Acute kidney injury and mortality risk in older adults with COVID-19.
Ontology highlight
ABSTRACT: Background
Research regarding COVID-19 and acute kidney injury (AKI) in older adults is scarce. We evaluated risk factors and outcomes of AKI in hospitalized older adults with and without COVID-19.Methods
Observational study of patients admitted to two geriatric clinics in Stockholm from March 1st to June 15th, 2020. The difference in incidence, risk factors and adverse outcomes for AKI between patients with or without COVID-19 were examined. Odds ratios (OR) for the risk of AKI and in-hospital death were obtained from logistic regression.Results
Three hundred-sixteen older patients were hospitalized for COVID-19 and 876 patients for non-COVID-19 diagnoses. AKI occurred in 92 (29%) patients with COVID-19 vs. 159 (18%) without COVID-19. The odds for developing AKI were higher in patients with COVID-19 (adjusted OR, 1.70; 95% confidence interval [CI] 1.04-2.76), low baseline kidney function as depicted by estimated glomerular filtration rate (eGFR) [4.19 (2.48-7.05), for eGFR 30 to < 60 mL/min, and 20.3 (9.95-41.3) for eGFR < 30 mL/min], and higher C reactive protein (CRP) (OR 1.81 (1.11-2.95) in patients with initial CRP > 10 mg/L). Compared to patients without COVID-19 and without AKI, the risk of in-hospital death was highest in patients with COVID-19 and AKI [OR 80.3, 95% CI (27.3-235.6)], followed by COVID-19 without AKI [16.3 (6.28-42.4)], and by patients without COVID-19 and with AKI [10.2 (3.66-28.2)].Conclusions
Geriatric patients hospitalized with COVID-19 had a higher incidence of AKI compared to patients hospitalized for other diagnoses. COVID-19 and reduced baseline kidney function were risk factors for developing AKI. AKI and COVID-19 were associated with in-hospital death.
SUBMITTER: Xu H
PROVIDER: S-EPMC7982881 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BACKGROUND:As more patients at lower cardiovascular (CV) risk are treated with statins, the balance between cardiovascular benefits and the risk of adverse events becomes increasingly important. METHODS:We did a population-based cohort study (May 1, 2002 to March 30, 2013) using province-wide laboratory and administrative data in Alberta. We studied new statin users aged 66 years of age and older who were not receiving renal replacement therapy at baseline. We assessed statin use at 30-day intervals to allow time-varying assessment of statin exposure in Cox proportional hazards models that examined the relation between statin use and hospitalization with acute kidney injury (AKI). RESULTS:Of the 128,140 new statin users, 47 and 46% were prescribed high- and medium-intensity regimens at the index date. During median follow-up of 4.6 years (interquartile range 2.2, 7.4), 9118 individuals were hospitalized for AKI. Compared to non-use, the use of high- and medium-intensity statin regimens was associated with significant increases in the adjusted risks of hospitalization with AKI: hazard ratios 1.16 [95% confidence interval (CI) 1.10, 1.23] and 1.07 (95% CI 1.01, 1.13), respectively. Risks of AKI were higher among women than men, and among users of angiotensin converting enzyme inhibitors/angiotensin receptor blockers than non-users, and among diuretic users (p for interaction 0.002, 0.01, and 0.04 respectively). CONCLUSIONS:We found a graded, independent association between the intensity of statin use and the risk of hospitalization with AKI, although the absolute magnitude of the excess risk was small.
| S-EPMC6434639 | biostudies-literature
Project description:Coronavirus disease 19 (COVID-19) is caused by severe acute respiratory syndrome-corona virus (SARS-CoV-2), a beta coronavirus, mainly involves the respiratory tract, and the clinical features simulate to a severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) of the past. The genome of the SARS-CoV-2, isolated from a cluster-patient with a typical pneumonia after visiting Wuhan, had 89% nucleotide identitical with bat SARS-like-CoVZXC21 and 82% with that of human SARS-CoV. It enters the respiratory tract through angiotensin converting enzyme-2 (ACE2) receptors on alveoli. It may induce lung injury through direct cytopathic effect, involving effector T cells or causing sepsis and inducing cytokine storm. With a similar mechanism, it can cause acute kidney injury (AKI). The overall incidence of AKI is 5.1%, and AKI is an independent risk factor for mortality. The hazard ratio of death increases with the increasing severity of AKI. Management of COVID-19 with AKI is primarily supportive care, and at present, there are no evidence based effective antivirals for the treatment.
