Acute kidney injury and urinary biomarkers in hospitalized patients with coronavirus disease-2019.
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ABSTRACT:
SUBMITTER: Husain-Syed F
PROVIDER: S-EPMC7454800 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
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Acute kidney injury and urinary biomarkers in hospitalized patients with coronavirus disease-2019.
Husain-Syed Faeq F Wilhelm Jochen J Kassoumeh Shadi S Birk Horst-Walter HW Herold Susanne S Vadász István I Walmrath Hans-Dieter HD Kellum John A JA Ronco Claudio C Seeger Werner W
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 20200701 7
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Project description:BackgroundRecent data have shown that severe acute respiratory syndrome coronavirus 2 can infect renal proximal tubular cells via Angiotensin Converting Enzyme 2 (ACE2) . Our objective was to determine whether Fanconi syndrome is a frequent clinical feature in coronavirus disease 2019 (COVID-19) patients.MethodsA retrospective cohort of 42 laboratory-confirmed COVID-19 patients without history of kidney disease hospitalized in University Hospital of Nancy was investigated. Patients were admitted to the intensive care unit (ICU) (n = 28) or the Medical department (n = 14) and were screened at least once for four markers of proximal tubulopathy.ResultsThe mean (standard deviation) follow-up was 19.7 (±12.2) days. Of the patients, 75% (30/40) showed at least two proximal tubule abnormalities (incomplete Fanconi syndrome). The main disorders were proteinuria (88%, n = 35), renal phosphate leak defined by renal phosphate threshold/glomerular filtration rate (TmPi/GFR) <0.77 (55%, n = 22), hyperuricosuria (43%, n = 17) and normoglycaemic glycosuria (30%, n = 12). At the time of the first renal evaluation, ICU patients presented more frequent (96 versus 62%, P = 0.0095) and more severe (844 ± 343 versus 350 ± 221 mg/g, P = 0.0001) proteinuria, and a trend for an increased number of proximal tubule abnormalities (P = 0.038). During follow-up, they presented a lower nadir of serum phosphate [median (interquartile range) 0.68 (0.43-0.76) versus 0.77 (0.66-1.07) mmol/L, P = 0.044] and Acute kidney Injury (AKI) during the hospitalization (P = 0.045). Fanconi syndrome preceded severe AKI KDIGO Stages 2 and 3 in 88% (7/8) of patients. Proximal tubular abnormalities (such as proteinuria, TmPi/GFR and glycosuria in five, two and two patients, respectively) were not detected anymore in recovering patients before hospital discharge.ConclusionIncomplete Fanconi syndrome is highly frequent in COVID-19 patients and precedes AKI or disappears during the recovery phase.
| S-EPMC7314200 | biostudies-literature
Project description:BackgroundAcute kidney injury (AKI) and chronic kidney disease (CKD) have become worldwide public health problems, but little information is known about the epidemiology of acute kidney disease (AKD)-a state in between AKI and CKD. We aimed to explore the incidence and outcomes of hospitalized patients with AKD after AKI, and investigate the prognostic value of AKD in predicting 30-day and one-year adverse outcomes.MethodsA total of 2,556 hospitalized AKI patients were identified from three tertiary hospitals in China in 2015 and followed up for one year.AKD and AKD stage were defined according to the consensus report of the Acute Disease Quality Initiative 16 workgroup. Multivariable regression analyses adjusted for confounding variables were used to examine the association of AKD with adverse outcomes.ResultsAKD occurred in 45.4% (1161/2556) of all AKI patients, 14.5% (141/971) of AKI stage 1 patients, 44.6% (308/691) of AKI stage 2 patients and 79.6% (712/894) of AKI stage 3 patients. AKD stage 1 conferred a greater risk of Major Adverse Kidney Events within 30 days (MAKE30) (odds ratio [OR], 2.36; 95% confidence interval 95% CI [1.66-3.36]) than AKD stage 0 but the association only maintained in AKI stage 3 when patients were stratified by AKI stage. However, compared with AKD stage 0, AKD stage 2-3 was associated with higher risks of both MAKE30 and one-year chronic dialysis and mortality independent of the effects of AKI stage with OR being 31.35 (95% CI [23.42-41.98]) and 2.68 (95% CI [2.07-3.48]) respectively. The association between AKD stage and adverse outcomes in 30 days and one year was not significantly changed in critically ill and non-critically ill AKI patients. The results indicated that AKD is common among hospitalized AKI patients. AKD stage 2-3 provides additional information in predicting 30-day and one-year adverse outcomes over AKI stage. Enhanced follow-up of renal function of these patients may be warranted.
