Covid-19 and acute kidney injury.

Since the onset of the corona virus disease 2019 pandemic the spectrum of disease caused by severe acute respiratory distress syndrome corona virus 2 (SARS-CoV-2) has been found to be very wide with a myriad of hematological manifestations. This chapter presents images of the peripheral blood features of two patients with acute kidney injury, which is part of this spectrum. The images from a 15-year-old Iraqi patient with β thalassemia major who was on regular transfusion and iron chelation therapy. He presented pericardiac arrest with ventricular tachycardia and acute kidney injury. He was found to have suffered hemorrhage from a duodenal ulcer, requiring emergency surgery and massive transfusion. The origin of acute kidney injury is multifactorial, including acute tubular damage and infiltration by lymphocytes and macrophages, with the virus having been identified within the glomerular endothelium and in tubular cells.

The most important feature of acute kidney injury (AKI) in COVID-19 is the absence of a single main link of pathogenesis. A thorough understanding of the mechanisms and main links of the pathogenesis of the disease will allow the identifi cation of early markers of AKI, which will contribute to early diagnosis, prognosis, personalized therapy and prevention of kidney damage in patients with COVID-19. Aim: to summarize data from clinical and scientifi c studies on the known mechanisms of AKI in COVID- 19. To identify markers of early kidney injury in COVID-19. Materials and methods. In the Web of Science, Scopus and RSCI databases, 81 sources were selected that contained relevant data from clinical and scientifi c researches on the topic of this review. Results: the main reported mechanisms of kidney damage in COVID-19 patients are as follows: intracellular activity of the virus leading to cell death, excessive release of pro-infl ammatory cytokines and cytokine storm, pathology of the renin-angiotensin-aldosterone system (RAAS), hyperergic infl ammation and immunothrombosis. The main effects of angiotensin II in the case of dysregulation of the RAAS, as well as the spectrum of pro-infl ammatory cytokines and their functions in the development of the cytokine storm, were determined. The possibility of a direct cytopathic effect of SARS-CoV-2 on the renal epithelium as an independent cause of AKI in COVID-19 was considered. The association between the hyperergic infl ammatory response and the process of immunothrombosis, which is mediated by many defense systems, including neutrophils, platelets and proteins of the complement system was presented. The risk of thrombotic complications in the renal vessels in patients with COVID-19 was anaysed. An analysis of potential early biomarkers of kidney injury in COVID-19 were also presented and compared with clinical biomarkers of AKI. Conclusions: AKI is one of the most common complications in critically ill patients with COVID-19, which signifi cantly worsens the prognosis of the disease. The study of the mechanisms of kidney injury contributes to the discovery of new markers necessary for early diagnosis, prognosis of the course of the disease, and further determination of the optimal personalized therapy. © 2021 JSC Vidal Rus. All Rights Reserved.

(1) Background: Acute kidney injury (AKI) in COVID-19 leads to an increase in patient mortality, especially among chronic kidney disease (CKD) patients. (2) Methods: A retrospective cohort of 519 adults admitted from 1 March 2020 to 1 March 2022 were reviewed for baseline characteristics and their association with renal outcomes. Patients were divided into diagnosed CKD, undiagnosed CKD, and normal eGFR. Chronic dialysis and kidney-transplant patients were excluded. Kaplan-Meier survival analysis at 7, 14, and 30 days from admission was performed. (3) Results: The overall incidence of AKI was 45.66%; the proportions among patients with diagnosed CKD, undiagnosed CKD, and normal eGFR were 76.64%, 38.75%, and 7.59%, respectively (p < 0.0001). Multivariate analysis showed that being male and inotrope use were significant risk factors for AKI, while higher eGFR was protective. AKI was associated with dialysis, invasive ventilation (p < 0.0001), prolonged hospitalization (p = 0.0001), and mortality (p < 0.0001). Renal recovery was 64%, 59%, and 23% in stages 1, 2, and 3 AKI, respectively, until 14 days from discharge (p < 0.0001). Patient survival was lower in cases of AKI: 83.16%, 70.59%, and 47.5% compared to non-AKI figures of 91.27%, 87.82%, and 76.95% at 7, 14, and 30 days respectively(p = 0.0001). (4) Conclusion: There was a higher incidence of AKI with worsening renal function. Intensified preventive measures for AKI are crucial to prevent its devastating consequences.