| S-EPMC7470203 | biostudies-literature
Project description:Background: Few epidemiologic studies on acute kidney injury (AKI) have focused on the older adult population. This study investigated the clinical features, risk factors, and clinical burden in this population. Methods: A retrospective observational study was performed with the clinical data of inpatients at Guangdong Geriatrics Institute from 1 August 2012, to 31 December 2016. AKI was classified into community-acquired AKI (CA-AKI) and hospital-acquired AKI (HA-AKI), and the risk factors for AKI were ranked by weight. The relationships between AKI and adverse outcomes during hospitalization were analyzed using univariate and multivariate logistic regression. Results: In total, 6126 patients were enrolled, and 1704 patients developed AKI (27.8%): 6.3% had CA-AKI, and 21.5% had HA-AKI. In total, 1425 (23.3%), 202 (3.3%), and 77 (1.3%) patients had stage 1, 2 and 3 AKI, respectively. Age, dementia, moderate/severe renal disease, moderate/severe liver disease, metastatic solid tumor, female sex, congestive heart failure, chronic pulmonary disease, diabetes mellitus with chronic complications, non-metastatic tumor and lymphoma were independent risk factors for HA-AKI. The first five were also independent risk factors for CA-AKI. After multiple adjustment, AKI was associated with intensive care admission (CA-AKI: OR 5.688, 95% CI 3.122-10.361; HA-AKI: OR 4.704, 95% CI 3.023-7.298) and in-hospital mortality (CA-AKI: OR 5.073, 95% CI 2.447-10.517; HA-AKI: OR 13.198, 95% CI 8.133-21.419). Conclusion: AKI occurs in >25% of older adults in the geriatric ward. In addition to traditional risk factors, dementia and tumors were risk factors for AKI in older adults. AKI is closely related to a poor prognosis.
| S-EPMC7671701 | biostudies-literature
Project description:As of 15 August 2020, Coronavirus disease 2019 (COVID-19) has been reported in >21 million people world-wide and is responsible for more than 750,000 deaths. The occurrence of acute kidney injury (AKI) in patients hospitalized with COVID-19 has been reported to be as high as 43%. This is comparable to AKI in other forms of pneumonia requiring hospitalization, as well as in non-infectious conditions like cardiac surgery. The impact of AKI on COVID-19 outcomes is difficult to assess at present but, similar to other forms of sepsis, AKI is strongly associated with hospital mortality. Indeed, mortality is reported to be very low in COVID-19 patients without AKI. Given that AKI contributes to fluid and acid-base imbalances, compromises immune response and may impair resolution of inflammation, it seems likely that AKI contributes to mortality in these patients. The pathophysiologic mechanisms of AKI in COVID-19 are thought to be multifactorial including systemic immune and inflammatory responses induced by viral infection, systemic tissue hypoxia, reduced renal perfusion, endothelial damage and direct epithelial infection with Severe Acute Respiratory Syndrome Coronavirus 2. Mitochondria play a central role in the metabolic deregulation in the adaptive response to the systemic inflammation and are also found to be vital in response to both direct viral damage and tissue reperfusion. These stress conditions are associated with increased glycolysis and reduced fatty acid oxidation. Thus, there is a strong rationale to target AKI for therapy in COVID-19. Furthermore, many approaches that have been developed for other etiologies of AKI such as sepsis, inflammation and ischemia-reperfusion, have relevance in the treatment of COVID-19 AKI and could be rapidly pivoted to this new disease.
| S-EPMC7665651 | biostudies-literature
Project description:Rationale & objectiveAcute kidney injury (AKI) is common in patients hospitalized with COVID-19, but validated, predictive models for AKI are lacking. We aimed to develop the best predictive model for AKI in hospitalized patients with coronavirus disease 2019 and assess its performance over time with the emergence of vaccines and the Delta variant.Study designLongitudinal cohort study.Setting & participantsHospitalized patients with a positive severe acute respiratory syndrome coronavirus 2 polymerase chain reaction result between March 1, 2020, and August 20, 2021 at 19 hospitals in Texas.ExposuresComorbid conditions, baseline laboratory data, inflammatory biomarkers.OutcomesAKI defined by KDIGO (Kidney Disease: Improving Global Outcomes) creatinine criteria.Analytical approachThree nested models for AKI were built in a development cohort and validated in 2 out-of-time cohorts. Model discrimination and calibration measures were compared among cohorts to assess performance over time.ResultsOf 10,034 patients, 5,676, 2,917, and 1,441 were in the development, validation 1, and validation 2 cohorts, respectively, of whom 776 (13.7%), 368 (12.6%), and 179 (12.4%) developed AKI, respectively (P = 0.26). Patients in the validation cohort 2 had fewer comorbid conditions and were younger than those in the development cohort or validation cohort 1 (mean age, 54 ± 16.8 years vs 61.4 ± 17.5 and 61.7 ± 17.3 years, respectively, P < 0.001). The validation cohort 2 had higher median high-sensitivity C-reactive protein level (81.7 mg/L) versus the development cohort (74.5 mg/L; P < 0.01) and higher median ferritin level (696 ng/mL) versus both the development cohort (444 ng/mL) and validation cohort 1 (496 ng/mL; P < 0.001). The final model, which added high-sensitivity C-reactive protein, ferritin, and D-dimer levels, had an area under the curve of 0.781 (95% CI, 0.763-0.799). Compared with the development cohort, discrimination by area under the curve (validation 1: 0.785 [0.760-0.810], P = 0.79, and validation 2: 0.754 [0.716-0.795], P = 0.53) and calibration by estimated calibration index (validation 1: 0.116 [0.041-0.281], P = 0.11, and validation 2: 0.081 [0.045-0.295], P = 0.11) showed stable performance over time.LimitationsPotential billing and coding bias.ConclusionsWe developed and externally validated a model to accurately predict AKI in patients with coronavirus disease 2019. The performance of the model withstood changes in practice patterns and virus variants.
