Tissue synthesis of some components of the renin-angiotensin system in hypertensive patients with localized kidney cancer

Background. In the last decade, the relationship between arterial hypertension and the risk of developing kidney cancer (KC) has been pointed out. Some studies have shown that the metabolic imbalance of the components of the renal renin-angiotensin system (RAS) is associated with the development and progression of KC.

Objective: to study the state of RAS in tumor and peritumoral tissues in patients with KC on the background of arterial hypertension.

Materials and methods. In patients with localized KC T1N0M0 and grade I–II arterial hypertension without special treatment (n = 40) in the samples of tumor, peritumoral and histologically unchanged tissue, the levels of angiotensins 1, 2, 1–7 (AT1, AT2, AT(1–7)) of angiotensin-converting enzymes (ACE, ACE2) were determined by ELISA. The comparison group consisted of patients with RC without impaired blood pressure (n = 55).

Results. In patients with KC, the level of AT1 is 1.5 times higher (p <0.05), and AT2 is 1.6 times higher (p <0.05) in tumor tissue against the background of unchanged content in peritumoral tissue compared with histologically unchanged tissue. The level of ACE is higher than histologically unchanged tissue by 2.7 times, ACE2 – by 1.6 times (in all cases p <0.05), and in peritumoral tissue it is identical in histologically unchanged tissue.

In patients with KC and arterial hypertension, the level of AT1 and AT2 in the tumor tissue is 1.8 times higher (p <0.05) and 2.1 times (p <0.01), respectively, the content of AT(1–7) is 1.6 times (p <0.01). In peritumoral tissue, AT1 is 1.6 times higher (p <0.01) and AT2 is 1.9 times higher (p <0.05). The level of AT(1–7) in the peritumoral tissue is identical to the values in the histologically unchanged tissue. The content of ACE and ACE2 in tumor tissue is 3.6 and 2.9 times higher, respectively, and in peritumoral tissue is identical to that in tumor tissue. Correlation analysis revealed a reliable direct relationship in the studied groups for all parameters, while in the peritumoral tissue of hypertensive patients, the relationship between the average blood pressure and the RAS peptide and enzymes content had a higher tightness.

Conclusion. An increase in the levels of AT1 and AT2, ACE and ACE2 in the tumor tissues and peritumoral tissue in patients with localized KC, regardless of the presence of arterial hypertension at initially higher values in hypertensive patients, was shown. The presence of arterial hypertension in patients with KC changes the metabolism of local RAS in peritumoral tissue and is associated with an increase in the correlation between changes in the components of RAS and arterial hypertension.

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