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.
Background. Allergic reactions to rituximab, which have been used for the past 20 years, are common in 32–62 % of patients. The purpose of the study: to develop an algorithm for controlling adverse reactions that occur during the introduction of rituximab. Materials and methods. The personal experience of treatment of 46 patients with various kidney diseases who received rituximab according to the indications according to the established diagnosis was analyzed. Evaluation of infusion allergic reactions was performed according to P.М. Kasi et al. (2012) for 5 classes of side effects. Results. It was found that allergic reactions to rituximab occurred in 46 % of patients in the range from 1 to 4 classes. The probability of their occurrence according to the class was almost the same, but somewhat less documented for the 4th grade. Re-administration of diphenhydramine, methylprednisolone 125 mg or hydrocortisone 125 mg, if necessary salbutamol, oxygen allowed to eliminate most of the reaction, and then resumed the introduction of rituximab, starting from 25 mg/h, gradually increasing to 300 mg/h. This administration, performed 1–2 times, was effective in 1–3 classes of allergic reactions. For fourth grade, one patient required omalizumab. Generalized experience allowed to give a graphical and descriptive algorithm of actions in case of infusion side effects for rituximab. Conclusions. Based on special data and literature analysis, an algorithm for controlling infusion allergic reactions with intravenous rituximab was formulated.
Background. SARS-CoV-2 infection in patients with chronic kidney disease (CKD) and hypertension degree 1–2 worsens the state of the cardiovascular system and may contribute to cardiovascular events and adverse renal risks. The presence of CKD in combination with hypertension degree 1–2 and its medical correction with renin-angiotensin-aldosterone system (RAAS) inhibitors causes a significant impact on the health of patients infected with SARS-CoV-2. SARS-CoV-2 uses RAAS, namely the receptor for angiotensin-converting enzyme (ACE) 2, as a tool to enter the cell. To choose further approaches and treatment, this combination of three pathological conditions requires careful analysis and research. Objective: to study the functional state of the kidneys in patients with CKD and hypertension infected with SARS-CoV-2. Materials and methods. The article is a fragment of the BIRCOV (ARB, ACE inhibitors, DRi in COVID-19) trial, which was designed according to the POEM (Patient-Oriented Evidence that Matters). The BIRCOV (two-center, open-label, initiative-randomized, in three parallel arms) prospective study enrolled 120 patients with CKD and hypertension degree 1–2, it lasted for 1 year and was registered at ClinicalTrials.gov (NCT03336203). One hundred and twelve outpatients with degree 1–2 hypertension, 83 with combination with CKD, were selected. At the end of the study, 108 patients remained, their results are presented in the article with subsequent statistical processing. Division into groups occurred depending on the drugs received (ACE inhibitors, angiotensin receptor blockers (ARBs) or direct renin inhibitor (DRIs)). Endpoints were: estimated glomerular filtration rate (eGFR), average blood pressure, albuminuria level. In 24 patients, the urine albumin to creatinine ratio was analyzed at the beginning of SARS-CoV-2, then 2, 4, 12, 24 weeks after the onset of the disease. Mathematical processing and statistical evaluation of the research results was done in the medical statistics package. Results. All patients were divided into 3 groups depending on the drug: 35 (32 %) of them received ARBs, 42 (39 %) ACE inhibitors, 31 (29 %) DRIs. At the manifestation of SARS-CoV-2, a decrease in blood pressure was recorded during the first two weeks, with the subsequent return to baseline on week 12 in the group of people who received ACE inhibitors, the lowest indicator was in the DRI group. The use of ACE inhibitors (risk ratio (RR) 1.648, 95% confidence interval (CI) 0.772–3.519, number needed to treat (NNT) 7.0) and ARBs (RR 13.023, 95% CI 1.815–93.426, NNT 19) in the treatment of hypertension significantly increased the risk of withdrawal compared to DRIs. Patients with CKD had similar dynamics of blood pressure during 24 weeks of observation. In CKD, higher mean blood pressure values were obtained compared to other participants of the BIRCOV trial. A simultaneous decrease in eGFR