| S-EPMC8990440 | biostudies-literature
Project description:Although the lungs are major targets for COVID-19 invasion, other organs-such as the kidneys-are also affected. However, the renal complications of COVID-19 are not yet well explored. This study aimed to identify the incidence of acute kidney injury (AKI) in patients with COVID-19 and to evaluate its impact on patient outcomes. This retrospective study included 704 patients with COVID-19 who were hospitalized at two hospitals in Daegu, Korea from February 19 to March 31, 2020. AKI was defined according to the serum creatinine criteria in the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines. The final date of follow-up was May 1, 2020. Of the 704 patients, 28 (4.0%) developed AKI. Of the 28 patients with AKI, 15 (53.6%) were found to have AKI stage 1, 3 (10.7%) had AKI stage 2, and 10 (35.7%) had AKI stage 3. Among these patients, 12 (42.9%) recovered from AKI. In the patients with AKI, the rates of admission to intensive care unit (ICU), administration of mechanical ventilator (MV), and in-hospital mortality were significantly higher than in patients without AKI. Multivariable analysis revealed that old age (Hazard ratio [HR] = 4.668, 95% confidence interval [CI] = 1.250-17.430, p = 0.022), high neutrophil-to-lymphocyte ratio (HR = 1.167, 95% CI = 1.078-1.264, p < 0.001), elevated creatinine kinase (HR = 1.002, 95% CI = 1.001-1.004, p = 0.007), and severe AKI (HR = 12.199, 95% CI = 4.235-35.141, p < 0.001) were independent risk factors for in-hospital mortality. The Kaplan-Meier curves showed that the cumulative survival rate was lowest in the AKI stage 3 group (p < 0.001). In conclusion, the incidence of AKI in patients with COVID-19 was 4.0%. Severe AKI was associated with in-hospital death.
| S-EPMC7725289 | biostudies-literature
Project description:ObjectiveTo determine the incidence of and risk factors for the development of acute kidney injury (AKI) and investigate the association between AKI and mortality in patients hospitalized with coronavirus disease 2019 (COVID-19) infection.Patients and methodsThis retrospective case series includes the first 370 patients consecutively hospitalized with confirmed COVID-19 illness between March 10, 2020, and May 13, 2020, at a 242-bed teaching hospital. To determine independent associations between demographic factors, comorbid conditions, and AKI incidence, multivariable logistic regression models were used to estimate odds ratios adjusted for clinical covariates.ResultsMedian age of patients was 71 (interquartile range, 59-82) years and 44.3% (145 of 327) were women. Patients with AKI were significantly older with a higher comorbid condition burden and mortality rate (58.1% [104 0f 179] vs 19.6% [29 of 148]; P<.001) when compared with those without AKI. Increasing age, chronic kidney disease, hyperlipidemia, and being of African American descent showed higher odds of AKI. Patients with AKI had significantly higher odds of mortality when compared with patients without AKI, and this effect was proportional to the stage of AKI. Increasing age and acute respiratory distress syndrome also revealed higher adjusted odds of mortality.ConclusionsAcute kidney injury is a common complication among hospitalized patients with COVID-19 infection. We found significantly higher odds of AKI with increasing age and among patients with hyperlipidemia, those with chronic kidney disease, and among African Americans. We demonstrate an independent association between AKI and mortality with increasingly higher odds of mortality from progressively worsening renal failure in hospitalized patients with COVID-19 infection.
