CKD and progression of chronic inflammation.