Mutual complications of impaired lung and kidney function in severe pneumonia (SP) complicated by acute kidney damage (AKP) are considered. The lungs and kidneys perform some similar functions, such as detoxification and regulation of acid-base balance. Lung damage is complicated by dysfunction or impaired renal function, and vice versa, AKI depressively affects lung function. Initially, all organs and tissues, including the kidneys, suffer from hypoxemic respiratory failure. SP is characterized by increased production of inflammatory mediators, decay products of microorganisms and their toxins and ejection them into the bloodstream. Endothelial vascular insufficiency, disseminated microvascular thrombosis, central hemodynamic disorders develop, and as a result, multiple organ failure develops. With the development of AKI, the elimination of uremic toxins and water is disrupted, hyperhydration is formed with an increase in the volume of extravascular water in the lungs on the background of the already existing broken airborne barrier. Uremic toxins depressively affect the heart muscle on the background of an acute pulmonary heart. There is evidence of a negative effect of mechanical ventilation on kidney function, and, conversely, of an adverse effect of AKI on the need and duration of ventilation. The progression of TP and AKP disrupts the acid - base balance due to excess CO2, impaired H+ ion release, and impaired synthesis of HCO3. The pathophysiological mechanisms underlying these relationships are complex, and their effect on the course of the disease is significant.
The clinical and epidemiological features of acute kidney injury in severe and extremely severe pneumonia associated with coronavirus disease-2019 (COVID-19) are considered. An observational prospective study was conducted with the inclusion of 117 patients, including 75 men and 42 women, suffering from severe and extremely severe pneumonia associated with COVID-19, who were treated in the intensive care unit of the 1586th Military Clinical Hospital in 20202022. Acute kidney injury was diagnosed in 21 (17.9%) patients (stage 1 in 10, stage 2 in 4, and stage 3 in 7 patients), kidney dysfunction was recorded in 22 (8.8%) patients (serum creatinine was higher than normal, but does not reach the diagnostic criteria of Kidney Disease Improving Global Outcomes). Four patients underwent renal replacement therapy. The probability of kidney damage increases with age (the average age of the patients with acute kidney damage is 65 (58; 71) years, and those without acute kidney damage was 47.5 (41; 55) years; p = 0.0001). Compared with patients without acute kidney injury, patients with acute kidney injury scored higher on the scales NEW (p = 0.000975), SMRT-CO (p = 0.011555), and Sequential Organ Failure Assessment (p = 0.000042). Among those suffering from acute kidney injury, significantly more pronounced manifestations of systemic inflammation were determined (leukocytes, p = 0.047324; platelets, p = 0.001230; ferritin, p = 0.048614; and D-dimer, p = 0.004496). In the general cohort, the mortality rate was 22.2%, whereas a significant intergroup difference in mortality was observed, i.e., 52.4% in patients with acute kidney injury and 15.62% in those without acute kidney injury (Chi-squared criterion, 13.468; p 0.001). Invasive artificial lung ventilation was performed in 19.66% of the patients, and a significant intergroup difference was identified, with 66.7% in patients with acute kidney injury and 9.38% in patients without acute kidney injury (Chi-squared criterion, 35.810; p 0.001). The durations of treatment in the intensive care unit in patients with and without acute kidney injury were 9 (7; 14) and 6 (4; 10) days, respectively. After the treatment, all patients with acute kidney injury had fully recovered kidney function upon discharge. In general, acute kidney injury occurs in almost every fifth patient with severe and extremely severe pneumonia associated with COVID-19, aggravates the condition of patients, and increases mortality. The alertness of doctors regarding acute kidney injury and early diagnosis and timely nephroprotective treatment may reduce the possibility of adverse disease outcomes.
Objective. To evaluate a potential of cystatin C blood concentration to predict acute kidney injury (AKI) in patients with severe and extremely severe pneumonia associated with a COVID-19.Materials and methods. An observational prospective study of 117 patients with severe and extremely severe pneumonia associated with a COVID-19 in an ICU setting was conducted in 2020-2022 (site: multi-functional Medical Center, 1586 Military Clinical Hospital of the Ministry of Defense of Russia, Moscow Region, Russia). Routine laboratory tests and instrumental examinations were performed according to generally accepted protocols. Cystatin C concentrations in blood (s-CysC) and urine (u-CysC) were measured by immunoturbidimetric method.Results. AKI was diagnosed in 21 (17.9%) patients, kidney dysfunction without AKI was found in 22 (18.8%) patients with severe and extremely severe pneumonia associated with COVID-19. s-CysC and u-CysC levels in the group of patients with AKI were statistically significantly higher compared to the levels in the group of patients without AKI. The levels of s-CysC obtained within Day 1 — T (-1), and Day 2 — T (-2) prior to AKI onset turned out to be the independent factors for AKI development in patients with severe and extremely severe pneumonia associated with COVID-19: OR 5.37, Wald chisquare 5.534 (CI: 1.324; 21.788); P=0.019 and OR 3.225, Wald chi-square 4.121 (CI: 1.041; 9.989); P=0.042, respectively. s-CysC T (-2) value is informative, and s- CysC T (-1) is a highly informative predictor of AKI development in severe and extremely severe pneumonia associated with COVID-19: ROC AUC 0.853 (95% CI, 0.74-0.966), P<0.001) with 90% sensitivity and 73% specificity at a cut-off of 1.67 mg/L, and ROC AUC 0.905 (95% CI, 0.837-0.973), P<0.001) with 90% sensitivity and 73% specificity at a cut-off of 1.69 mg/l, respectively. Serum CysC levels started increasing 3 days prior to AKI onset, outpacing the increase of SCr levels. The u-CysC levels were not predictive of AKI development. Impaired renal function probability was increasing with patients' age (P<0.0001).Conclusions. Serum CysC seems to be a statistically significant predictor of AKI. s-CysC levels started increasing 3 days prior to AKI onset, surpassing the increase of SCr levels in patients with severe and extremely severe pneumonia associated with COVID-19. Urine CysC did not achieve statistical significance as a predictor for AKI, although u-CysC concentrations were significantly higher on days 3, 2, 1 prior to AKI onset and on the day of AKI onset in the group of patients with AKI.
The results of published studies of modern biomarkers used in the diagnosis of acute kidney injury (AKI) were summarized. The search was carried out in the PubMed/MEDLINE, Scopus, eLibrary databases. AKI occurs in 10–15% of all inpatients and 50% of intensive care patients, and affects economic aspects of treatment and rehabilitation. The literature review allowed to draw conclusions about the significant advantage of new AKI biomarkers (cystatin C, neutrophil gelatinase-associated lipocalin, β2-microglobulin, kidney injury molecule-1, fatty acid binding protein) over the conventional glomerular filtration rate, serum creatinine and urinary volume. Serum creatinine increases only in cases when 50–60% of nephrons are damaged, urinary volume has limitations such as the overdiagnosis of AKI in dehydrated patients, the inability to assess based on a single measurement, and the need for regular and frequent follow-up. Modern biomarkers make it possible to verify renal dysfunction in advance, at the subclinical level. This allows to make a correction in the therapy of the underlying disease and initiate nephroprotection to prevent the development of AKI and the further development of multiple organ failure, which may be more effective than the treatment of already developed AKI.
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