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Background. Acute kidney injury often complicates the course of COVID-19; in many patients it develops even before hospitalization, and the reasons for its development are not sufficiently clear. Aim. To study the role of dehydration in the development of community-onset acute kidney injury in COVID-19. Material and methods. 329 patients with COVID-19 were examined (age 58.014.3 years, 172 men, 157 women). Acute kidney injury was diagnosed according to the Russian recommendations of 2020. To determine prerenal acute kidney injury, the ratio of blood urea nitrogen to blood creatinine was calculated, and to diagnose dehydration the calculated osmolarity of blood serum. Data are presented for a normal distribution as the arithmetic mean and standard deviation (MSD), for a non-normal distribution as a median (Me) and interquartile range (IQR). Univariate and multivariate logistic regression analyzes were used. To assess the diagnostic significance of quantitative characteristics in predicting a certain outcome, the ROC curve analysis method was used. Differences were considered statistically significant at p 0.05. Results. Acute kidney injury was diagnosed in 70 (21.3%) patients, of which 58 (82.9%) were community-acquired. In 16 (27.6%) patients with community-onset acute kidney injury, it was of a prerenal nature, of which in 13 (81.3%) the calculated serum osmolarity exceeded 295 mOsm/L. Independent factors directly associated with prerenal prehospital acute kidney injury were estimated serum osmolarity (p 0.001), C-reactive protein level (p 0.001) and age (p=0.003) (R2=0.23, F=33,34). Conclusion. Acute kidney injury complicates the course of COVID-19, and in most patients, it develops even at the prehospital stage. Estimated serum osmolarity is directly and independently associated with prerenal community-onset acute kidney injury, suggesting the important role of dehydration in its development.
Background. Acute kidney injury often complicates the course of COVID-19; in many patients it develops even before hospitalization, and the reasons for its development are not sufficiently clear. Aim. To study the role of dehydration in the development of community-onset acute kidney injury in COVID-19. Material and methods. 329 patients with COVID-19 were examined (age 58.014.3 years, 172 men, 157 women). Acute kidney injury was diagnosed according to the Russian recommendations of 2020. To determine prerenal acute kidney injury, the ratio of blood urea nitrogen to blood creatinine was calculated, and to diagnose dehydration the calculated osmolarity of blood serum. Data are presented for a normal distribution as the arithmetic mean and standard deviation (MSD), for a non-normal distribution as a median (Me) and interquartile range (IQR). Univariate and multivariate logistic regression analyzes were used. To assess the diagnostic significance of quantitative characteristics in predicting a certain outcome, the ROC curve analysis method was used. Differences were considered statistically significant at p 0.05. Results. Acute kidney injury was diagnosed in 70 (21.3%) patients, of which 58 (82.9%) were community-acquired. In 16 (27.6%) patients with community-onset acute kidney injury, it was of a prerenal nature, of which in 13 (81.3%) the calculated serum osmolarity exceeded 295 mOsm/L. Independent factors directly associated with prerenal prehospital acute kidney injury were estimated serum osmolarity (p 0.001), C-reactive protein level (p 0.001) and age (p=0.003) (R2=0.23, F=33,34). Conclusion. Acute kidney injury complicates the course of COVID-19, and in most patients, it develops even at the prehospital stage. Estimated serum osmolarity is directly and independently associated with prerenal community-onset acute kidney injury, suggesting the important role of dehydration in its development.
During the pandemic caused by SARS-CoV-2, cardiovascular disease has been found to be an important risk factor for COVID-19. At the same time, it turned out that patients who did not suffer from cardiovascular pathology before infection with SARS-CoV-2 often had cardiovascular complications in the form of myocarditis, arrhythmias, and heart failure. It is extremely important to elucidate the pathogenetic mechanisms that determine the relationship between COVID-19 and cardiovascular pathology. Analysis of the data of the scientific literature suggests that an imbalance in the renin-angiotensin-aldosterone system (RAAS), expressed in the hyperproduction of angiotensin II and the deficiency of angiotensin 1-7, is an important factor in the pathogenetic link that causes comorbidity of COVID-19 and cardiovascular pathology. According to modern concepts, the RAAS is a complex, multicomponent, multi-level, two-axis system that has, both cardio- and vasoprotective (ACE2/Ang1-7/MasR axis) and damaging effects on the heart and blood vessels (ACE/Ang II/AT1R axis). Patients with cardiovascular diseases, as a rule, already have an imbalance of the RAAS, characterized by hyperproduction of cardiotoxic angiotensin II. Coronavirus, interacting with ACE2 an important component of the cardioprotective axis of RAAS, and reducing its quantity and activity, increases this imbalance, which aggravates the damage to the cardiovascular system. In addition, an imbalance of RAAS can lead to an imbalance in the kallikrein-kinin system with the accumulation of vascular permeability-increasing des-Arg9-bradykinin, potentiate inflammation, create prerequisites for the development of COVID-19 associated coagulopathy and acute respiratory distress syndrome. In the pathogenetic therapy of coronavirus infection, complicated by lesions of the cardiovascular system, it may be advisable to use drugs that correct changes in the renin-angiotensin-aldosterone system.
Kidney disease and chronic renal failure are among the main comorbidities of the complicated course of COVID-19.Objective: to identify the clinical features of the course of a new coronavirus SARS-CoV-2-infection in a child aged 2 years 2 months with chronic kidney disease and dialysis-dependent renal failure.A new coronavirus infection typically began with a moderate intoxication syndrome and catarrhal symptoms, confirmed by the detection of SARS-CoV-2 RNA. Computed tomography of the chest revealed signs of bilateral pneumonia, 30% damage to the lung tissue. Progression occurred by the 4th day of hospitalization with the development of a multisystem inflammatory syndrome, including damage to the cardiovascular system of the digestive system against the background of the existing end-stage renal failure. Laboratory criteria for multisystem inflammatory syndrome were an increase procalcitonin, C-reactive protein, and ferritin. As a result of the developed multiple organ failure, a fatal outcome occurred.
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