| S-EPMC8158174 | biostudies-literature
Project description:Since the outbreak of Coronavirus Disease 2019 (COVID-19) in Wuhan, China, in December of 2019, it has rapidly become a global pandemic. Although acute respiratory disorder is the main manifestation of COVID-19, acute kidney injury (AKI) is another important extrapulmonary complication, which has a critical impact on the prognosis and mortality of patients. Current understanding about the exact pathogenesis of AKI in COVID-19 is unclear. Several studies have suggested that intrarenal, pre-renal and post-renal factors mediated collaboratively by direct virus attack, overloaded immune responses, drugs, sepsis, coagulation dysfunction, and underlying diseases may all be involved in the pathogenesis of AKI. This article reviews the current understanding of the pathogenesis of AKI in COVID-19.
| S-EPMC7928360 | biostudies-literature
Project description:BackgroundThe 2019 novel coronavirus disease (CO-VID-19) is a newly defined serious infectious disease caused by the SARS-CoV-2 virus. The epidemic started in Wuhan, China, in December of 2019 and quickly spread to over 200 countries. It has affected 4,258,666 people, with 294,190 deaths worldwide by May 15, 2020. COVID-19 is characterized by acute respiratory disease, with 80% of patients presenting mild like flu-like symptoms; however, 20% of patients may have a severe or critical clinical presentation, which likely causes multiple organ injuries (e.g., kidney, heart, blood, and nervous system). Among them, acute kidney injury (AKI) is a critical complication due to its high incidence and mortality rate. Here we present a review of the current understanding of AKI in COVID-19.SummaryCO-VID-19 is a catastrophic contagious disease caused by the coronavirus, and the AKI induced by COVID-19 significantly increases the mortality rate. In this review, we summarize the clinical characteristics of COVID-19 induced AKI by focusing on its epidemiology, pathogenesis, clinical diagnosis, and treatment.Key messagesMultiple studies have shown that COVID-19 may involve the kidneys and cause AKI. This article reviews the characteristics of COVID-19-induced AKI largely based on up-to-date studies in the hope that it will be helpful in the current global fight against and treatment of COVID-19.
| S-EPMC7360511 | biostudies-literature
Project description:BackgroundData on clinical characteristics and outcomes of people living with HIV (PLWH) hospitalized with coronavirus disease 2019 (COVID-19) who develop acute kidney injury (AKI) are limited.SettingLarge tertiary health care system in the Bronx, NY.MethodsWe performed a retrospective cohort study of 83 PLWH and 4151 patients without HIV hospitalized with COVID-19 from March 10, 2020, to May 11, 2020. We compared the clinical characteristics and outcomes associated with AKI by HIV serostatus and evaluated HIV-related factors for AKI among PLWH. AKI was defined and staged using Kidney Disease Improving Global Outcomes criteria.ResultsThe incidence of AKI in hospitalized patients with COVID-19 did not differ significantly by HIV serostatus (54.2% in PLWH vs 49.5% in patients without HIV, P = 0.6). Despite a higher incidence of stage 3 AKI (28.9% vs 17.1% P = 0.05) in PLWH compared with those without HIV, there was no significant difference in the need for renal replacement therapy (22.2% vs 13.4% P = 0.12), renal recovery (76.9% vs 82.5% P = 0.61), or dependence on renal replacement therapy (7.7% vs 3.8% P = 0.27). CD4 T-cell count, HIV-1 RNA viral suppression, and antiretroviral therapy use were not associated with AKI. AKI was associated with increased need for invasive ventilation and in-hospital death, but HIV was not an independent risk factor of in-hospital death after AKI [adjusted hazard ratio 1.01 (95% CI: 0.59 to 1.72), P = 0.98].ConclusionsHIV-related factors were not associated with increased risk of AKI in PLWH hospitalized with COVID-19. PLWH hospitalized with COVID-19 had more stage 3 AKI, but outcomes after AKI were similar to those without HIV.
