Impact of Kidney Damage on the Course and Prognosis of COVID-19 Infection According to the International Registry <<Analysis of Chronic Non-Infectious Diseases Dynamics After Covid-19 Infection in Adult Patients>>

Objective. To study the course of the new coronavirus infection in patients with chronic kidney disease (CKD), to identify cases of acute kidney injury (AKI) in the setting of COVID-19 infection, and to access the impact of renal function on prognosis in these categories of patients during the acute phase and after hospitalization, at 3, 6, and 12 months after recovery. Materials and methods. The ACTIV and ACTIV 2 registries included men and women older than 18 years with a diagnosis of COVID-19 based on a positive PCR test for COVID-19 and a characteristic chest X-ray or computed tomography chest scan. Results. A total of 9364 patients (4404 men, average age59 [48-69]) were included in the analysis. 716 (7.67 %) patients had CKD. 8496 (90,7 %) patients had their glomerular filtration rate (GFR) measured during hospitalization, and the values were distributed as follows: >=90 ml/min/1.73m2 - in 4289 (50,5 %) patients, 89-60 ml/min/1.73m2 - in 3150 (37,1 %) patients, 59-45 ml/min/1.73m2 - in 613 (7,22 %), 44-30 ml/min/1.73m2 - in 253 (2,98 %), 29-15 ml/min/1.73m2 - in 110 (1,29 %), <15 ml/min/1.73m2 - in 81 (0,95 %) patients. 11.6 % of the subjects (n=1068) developed AKI during hospitalization. This complication was reported more often than cytokine storm (in 7.46 % in 687 patients, p<0,001) or sepsis (in 0.17 % in 16 patients, p=620). CKD increased the risk of death by 3.94-fold in patients with COVID-19 during hospitalization compared with patients without CKD. The mortality of patients with AKI during hospitalization was 3.94 times higher than the mortality of those without AKI. CKD also affected long-term survival after hospitalization: within 3 months of follow-up, the risk of death in patients with CKD increased 4.88-fold, within 6 months - 4.24-fold, after 12 months - 8.36-fold. Conclusion. The prevalence of CKD in COVID-19 patients is similar to that in the general population. AKI developed in 11.6 % of cases with COVID-19 infection and was observed more frequently in patients with overweight and hyperglycemia. CKD and AKI increased the risk of hospital mortality in patients with COVID-19. In the group of patients with CKD, mortality increased in the post-COVID period, 3, 6 and 12 months after. The high mortality rate of patients who had AKI during the coronavirus infection was observed only in the first 3 months of follow-up in the post-COVID period.Copyright © 2023 The authors.

Remdesivir May Be Associated with Acute Kidney Injury in Covid-10 Patients: A Cohort Study

Objective: To assess the outcomes of coronavirus disease-2019 patients with acute renal damage who received remdesivir against placebo at a private hospital in Karachi, Pakistan. Methodology: At the COVID-19 ICU of Hussain Lakhni Hospital, a cohort study was conducted from July 2021 to February 2022. Male and female study participants with COVID-19 and acute renal injury ranged in age from 40 to 80. Remdesivir-treated individuals with COVID-19 acute kidney injury were exposed, but placebo-treated patients with COVID-19 acute kidney injury were not exposed. In-hospital mortality, elevated serum creatinine levels, and prolonged hospital stays were the results. The data was analyzed using SPSS version 23. Result(s): Patients who took remdesivir had a lower mortality rate than those who were placebo (32.2% vs 67.8%, OR=0.38, 95 percent CI=0.27-0.52), with a p-value of 0.001. Remdesivir was also associated with a shorter hospital stay (4.2% versus 95.8%, OR=0.005, 95 percent CI=.003-0.009) with a p-value of 0.001). However, increased serum creatinine revealed statistically insignificant differences between groups. The odds of in-hospital mortality were 0.376 times lower (AOR=0.376, 95 percent CI=0.275-0.514, p=0.0001) and the odds of a prolonged hospital stay were 0.030 times lower (AOR=0.030, 95 percent CI=0.012-0.074, p=0.001) in the remdesivir group than in the placebo group after controlling for covariates. Practical implication: In literature Remdesvir was associated with acute kidney injury (rise in serum creatinine) and in many centres,it was not used in patients with acute kidney injury although it has very beneficial effect in patients of severe covid pneumonia,many centres were not using it in patients of acute renal failure. in our study, rise in serum creatinine was not significant in remdesvir group in patient with acute kidney injury,so remdesvir must not be withheld in this group of patients as it can decrease the severity of covid pneumonia and saves patients lives Conclusion(s): Remdesivir is an effective medicine in COVID-19 patients with acute renal damage in terms of in-hospital mortality and duration of stay. Copyright © 2022 Lahore Medical And Dental College. All rights reserved.

