BACKGROUND. The presence and drug correction of arterial hypertension (AH) with inhibitors of the renin-angiotensin system (RAS), as well as chronic kidney disease (CKD) and its role in the regulation of RAS, can significantly affect the condition of a person with COVID-19. OBJECTIVE: to study the features of the functional state of the kidneys in patients with grade 1-2 hypertension who have fallen ill with COVID-19. PATIENTS AND METHODS. A subanalysis of patients with CKD, participants in the BIRCOV study (ARB, ACEi, DRi in COVID-19) is presented: 112 outpatient patients with grade 1-2 hypertension, 83 of whom had CKD. The participants were divided into groups receiving ACE inhibitors (group 1 – 39 %), ARBs (group 2 – 32 %), or a direct renin inhibitor (PIR) (group 3 – 29 %) as the main therapy of hypertension. The value of blood pressure, eGFR, albuminuria level were analyzed at the debut of COVID-19 and at 2, 4, 12, 24 weeks from the onset of the disease. RESULTS. In the first two weeks of COVID-19, there was a decrease in blood pressure with a gradual return to baseline values in patients of group 1 and group 3 (to a lesser extent). The use of ACE inhibitors in the treatment of hypertension increased the risk of withdrawal compared to PIR and ARBs due to COVID-19. In patients with CKD, higher values of mean blood pressure were obtained with similar dynamics. A synchronous decrease in eGFR and systolic blood pressure has been documented, more pronounced in patients with CKD, especially when taking aCEI. The decrease in eGFR correlated with the stage of CKD. With stable renal function in patients with CKD during the first 12 weeks of COVID-19, the urine albumin/creatinine ratio (UAC) increased without further normalization. By the second week of the disease, eGFR decreased with a reciprocal increase in the level of uric acid in the blood. The use of dexamethasone was accompanied by a decrease in eGFR in CKD stages 3b-4. CONCLUSION. When taking ACE inhibitors, the effect of lowering blood pressure was comparable to a double block of RAS: ACE inhibitors + ARBs.