and systolic blood pressure was documented, it was most pronounced in patients with CKD. The lowest results were in people who took ACE inhibitors for 0–24 weeks: the correlation coefficient was 0.815. A decrease in eGFR correlated with the degree of CKD. There was a decrease in eGFR of less than 60 ml/min during the first 4 weeks from the onset of SARS-CoV-2 in 28 people who took ACE inhibitors versus 22 who used ARBs or DRIs: absolute risk was 0.667 (RR 2.00, 95% CI 1.337–2.92, NNT 3.0). The relative risk of eGFR reduction was 16.6 (95% CI 5.263–52.360, NNT 1.774) for people receiving ACE inhibitors versus all patients with CKD, 2.049 for ARBs (95% CI 0.361–11.22, NNT 1.774) and 1.064 for DRIs versus the entire sample of people with CKD (95% CI 0.116–9.797, NNT 431.6). After 12 weeks of follow-up, eGFR almost returned to baseline in CKD stage 2–3a. An increase in the urine albumin to creatinine ratio (which did not reach the baseline within 24 weeks from the onset of the disease) was recorded in CKD patients with stable renal function during the first 12 weeks from the onset of SARS-CoV-2 (the mean values of eGFR were not statistically different within 2–24 weeks). Males had a higher risk of CKD progression to end-stage renal disease. In people with SARS-CoV-2, on the second week from the onset of the disease, a decrease in eGFR was observed with a reciprocal increase in the level of blood uric acid, which differed significantly from the baseline values. The use of dexamethasone was accompanied by a decrease in eGFR (Р ≤ 0.05) and the preservation of these disorders in people with CKD stage 3b-4 up to 24 weeks of observation (RR 0.686, 95% CI 0.264–1.780, NNT 7.636). Conclusions. The course of SARS-CoV-2 in people with hypertension degree 1–2 was characterized by the development of significant hypotension among those taking ACE inhibitors, and in patients with CKD and hypertension taking ACE inhibitors — by a decrease in GFR, hypotension, an increase in albuminuria and in the urine albumin to creatinine ratio, which was transient in most cases. Albuminuria increased less significantly in patients taking ARBs and was practically unchanged when using DRIs. Patients with CKD stage 4 and hypertension degree 2 had the greatest risks of an unfavorable prognosis. The authors hypothesized about the mechanism of SARS-CoV-2 effect when using ACE inhibitors that was similar to that of ARBs (ARB effect), i.e., in people who took ACE inhibitors, the effect of reducing blood pressure was comparable to that of the dual RAAS blockade with ACE inhibitors and ARBs.
Introduction and aim. There is evidence in the literature about a change in the effectiveness of inhibitors of the renin-angiotensin system (iRAS) in people with COVID-19. Considering different mechanisms of pressure reduction by different iRAS groups, one can expect differences in people with COVID-19 receiving these drugs. The aim of angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor blockers (ARB) and direct renin inhibitors (DRi) usage in COVID-19 (BIRCOV study) was to pinpoint clinical and laboratory differences in people with hypertension who received iRAS and suffered coronavirus infection. Material and methods. An open prospective trial of 108 patients was performed in subjects suffering from COVID-19 who have been receiving iRAS: ACEi, ARB or DRi as basic antihypertensive therapy. The disease follow-up was 12 and 24 weeks. A blood pressure (BP) measurement was performed the week before COVID-19 and up to 24 weeks from the disease onset. Subanalysis in patients with chronic kidney disease (CKD) was performed. Results. In patients with COVID-19, a change in the effectiveness of antihypertensive therapy depending on the type of drug in the iRAS group has been documented in the first 4 weeks from the onset of the disease. The use of ACEi had significantly increased the risk of severe hypotension, unlike ARBs that do not cause hypotension. The synchronous decline of estimated glomerular filtration rate (eGFR) and systolic BP was more pronounced in CKD patients followed by albuminuria incidence. The greatest decrease in eGFR was in people taking ACEi. Conclusion. People with grade 1-2 hypertension who are constantly receiving RAS inhibitors suffering from COVID-19 may develop hypotension with ACEi. COVID-19 leads to transient albuminuria and decreased glomerular filtration rate, which is especially dangerous for people with CKD 4-5.
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