SARS-CoV-2 versus other minor viral infection on kidney injury in asymptomatic and mildly symptomatic patients.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has become a global pandemic since December 2019. Most of the patients are mild or asymptomatic and recovered well as those suffered from other respiratory viruses. SARS-CoV-2 infection is supposed to demonstrate more sequelae. Acute kidney injury (AKI) is common among COVID-19 patients and is associated with disease severity and outcomes. Only a few studies focused on a detailed analysis of kidney damage in asymptomatic or mildly symptomatic COVID-19 patients. Whether any minor viral infection is likely to exhibit similar minor effect on renal function as COVID-19 is still unclear, and the definite pathophysiology of viral invasion is not fully understood. Currently, the proposed mechanisms of AKI include direct effects of virus on kidney, dysregulated immune response, or as a result of multi-organs failure have been proposed. This study will discuss the difference between COVID-19 and other viruses, focusing on proposed mechanisms, biomarkers and whether it matters with clinical significance.

High mortality and residual kidney damage with Coronavirus disease-19-associated acute kidney injury in northern India.

BACKGROUND: Acute kidney injury (AKI) is associated with morbidity and mortality in COVID-19 patients. The incidence of AKI and its outcomes vary in different parts of the world. We aimed to analyze the AKI incidence, predictors of AKI, mortality, and renal function outcomes on follow-up in hospitalized patients with COVID-19. MATERIALS AND METHODS: The study was designed as a retrospective, observational study of electronically captured data on the hospital information system of laboratory-confirmed COVID-19 patients, with and without AKI, between March 2020 to June 2021. The predictor of AKI and mortality and residual damage in recovered AKI patients were analyzed. RESULTS: Of the 3395 patients, 3010 COVID-19 patients were eligible. AKI occurred in 951 (31.5%); with stages 1, 2, and 3 in 605 (63.7%), 138 (14.5%), and 208 (21.8%) patients, respectively. AKI severity increased with COVID-19 severity. Of 951 AKI patients, 403 died, and 548 were discharged. AKI group had higher mortality (42.3%) than the non-AKI (6.6%). At discharge, complete recovery was noticed in 370(67.5%), while 178 (32.5%) had residual damage. At three months of follow-up, 108 (69.6%) of 155 patients showed complete recovery. Residual damage was observed in 47 (30.3%). In 14 (9%) patients, serum creatinine remained elevated above the baseline. Thirty-three (21.2%) patients showed proteinuria (n = 24) and microscopic hematuria (n = 9). CONCLUSIONS: AKI is common among patients hospitalized with COVID-19 and is associated with high mortality. Residual kidney damage post-COVID-19 in recovered AKI patients may increase the CKD burden.

Organ manifestations of COVID-19: what have we learned so far (not only) from autopsies?

The use of autopsies in medicine has been declining. The COVID-19 pandemic has documented and rejuvenated the importance of autopsies as a tool of modern medicine. In this review, we discuss the various autopsy techniques, the applicability of modern analytical methods to understand the pathophysiology of COVID-19, the major pathological organ findings, limitations or current studies, and open questions. This article summarizes published literature and the consented experience of the nationwide network of clinical, neuro-, and forensic pathologists from 27 German autopsy centers with more than 1200 COVID-19 autopsies. The autopsy tissues revealed that SARS-CoV-2 can be found in virtually all human organs and tissues, and the majority of cells. Autopsies have revealed the organ and tissue tropism of SARS-CoV-2, and the morphological features of COVID-19. This is characterized by diffuse alveolar damage, combined with angiocentric disease, which in turn is characterized by endothelial dysfunction, vascular inflammation, (micro-) thrombosis, vasoconstriction, and intussusceptive angiogenesis. These findings explained the increased pulmonary resistance in COVID-19 and supported the recommendations for antithrombotic treatment in COVID-19. In contrast, in extra-respiratory organs, pathological changes are often nonspecific and unclear to which extent these changes are due to direct infection vs. indirect/secondary mechanisms of organ injury, or a combination thereof. Ongoing research using autopsies aims at answering questions on disease mechanisms, e.g., focusing on variants of concern, and future challenges, such as post-COVID conditions. Autopsies are an invaluable tool in medicine and national and international interdisciplinary collaborative autopsy-based research initiatives are essential.