PurposeTo develop and externally validate a multivariate prediction model for the prediction of acute kidney injury (AKI) in COVID-19, based on baseline renal perfusion from contrast-enhanced CT together with clinical and laboratory parameters.MethodsIn this retrospective IRB-approved study, we identified COVID-19 patients who had a standard-of-care contrast-enhanced abdominal CT scan within 5 days of their COVID-19 diagnosis at our institution (training set; n = 45, mean age 65 years, M/F 23/22) and at a second institution (validation set; n = 41, mean age 61 years, M/F 22/19). The CT renal perfusion parameter, cortex-to-aorta enhancement index (CAEI), was measured in both sets. A multivariate logistic regression model for predicting AKI was constructed from the training set with stepwise feature selection with CAEI together with demographical and baseline laboratory/clinical data used as input variables. Model performance in the training and validation set was evaluated with ROC analysis.ResultsAKI developed in 16 patients (35.6%) of the training set and in 6 patients (14.6%) of the validation set. Baseline CAEI was significantly lower in the patients that ultimately developed AKI (P = 0.003). Logistic regression identified a model combining baseline CAEI, blood urea nitrogen, and gender as most significant predictor of AKI. This model showed excellent diagnostic performance for prediction of AKI in the training set (AUC = 0.89, P < 0.001) and good performance in the validation set (AUC 0.78, P = 0.030).ConclusionOur results show diminished renal perfusion preceding AKI and a promising role of CAEI, combined with laboratory and demographic markers, for prediction of AKI in COVID-19.

Background and Objectives: Within a year, COVID-19 has advanced from an outbreak to a pandemic, spreading rapidly and globally with devastating impact. The pathophysiological link between COVID-19 and acute kidney injury (AKI) is currently being debated among scientists. While some studies have concluded that the mechanisms of AKI in COVID-19 patients are complex and not fully understood, others have claimed that AKI is a rare complication of COVID-19-related disorders. Considering this information gap and its possible influence on COVID-19-associated AKI management, our study aimed to explore the prevalence of AKI and to identify possible risk factors associated with AKI development among COVID-19 hospitalized patients. Materials and Methods: A retrospective cohort study included 83 laboratory-confirmed COVID-19 patients hospitalized at the isolation department in a tertiary hospital in Zagazig City, Egypt between June and August 2020. Patients younger than 18 years of age, those diagnosed with end-stage kidney disease, or those on nephrotoxic medications were excluded. All study participants had a complete blood count, liver and renal function tests, hemostasis parameters examined, inflammatory markers, serum electrolytes, routine urinalysis, arterial blood gas, and non-enhanced chest and abdominal computer tomography (CT) scans. Results: Of the 83 patients, AKI developed in 24 (28.9%) of them, of which 70.8% were in stage 1, 8.3% in stage 2, and 20.8% in stage 3. Patients with AKI were older than patients without AKI, with hypertension and diabetes being the most common comorbidities. Risk factors for AKI include increased age, hypertension, diabetes mellitus, and a higher sequential organ failure assessment (SOFA) score. Conclusions: AKI occurs in a considerable percentage of patients with COVID-19, especially in elderly males, those with hypertension, diabetes, and a higher sequential organ failure assessment (SOFA) score. Hence, the presence of AKI should be taken into account as an important index within the risk spectrum of disease severity for COVID-19 patients.

Recalcitrant verruca vulgaris regression following severe SARS-CoV-2 infection

Renal involvement is frequent in COVID-19 (4–37%). This study evaluated the incidence and risk factors of acute kidney injury (AKI) in hospitalized patients with COVID-19.Methodology: This study represents a prospective cohort in a public and tertiary university hospital in São Paulo, Brazil, during the first 90 days of the COVID-19 pandemic, with patients followed up until the clinical outcome (discharge or death).Results: There were 101 patients hospitalized with COVID-19, of which 51.9% were admitted to the intensive care unit (ICU). The overall AKI incidence was 50%; 36.8% had hematuria or proteinuria (66.6% of those with AKI), 10.2% had rhabdomyolysis, and mortality was 36.6%. Of the ICU patients, AKI occurred in 77.3% and the mortality was 65.4%. The mean time for the AKI diagnosis was 6 ± 2 days, and Kidney Disease Improving Global Outcomes (KDIGO) stage 3 AKI was the most frequent (58.9%). Acute renal replacement therapy was indicated in 61.5% of patients. The factors associated with AKI were obesity [odds ratio (OR) 1.98, 95% confidence interval (CI) 1.04–2.76, p < 0.05] and the APACHE II score (OR 1.97, 95% CI 1.08–2.64, p < 0.05). Mortality was higher in the elderly (OR 1.03, 95% CI 1.01–1.66, p < 0.05), in those with the highest APACHE II score (OR 1.08, 95% CI 1.02–1.98, p < 0.05), and in the presence of KDIGO stage 3 AKI (OR 1.11, 95% CI 1.05–2.57, p < 0.05).Conclusion: AKI associated with severe COVID-19 in this Brazilian cohort was more frequent than Chinese, European, and North American data, and the risk factors associated with its development were obesity and higher APACHE II scores. Mortality was high, mainly in elderly patients, in those with a more severe disease manifestation, and in those who developed KDIGO stage 3 AKI.