| S-EPMC8629144 | biostudies-literature
Project description:BackgroundThe clinical significance of Coronavirus disease 2019 (COVID-19) as an associate of myocardial injury is controversial.HypothesisType 2 MI/Myocardial Injury are associated with worse outcomes if complicated by COVID-19.MethodsThis longitudinal cohort study involved consecutive patients admitted to a large urban hospital. Myocardial injury was determined using laboratory records as ≥1 hs-TnI result >99th percentile (male: >34 ng/L; female: >16 ng/L). Endotypes were defined according to the Fourth Universal Definition of Myocardial Infarction (MI) and COVID-19 determined using PCR. Outcomes of patients with myocardial injury with and without COVID-19 were assessed.ResultsOf 346 hospitalized patients with elevated hs-TnI, 35 (10.1%) had laboratory-confirmed COVID-19 (median age [IQR]; 65 [59-74]; 64.8% male vs. COVID-19 negative: 74 [63-83] years; 43.7% male). Cardiac endotypes by COVID-19 status (yes vs. no) were: Type 1 MI (0 [0%] vs. 115 [100%]; p < .0005), Type 2 MI (13 [16.5%] vs. 66 [83.5%]; p = .045), and non-ischemic myocardial injury (cardiac: 4 [5.8%] vs. 65 [94.2%]; p = .191, non-cardiac:19 [22.9%] vs. 64 [77.%]; p < .0005). COVID-19 patients had less comorbidity (median [IQR] Charlson Comorbidity Index: 3.0 [3.0] vs. 5.0 [4.0]; p = .001), similar hs-TnI concentrations (median [IQR] initial: 46 [113] vs. 62 [138]; p = .199, peak: 122 [474] vs. 79 [220] ng/L; p = .564), longer admission (days) (median [IQR]: 14[19] vs. 6[12]; p = .001) and higher in-hospital mortality (63.9% vs. 11.3%; OR = 13.2; 95%CI: 5.90, 29.7).ConclusionsCardiac sequelae of COVID-19 typically manifest as Non-cardiac myocardial injury/Type 2MI in younger patients with less co-morbidity. Paradoxically, the admission duration and in-hospital mortality are increased.
| S-EPMC7943910 | biostudies-literature
Project description: Not available
| S-EPMC7272937 | biostudies-literature
Project description:ObjectiveThe epidemiology and outcomes of acute kidney disease (AKD) after acute kidney injury (AKI) in hospitalized children are poorly described. The aim of this study is to investigate the prevalence, predictive factors, and clinical outcomes of AKD in hospitalized children with AKI.MethodsChildren (1 month-18 years) with AKI during hospitalization in the Second Xiangya Hospital from January 2015 to December 2020 were identified. AKD was defined based on the consensus report of the Acute Disease Quality Initiative 16 workgroup. The endpoints include adverse outcomes in 30 and 90 days. Multivariable logistic regression analyses were used to estimate the odds ratio of 30- and 90-day adverse outcomes associated with AKD and identify the risk factors of AKD.ResultsAKD was developed in 42.3% (419/990) of the study patients, with 186 in AKD stage 1, 107 in AKD stage 2, and 126 in AKD stage 3. Pediatric patients with AKD stages 2-3 had significantly higher rates of developing 30- and 90-day adverse outcomes than those with AKD stage 0 and 1. The adjusted odds ratio of AKD stage 2-3 was 12.18 (95% confidence interval (CI), 7.38 - 20.09) for 30-day adverse outcomes and decreased to 2.49 (95% CI, 1.26 - 4.91) for 90-day adverse outcomes. AKI stages 2 and 3, as well as glomerulonephritis, were the only predictive factors for AKD stage 2-3.ConclusionAKD is frequent among hospitalized pediatric AKI patients. AKD stage 2-3 represents a high-risk subpopulation among pediatric AKI survivors and is independently associated with 30- and 90-day adverse outcomes. Awareness of the potential risks associated with AKD stage 2-3 and its risk factors may help improve outcomes through careful monitoring and timely intervention.