COVID-19 pandemic and kidney disease in children: literature review and own regional observations

Introduction. Currently, the coronavirus infection pandemic caused by the SARS-CoV-2 virus continues around the world. Research data from domestic and foreign authors indicate that the kidneys are a target organ for a new infection, lesions vary from pro-teinuria and hematuria to acute kidney injury. Aim of the study – to determine the frequency and nature of kidney damage in children with confirmed coronavirus infection. Materials and methods. A retrospective and prospective analysis of cases of confirmed COVID-19 infection in children (n = 441) admitted to the Samara Regional Children’s Infectious Diseases Hospital from March 2020 to July 2021 was carried out. SARS-CoV-2 RNA was detected in all patients by a one-step reverse transcription reaction combined with a polymerase chain reaction. The changes in the kidneys that occurred in 57 children were studied. The research results were processed using the Statistica 7.0 software (StatSoft, USA). Results. The involvement of the kidneys in the infectious process was detected in every 8 children with COVID-19 (12.9%), more often in the form of isolated urinary syndrome, the detection rate of which correlated with the severity of the course of corona-virus infection: in severe cases, proteinuria was detected in 31.6% of patients, hematuria – in 21%, acute kidney injury – in 10.5%, diabetic nephropathy – in 5.3%. Kidney damage was combined with damage to the respiratory and gastrointestinal tract, charac-terized by rapid recovery of urine output and azotemia parameters without special renal therapy. A clinical case of the onset of nephrotic syndrome that developed 2 weeks after suffering a coronavirus infection is described. Conclusions. Children with COVID-19 require kidney function monitoring for early detection and correction in case of impairment. Patients with isolated urinary syndrome in the acute period require long-term observation in order to detect latent renal pathology. © 2022, Remedium Group Ltd. All rights reserved.

Does Oxidative Stress Management Help Alleviation of COVID-19 Symptoms in Patients Experiencing Diabetes?

Severe acute respiratory syndrome (SARS)-CoV-2 virus causes novel coronavirus disease 2019 (COVID-19) with other comorbidities such as diabetes. Diabetes is the most common cause of diabetic nephropathy, which is attributed to hyperglycemia. COVID-19 produces severe complications in people with diabetes mellitus. This article explains how SARS-CoV-2 causes more significant kidney damage in diabetic patients. Importantly, COVID-19 and diabetes share inflammatory pathways of disease progression. SARS-CoV-2 binding with ACE-2 causes depletion of ACE-2 (angiotensin-converting enzyme 2) from blood vessels, and subsequently, angiotensin-II interacts with angiotensin receptor-1 from vascular membranes that produce NADPH (nicotinamide adenine dinucleotide hydrogen phosphate) oxidase, oxidative stress, and constriction of blood vessels. Since diabetes and COVID-19 can create oxidative stress, we hypothesize that COVID-19 with comorbidities such as diabetes can synergistically increase oxidative stress leading to end-stage renal failure and death. Antioxidants may therefore prevent renal damage-induced death by inhibiting oxidative damage and thus can help protect people from COVID-19 related comorbidities. A few clinical trials indicated how effective the antioxidant therapy is against improving COVID-19 symptoms, based on a limited number of patients who experienced COVID-19. In this review, we tried to understand how effective antioxidants (such as vitamin D and flavonoids) can act as food supplements or therapeutics against COVID-19 with diabetes as comorbidity based on recently available clinical, preclinical, or in silico studies.

Abnormal Indexes of Liver and Kidney Injury Markers Predict Severity in COVID-19 Patients.