| S-EPMC7368916 | biostudies-literature
Project description:IntroductionUrea is a toxin present in acute kidney injury (AKI). We hypothesize that reduction in serum urea levels might improve clinical outcomes. We examined the association between the reduction in urea and mortality.MethodsPatients with AKI admitted to the Hospital Civil de Guadalajara were enrolled in this retrospective cohort study. We create 4 groups of urea reduction ratio (UXR) stratified by their decrease in urea from the highest index value in comparison to the value on day 10 (0%, 1-25%, 26-50%, and >50%), or at the time of death or discharge if prior to 10 days. Our primary endpoint was to observe the association between UXR and mortality. Secondary observations included determination of which types of patients achieved a UXR >50%, whether the modality of kidney replacement therapy (KRT) effected changes in UXR, and if serum creatinine (sCr) value changes were similarly associated with patient mortality.ResultsA total of 651 AKI patients were enrolled. The mean age was 54.1 years, and 58.6% were male. AKI 3 was present in 58.5%; the mean admission urea was 154 mg/dL. KRT was started in 32.4%, and 18.9% died. A trend toward decreased risk of death was observed in association with the magnitude of UXR. The best survival (94.3%) was observed in patients with a UXR >50%, and the highest mortality (72.1%) was observed in patients achieving a UXR of 0%. After adjusting for age, sex, diabetes mellitus, CKD, antibiotics, sepsis, hypovolemia, cardio-renal syndrome, shock, and AKI stage, the 10-day mortality was higher in groups that did not achieve a UXR of at least 25% (OR: 1.20). Patients achieving a UXR >50% were most likely initiated on dialysis due to a diagnosis of the uremic syndrome or had a diagnosis of obstructive nephropathy. Percentage change in sCr was also associated with increased mortality risk.ConclusionsIn our retrospective cohort of AKI patients, the percent decrease in UXR from admission was associated with a stratified risk of death. Patients with a UXR >25% had the best associated outcomes. Overall, a greater magnitude in UXR was associated with improved patient survival.
| S-EPMC10308539 | biostudies-literature
Project description:BackgroundCOVID-19 is a multisystemic disorder that frequently causes acute kidney injury (AKI). However, the precise clinical and biochemical variables associated with AKI progression in patients with severe COVID-19 remain unclear.MethodsWe performed a retrospective study on 278 hospitalized patients who were admitted to the ward and intensive care unit (ICU) with COVID-19 between March 2020 and June 2020, at the University Hospital, São Paulo, Brazil. Patients aged ≥ 18 years with COVID-19 confirmed on RT-PCR were included. AKI was defined according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria. We evaluated the incidence of AKI, several clinical variables, medicines used, and outcomes in two sub-groups: COVID-19 patients with AKI (Cov-AKI), and COVID-19 patients without AKI (non-AKI). Univariate and multivariate analyses were performed.ResultsFirst, an elevated incidence of AKI (71.2%) was identified, distributed across different stages of the KDIGO criteria. We further observed higher levels of creatinine, C-reactive protein (CRP), leukocytes, neutrophils, monocytes, and neutrophil-to-lymphocyte ratio (NLR) in the Cov-AKI group than in the non-AKI group, at hospital admission. On univariate analysis, Cov-AKI was associated with older age (>62 years), hypertension, CRP, MCV, leucocytes, neutrophils, NLR, combined hydroxychloroquine and azithromycin treatment, use of mechanical ventilation, and vasoactive drugs. Multivariate analysis showed that hypertension and the use of vasoactive drugs were independently associated with a risk of higher AKI in COVID-19 patients. Finally, we preferentially found an altered erythrocyte and leukocyte cellular profile in the Cov-AKI group compared to the non-AKI group, at hospital discharge.ConclusionsIn our study, the development of AKI in patients with severe COVID-19 was related to inflammatory blood markers and therapy with hydroxychloroquine/azithromycin, with vasopressor requirement and hypertension considered potential risk factors. Thus, attention to the protocol, hypertension, and some blood markers may help assist doctors with decision-making for the management of COVID-19 patients with AKI.
| S-EPMC8148326 | biostudies-literature
Project description:Acute kidney injury (AKI) is common among hospitalized patients with coronavirus disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. An improved knowledge of the pathology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who develop AKI during COVID-19. In this review, we summarize the published cases and case series of various kidney pathologies seen with COVID-19. Both live kidney biopsies and autopsy series suggest acute tubular injury as the most commonly encountered pathology. Collapsing glomerulopathy and thrombotic microangiopathy are other encountered pathologies noted in both live and autopsy tissues. Other rare findings such as anti-neutrophil cytoplasmic antibody vasculitis, anti-glomerular basement membrane disease and podocytopathies have been reported. Although direct viral infection of the kidney is possible, it is certainly not a common or even widespread finding reported at the time of this writing (November 2020).
| S-EPMC7929005 | biostudies-literature