| S-EPMC9168069 | biostudies-literature
Project description:BackgroundCoronavirus disease 2019 (COVID-19) has emerged as a major global health threat with a great number of deaths worldwide. Acute kidney injury (AKI) is a common complication in patients admitted to the intensive care unit. We aimed to assess the incidence, risk factors and in-hospital outcomes of AKI in COVID-19 patients admitted to the intensive care unit.MethodsWe conducted a retrospective observational study in the intensive care unit of Tongji Hospital, which was assigned responsibility for the treatments of severe COVID-19 patients by the Wuhan government. AKI was defined and staged based on Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Mild AKI was defined as stage 1, and severe AKI was defined as stage 2 or stage 3. Logistic regression analysis was used to evaluate AKI risk factors, and Cox proportional hazards model was used to assess the association between AKI and in-hospital mortality.ResultsA total of 119 patients with COVID-19 were included in our study. The median patient age was 70 years (interquartile range, 59-77) and 61.3% were male. Fifty-one (42.8%) patients developed AKI during hospitalization, corresponding to 14.3% in stage 1, 28.6% in stage 2 and 18.5% in stage 3, respectively. Compared to patients without AKI, patients with AKI had a higher proportion of mechanical ventilation mortality and higher in-hospital mortality. A total of 97.1% of patients with severe AKI received mechanical ventilation and in-hospital mortality was up to 79.4%. Severe AKI was independently associated with high in-hospital mortality (OR: 1.82; 95% CI: 1.06-3.13). Logistic regression analysis demonstrated that high serum interleukin-8 (OR: 4.21; 95% CI: 1.23-14.38), interleukin-10 (OR: 3.32; 95% CI: 1.04-10.59) and interleukin-2 receptor (OR: 4.50; 95% CI: 0.73-6.78) were risk factors for severe AKI development.ConclusionsSevere AKI was associated with high in-hospital mortality, and inflammatory response may play a role in AKI development in critically ill patients with COVID-19.
| S-EPMC7649690 | biostudies-literature
Project description:BackgroundThe development of acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19) is associated with a high risk of death. Published data demonstrate the possibility of severe kidney injury in patients suffering from COVID-19. However, these data are still controversial.MethodsA total of 1,280 patients with a proven diagnosis of COVID-19 were included in our study. COVID-19 was confirmed in all patients using reverse transcriptase polymerase chain reaction test of a nasopharyngeal swab, and based on the typical computed tomography findings. Demographic data, underlying comorbidities, and laboratory blood tests were assessed. We assessed the incidence of AKI and its associated mortality defined by survival status at discharge.ResultsProteinuria was identified with 648 patients (50.6%) with COVID-19. AKI was identified in 371 patients (29.0%). Ten of these patients (2.7%) required dialysis. The risk factors for AKI included age of > 65 years, augmentation of C-reactive protein, ferritin and an increase in values of activated partial thromboplastin time. Overall, 162 of the 1,280 hospitalized patients (12.7%) and 111 of the 371 patients (29.9%) with AKI did not survive. The hazard ratio (HR) for mortality was 3.96 (95% confidence interval, 2.83-5.54) for patients with AKI vs. no AKI.ConclusionAKI was a relatively common finding among patients with COVID-19. The risk factors for AKI in COVID-19 included old age, the inflammatory response, the severity of lung involvement, and disseminated intravascular coagulation. These same factors, in addition to arterial hypertension, were found to increase the risk of mortality.
| S-EPMC8237114 | biostudies-literature