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.&#x0D; Aim. To study the role of dehydration in the development of community-onset acute kidney injury in COVID-19.&#x0D; 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.&#x0D; 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).&#x0D; 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.

BackgroundTo investigate the temporal characteristics of clinical variables of hospital-acquired acute kidney injury (AKI) in COVID-19 patients and to longitudinally predict AKI onset.MethodsThere were 308 hospital-acquired AKI and 721 non-AKI (NAKI) COVID-19 patients from Stony Brook Hospital (New York, USA) data, and 72 hospital-acquired AKI and 303 NAKI COVID-19 patients from Tongji Hospital (Wuhan, China). Demographic, comorbidities, and longitudinal (3 days before and 3 days after AKI onset) clinical variables were used to compute odds ratios for and longitudinally predict hospital-acquired AKI onset.ResultsCOVID-19 patients with AKI were more likely to die than NAKI patients (31.5% vs 6.9%, adjusted p < 0.001, OR = 4.67 [95% CI 3.1, 7.0], Stony Brook data). AKI developed on average 3.3 days after hospitalization. Procalcitonin was elevated prior to AKI onset (p < 0.05), peaked, and remained elevated (p < 0.05). Alanine aminotransferase, aspartate transaminase, ferritin, and lactate dehydrogenase peaked the same time as creatinine, whereas d-dimer and brain natriuretic peptide peaked a day later. C-reactive protein, white blood cell and lymphocyte showed group differences − 2 days prior (p < 0.05). Top predictors were creatinine, procalcitonin, white blood cells, lactate dehydrogenase, and lymphocytes. They predicted AKI onset with areas under curves (AUCs) of 0.78, 0.66, and 0.56 at 0, − 1, and − 2 days prior, respectively. When tested on the Tongji Hospital data, the AUCs were 0.80, 0.79, and 0.77, respectively.ConclusionsTime-locked longitudinal data provide insight into AKI progression. Commonly clinical variables reasonably predict AKI onset a few days prior. This work may lead to earlier recognition of AKI and treatment to improve clinical outcomes.

Acute Kidney Injury (AKI) complicates a substantial part of patients withCOVID-19. Direct viral penetration of renal cells through the Angiotensin Converting Enzyme 2 receptor, and indirect damage by the aberrant inflammatory response characteristic of COVID-19 are likely mechanisms. Nevertheless, other common respiratory viruses such as Influenza and Respiratory Syncytial Virus (RSV) are also associated with AKI. We retrospectively compared the incidence, risk factors and outcomes of AKI among patients who were admitted to a tertiary hospital because of infection withCOVID-19, influenza (A + B) or RSV. We collected data of 2593 patients hospitalized withCOVID-19, 2041patients with influenza and 429 withRSV. Patients affected byRSV were older, had more comorbidities and presented with higher rates of AKI at admission and within 7 days (11.7% vs. 13.3% vs. 18% for COVID-19, influenza and RSV, respectively p = 0.001). Nevertheless, patients hospitalized withCOVID-19 had higher mortality (18% with COVID-19vs. 8.6% and 13.5% forinfluenza and RSV, respectively P < 0.001) and higher need ofmechanical ventilation (12.4% vs. 6.5% vs.8.2% for COVID-19, influenza and RSV, respectively, P = 0.002). High ferritin levels and low oxygen saturation were independent risk factors for severe AKI only in the COVID-19 group. AKI in the first 48h of admission and in the first 7 days of hospitalization were strong independent risk factors for adverse outcome in all groups. Despite many reports of direct kidney injury by SARS-COV-2, AKI was less in patients with COVID-19 compared to influenza and RSV patients. AKI was a prognostic marker for adverse outcome across all viruses.

Background and Objectives: The recent worldwide pandemic of COVID-19 has been a serious, multidimensional problem that has left a detrimental worldwide impact on individuals of all ages and several organ systems. The typical manifestation of kidney involvement is acute kidney injury (AKI); however, there is a lack of consensus data regarding AKI epidemiology in COVID-19. This systematic literature review aims to bridge this knowledge gap. Design, Setting, Participants, and Measurements: MEDLINE and Cochrane library were systematically searched for the literature related to AKI in COVID-19 patients of all ages. MedRxIV was searched for relevant unpublished manuscripts. Two reviewers independently assessed the literature on the incidence of AKI and mortality, extracting the need for kidney replacement therapy (KRT). Results: Sixty studies (n = 43,871 patients) were included in this review. The pooled incidence of AKI among COVID-19 patients was 19.45% (95% confidence intervals [95% CI]: 14.63–24.77%), while the pooled incidence of AKI COVID-19 patients requiring KRT was 39.04% (16.38–64.57%). The pooled proportion of COVID+ patients was significantly lower at 8.83% (5.64% to 12/66%). The overall mortality of COVID-19 patients was calculated to be 17.71% (95% CI: 11.49–24.93%), while the mortality among patients with AKI was higher at 54.24% (95% CI: 44.70–63.63%). Conclusion: This comprehensive systematic review summarizes the available literature pertaining to AKI epidemiology in COVID-19 patients and highlights the incidence, associated mortality, and the need for KRT in this susceptible population.

