ABSTRACT
Objective: To assess clinical and pathomorphological features of kidney damage in patients with arterial hypertension (AH) who died of the new coronavirus infection COVID-19. Design and method: A complex analysis of 268 kidney autopsies was carried out, including the study of macro- and microscopic changes reflected in the protocols of pathological and anatomical autopsies and identified during the histological examination. In 224 patients (83.6%) with AH, the diagnosis was confirmed by isolating the SARS-CoV-2 RNA using the polymerase chain reaction;in 44 (16.4%) - through computed tomography of the lungs. The causes of deaths were the following: in 31 patients (11.6%) acute myocardial infarction;in 40 (14.9%) cerebrovascular accident;in 11 (4.1%) pulmonary embolism;222 patients (83%) had acute respiratory distress syndrome. The analysis included 130 men aged 36 to 92 (72.6 years old on average) and 138 women aged 40 to 106 (77.1 years old on average). Results: In the kidneys we detected ischemic changes caused by disturbances in the microvasculature. These are stases, sludges, erythrocyte and fibrin thrombi predominantly in the medulla. In the glomeruli diapedesis hemorrhages, mesangial cells proliferation, basement membrane thickening and fibrinoid necrosis of the capillary wall were observed. In the epithelium of the convoluted tubules, a granular, hyaline-drop dystrophy and a necrosis as the extreme degree of the damage were noted. In the kidneys, a pronounced lymphoid and leukocyte infiltration was detected. These changes were accompanied by inflammation and renal failure symptoms. In particular, the level of C-reactive protein was 140.6 ± 7.42 mg/l;blood ferritin 1258.0 ± 110.1 mcg/l;blood leukocytes 15.0 ± 0.67 10
ABSTRACT
Objective: To determine risk factors for post-COVID-19 syndrome development in patients with arterial hypertension (AH). Design and method: A total of 81 patients with AH were examined 3-6 months after COVID-19. 48 people (group 1: 27 women, 21 men) suffered from SARSCoV- 2 pneumonia with lungs lesion from 15% to 74%. The patients' age was 18-87 years old (65 years old on average). In 38 patients chronic ischemic heart disease (IHD) was diagnosed;in 18 - myocardial infarction (MI);in 10 - permanent atrial fibrillation (AF);in 12 - AF paroxysms. 33 people (group 2: 18 women, 15 men) suffered from COVID-19 in the form of an acute respiratory illness without pneumonia. These patients were aged from 41 to 74 (56.9 years old on average). 25 patients had coronary artery disease;2 - MI;2 - permanent AF;4 - AF paroxysms. Results: Comparing to group 2, in group 1 the patients had higher blood pressure;higher left atrial volume index (LAVI) (35.1 ± 3.3 ml/m2 vs. 29.6 ± 3.2 ml/m2;p < 0.05);higher left ventricular (LV) end-diastolic volume index (EDVI) (76.1 ± 8.8 ml/m2 vs. 62.6 ± 10.3 ml/m2;p < 0.05);lower LV ejection fraction (EF) (56.1 ± 8.1% vs. 63.2 ± 3.9%;p < 0.05). In 7 group 1 patients, an increase in the frequency of AF attacks was detected. In group 1 symptoms of inflammation persisted for a long time: higher levels of C-reactive protein (15 ± 4.9 mg/l vs. 5.5 ± 3.8 mg/l), of blood ferritin (275 ± 106.3 mcg/l vs. 155.6 ± 85.8 mcg/l;p < 0.05), of D-dimer (919.3 ± 77.1 ng/ml vs. 609 ± 87.4 ng/ml;p < 0.05) as well as of total cholesterol (5.8 ± 1.2 mmol/l vs. 4.9 ± 1.1 mmol/l;p < 0.05) and of LDL (4.1 ± 1.1 mmol/l vs. 3.2 ± 1.3 mmol/l;p < 0.05). Conclusions: The revealed risk factors were high blood pressure, an increase in LAVI and LV EDVI, a decrease in LVEF, an increase in LDL, previous MI, and an increase in the frequency of AF paroxysms.