BACKGROUND: SARS-CoV-2 can damage not only the lungs but also the liver and kidney. Most critically ill patients with coronavirus disease 2019 (COVID-19) have liver and kidney dysfunction. We aim to investigate the levels of liver and kidney function indexes in mild and severe COVID-19 patients and their capability to predict the severity of the disease. METHODS: The characteristics and laboratory indexes were compared between patients with different conditions. We applied binary logistic regression to find the independent risk factors of severe patients. Receiver operating characteristic (ROC) analysis was used to predict the severity of COVID-19 using the liver and kidney function indexes. RESULTS: This study enrolled 266 COVID-19 patients, including 235 mild patients and 31 severe patients. Compared with mild patients, severe patients had lower albumin (ALB) and higher alanine aminotransferase (ALT), aspartate aminotransferase (AST), and urea nitrogen (BUN) (all p<0.001). Binary logistic regression analysis also identified ALB [OR=0.273 (0.079-0.947), p=0.041] and ALT [OR=2.680 (1.036-6.934), p=0.042] as independent factors of severe COVID-19 patients. Combining ALB, ALT, BUN, and LDH exhibited the area under ROC at 0.914, with a sensitivity of 86.7% and specificity of 83.0%. CONCLUSION: COVID-19 patients, especially severe patients, have damage to liver and kidney function. ALT, AST, LDH, and BUN could be independent factors for predicting the severity of COVID-19. Combining the ALB, ALT, BUN, and LDH could predict the transition from mild to severe in COVID-19 patients.

Outcomes of COVID-19 Among Hospitalized Patients With Non-dialysis CKD.

Background: Coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome-Corona Virus 2 has generated significant impact on global health worldwide. COVID-19 can cause pneumonia and organ injury. Chronic kidney disease (CKD) has been associated with increased mortality in previous epidemics, but there is a paucity of data regarding actual risks for non-dialysis CKD patients with COVID-19. Methods: Multicenter, observational cohort study including 136 non-dialysis CKD patients and 136 age- and sex-matched controls that required hospitalization due to COVID-19. Patients with end-stage renal disease, a kidney transplant or without registered baseline glomerular filtration rate prior to COVID-19 infection were excluded. CKD and acute kidney injury (AKI) were defined according to KDIGO criteria. Results: CKD patients had higher white blood cell count and D-dimer and lower lymphocyte percentage. No differences were found regarding symptoms on admission. CKD was associated with higher rate of AKI (61 vs. 24.3%) and mortality (40.4 vs. 24.3%). Patients with AKI had the highest hazard for death (AKI/non-CKD HR:7.04, 95% CI:2.87-17.29; AKI/CKD HR:5.25, 95% CI: 2.29-12.02), followed by CKD subjects without AKI (HR:3.39, 95% CI:1.36-8.46). CKD status did not condition ICU admission or length of in-hospital stay. Conclusions: CKD patients that require hospitalization due to COVID-19 are exposed to higher risk of death and AKI.

[Clinical analysis of early damage in multiple extra-pulmonary organs in COVID-19].

OBJECTIVE: To analyze the clinical manifestations of heart, liver and kidney damages in the early stage of COVID-19 to identify the indicators for these damages. METHODS: We analyzed the clinical features, underlying diseases, and indicators of infection in 12 patients with COVID-19 on the second day after their admission to our hospital between January 20 and February 20, 2020.The data including CK-MB, aTnI, BNP, heart rate, changes in ECG, LVEF (%), left ventricular general longitudinal strain (GLS, measured by color Doppler ultrasound) were collected.The changes of liver function biochemical indicators were dynamically reviewed.BUN, UCR, eGFR, Ccr, and UACR and the levels of MA, A1M, IGU, and TRU were recorded. RESULTS: The 12 patients included 2 severe cases, 8 common type cases, and 2 mild cases.Four of the patients presented with sinus tachycardia, ECG changes and abnormal GLS in spite of normal aTNI and LVEF; 1 patient had abnormal CKMB and BNP.On the first and third days following admission, the patients had normal ALT, AST and GGT levels.On day 7, hepatic function damage occurred in the severe cases, manifested by elevated ALT and AST levels.Abnormalities of eGFR, Ccr and UACR occurred in 8, 5 and 5 of the patients, respectively.Abnormal elevations of MA, A1M, IGU and TRU in urine protein were observed in 4, 4, 5, and 2 of the patients, respectively. CONCLUSIONS: In patients with COVID-19, heart damage can be identified early by observing the GLS and new abnormalities on ECG in spite of normal aTNI and LVEF.Early liver injury is not obvious in these patients, but dynamic monitoring of the indicators of should be emplemented, especially in severe cases. In cases with normal CR and BUN, kidney damage can be detected early by calculating eGFR, Ccr and UACR and urine protein tests.