.Despite myriad improvements in the care of COVID-19 patients, atypical manifestations are least appreciated during the current pandemic. Because COVID-19 is primarily manifesting as an acute respiratory illness with interstitial and alveolar pneumonia, the possibility of viral invasions into the other organs cannot be disregarded. Acute kidney injury (AKI) has been associated with various viral infections including dengue, chikungunya, Zika, and HIV. The prevalence and risks of AKI during the course of COVID-19 have been described in few studies. However, the existing literature demonstrate great disparity across findings amid variations in methodology and population. This article underscores the propensity of AKI among COVID-19 patients, limitations of the exiting evidence, and importance of timely identification during the case management. The prevalence of AKI is variable across the studies ranging from 4.7% to 81%. Evidence suggest old age, comorbidities, ventilator support, use of vasopressors, black race, severe infection, and elevated levels of baseline serum creatinine and d-dimers are independent risk factors of COVID-19 associated with AKI. COVID-19 patients with AKI also showed unsatisfactory renal recovery and higher mortality rate as compared with patients without AKI. These findings underscore that AKI frequently occurs during the course of COVID-19 infection and requires early stratification and management.

Introduction:Acute kidney injury (AKI) can be a severe complication of the coronavirus 2019 (COVID-19) infection. Follow-up data of these AKI patients, including the rate of progression to chronic kidney disease (CKD), is limited.Methods:COVID-19 patients with AKI, admitted from June 1, 2020, to August 25, 2020, were enrolled prospectively. Their clinical profile, biochemical investigations, urine analysis, treatment, and outcome in terms of mortality or discharge were analyzed. The discharged patients were followed up 3 months later to determine their renal recovery status.Results:AKI was noted in 146 out of 4,613 COVID-19 patients with an incidence of 3.16%. The outcome was available for 111 patients. According to the KDIGO (Kidney Disease Improving Global Outcomes) AKI criteria, 20 (18%) patients were in Stage 1, 16 (14%) in Stage 2, and 75 (68%) in Stage 3 AKI. Proteinuria and hematuria were present in 66% and 41%, respectively. Renal replacement therapy (RRT) was required in 45 (40.5%) patients. A total of 53 (47.7%) patients turned RT-PCR negative and were discharged. The renal recovery at discharge was complete in 31 of 111 (28%), partial in 20 of 111 (18%), and none in two (2%) patients. At 3 months follow-up of discharged patients, total mortality rate was 55.85%. Twenty three of 53 (43%) recovered their renal functions to baseline and 26 of 53 (49%) had progressed to CKD. Diabetes mellitus, dyspnea, altered sensorium, severe acute respiratory distress syndrome, need for RRT, lymphopenia, high neutrophil–lymphocyte ratio, hyperglycemia, raised inflammatory markers, and hematuria were associated with high mortality rate and reached statistical significance.Conclusion:AKI in COVID-19 patients has a high mortality rate (55.85%) with a high CKD progression rate among survivors (49%).

Although initially kidney involvement in COVID-19 infection was felt to occur relatively infrequently, this has proved not to be the case. In critically ill patients with COVID-19, multiorgan failure including acute kidney injury (AKI) is common and is associated with an increased risk of mortality and morbidity. This review focuses briefly on the epidemiology and pathophysiology of COVID-19 associated AKI as well as options for management. The risk factors for AKI are common to both noncovid-related AKI and COVID-19 associated AKI. Kidney injury in COVID-19 associated AKI may arise through several mechanisms, including not only direct effects on the kidney leading to tubular injury but also through the effects of treatment of multiorgan failure complicating infection. During surge conditions, the use of kidney replacement therapy has embraced all modalities including the use of peritoneal dialysis. The use of blood purification techniques has been proposed, but to date, the results are variable. COVID-19 associated AKI is common, affecting approximately a quarter of patients hospitalized with COVID-19. Glomerular injury can occur, but in the main tubular injury seems most likely leading to AKI, which should be managed following clinical pathways informed by accepted guidelines.

Thromboelastometry and D-Dimer Elevation in Coronavirus-2019