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1.
Biomolecules ; 12(2)2022 02 08.
Article in English | MEDLINE | ID: covidwho-1674482

ABSTRACT

A high proportion of critically ill patients with COVID-19 develop acute kidney injury (AKI) and die. The early recognition of subclinical AKI could contribute to AKI prevention. Therefore, this study was aimed at exploring the role of the urinary biomarkers NGAL and [TIMP-2] × [IGFBP7] for the early detection of AKI in this population. This prospective, longitudinal cohort study included critically ill COVID-19 patients without AKI at study entry. Urine samples were collected on admission to critical care areas for determination of NGAL and [TIMP-2] × [IGFBP7] concentrations. The demographic information, comorbidities, clinical, and laboratory data were recorded. The study outcomes were the development of AKI and mortality during hospitalization. Of the 51 individuals that were studied, 25 developed AKI during hospitalization (49%). Of those, 12 had persistent AKI (23.5%). The risk factors for AKI were male gender (HR = 7.57, 95% CI: 1.28-44.8; p = 0.026) and [TIMP-2] × [IGFBP7] ≥ 0.2 (ng/mL)2/1000 (HR = 7.23, 95% CI: 0.99-52.4; p = 0.050). Mortality during hospitalization was significantly higher in the group with AKI than in the group without AKI (p = 0.004). Persistent AKI was a risk factor for mortality (HR = 7.42, 95% CI: 1.04-53.04; p = 0.046). AKI was frequent in critically ill COVID-19 patients. The combination of [TIMP-2] × [IGFBP7] together with clinical information, were useful for the identification of subclinical AKI in critically ill COVID-19 patients. The role of additional biomarkers and their possible combinations for detection of AKI in ritically ill COVID-19 patients remains to be explored in large clinical trials.


Subject(s)
Acute Kidney Injury/diagnosis , Acute Kidney Injury/urine , COVID-19/diagnosis , COVID-19/urine , Critical Illness/mortality , Acute Kidney Injury/complications , Acute Kidney Injury/mortality , Adult , Aged , Biomarkers/urine , COVID-19/complications , COVID-19/mortality , Female , Humans , Insulin-Like Growth Factor Binding Proteins/urine , Kaplan-Meier Estimate , Lipocalin-2/urine , Longitudinal Studies , Male , Middle Aged , Prospective Studies , Risk Factors , Tissue Inhibitor of Metalloproteinase-2/urine
2.
JCI Insight ; 6(24)2021 12 22.
Article in English | MEDLINE | ID: covidwho-1518199

ABSTRACT

Kidneys are critical target organs of COVID-19, but susceptibility and responses to infection remain poorly understood. Here, we combine SARS-CoV-2 variants with genome-edited kidney organoids and clinical data to investigate tropism, mechanism, and therapeutics. SARS-CoV-2 specifically infects organoid proximal tubules among diverse cell types. Infections produce replicating virus, apoptosis, and disrupted cell morphology, features of which are revealed in the context of polycystic kidney disease. Cross-validation of gene expression patterns in organoids reflects proteomic signatures of COVID-19 in the urine of critically ill patients indicating interferon pathway upregulation. SARS-CoV-2 viral variants alpha, beta, gamma, kappa, and delta exhibit comparable levels of infection in organoids. Infection is ameliorated in ACE2-/- organoids and blocked via treatment with de novo-designed spike binder peptides. Collectively, these studies clarify the impact of kidney infection in COVID-19 as reflected in organoids and clinical populations, enabling assessment of viral fitness and emerging therapies.


Subject(s)
Acute Kidney Injury/urine , COVID-19/urine , Kidney Tubules, Proximal/virology , Kidney/virology , Organoids/virology , SARS-CoV-2/pathogenicity , Acute Kidney Injury/etiology , Adult , Aged , Angiotensin-Converting Enzyme 2/genetics , Animals , Apoptosis , Bowman Capsule/cytology , Bowman Capsule/virology , COVID-19/complications , Chlorocebus aethiops , Female , Gene Knockout Techniques , Hospital Mortality , Hospitalization , Humans , Kidney/metabolism , Kidney/pathology , Kidney Tubules, Proximal/metabolism , Kidney Tubules, Proximal/pathology , Male , Middle Aged , Organoids/metabolism , Podocytes/virology , Polycystic Kidney Diseases , Proteome , Receptors, Coronavirus/genetics , Reproducibility of Results , Transcriptome , Vero Cells , Viral Tropism , Virus Replication
3.
Clin Exp Nephrol ; 25(11): 1240-1246, 2021 Nov.
Article in English | MEDLINE | ID: covidwho-1303328

ABSTRACT

BACKGROUND: Severe acute respiratory syndrome Coronavirus 2 has rapidly spread worldwide, with acute kidney injury (AKI) as one of the manifestations with unknown causal mechanisms. We aimed to investigate tubular injury by assessing tubular markers and their association with the severity of Coronavirus disease 2019 (COVID-19). METHODS: We examined the associations between laboratory markers and urinary levels of N-acetyl-ß-D-glucosaminidase (uNAG), ß2-microglobulin (u ß2MG), α1-microglobulin (u α1MG), and liver-type fatty acid binding protein (L-FABP). We studied 18 COVID-19 patients without previous chronic kidney disease and analyzed the relationship between the urinary biomarkers and inflammatory markers in patients with severe (n = 7) or non-severe (n = 11) COVID-19, defined by requirements of supplemental oxygen. RESULTS: Fourteen patients (78%) showed abnormal urinalysis findings and two (11%) developed AKI. Patients with severe COVID-19 had significantly higher levels of proteinuria, uNAG, uß2MG, uα 1MG, and L-FABP than those with non-severe disease. Serum levels of interleukin-6 (IL-6) were significantly higher on admission in all severe COVID-19 cases and correlated with the levels of L-FABP, uß2MG, uα1MG, uNAG, and proteinuria. Moreover, the changes in serum IL-6 (ΔIL-6) levels from baseline to 7 days after admission significantly correlated with ΔL-FABP and Δuß2MG. CONCLUSIONS: Levels of tubular injury markers, especially L-FABP and uß2MG, were significantly associated with IL-6 levels even in patients with no evident AKI. This suggests that L-FABP and uß2MG could be useful as early detective biomarkers for COVID-19 associated renal injury.


Subject(s)
Acute Kidney Injury/blood , COVID-19/blood , Cytokines/blood , Inflammation Mediators/blood , Acute Kidney Injury/diagnosis , Acute Kidney Injury/etiology , Acute Kidney Injury/urine , Adult , Aged , Biomarkers/blood , Biomarkers/urine , COVID-19/complications , COVID-19/diagnosis , Fatty Acid-Binding Proteins/urine , Female , Humans , Interleukin-6/blood , Male , Middle Aged , Proteinuria/blood , Proteinuria/etiology , Proteinuria/urine , Retrospective Studies , Severity of Illness Index , Up-Regulation , beta 2-Microglobulin/urine
4.
Int Urol Nephrol ; 54(3): 627-636, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1293420

ABSTRACT

PURPOSE: To evaluate urinary kidney injury molecule-1 (uKIM-1), which is a proximal tubule injury biomarker in subclinical acute kidney injury (AKI) that may occur in COVID-19 infection. METHODS: The study included proteinuric (n = 30) and non-proteinuric (n = 30) patients diagnosed with mild/moderate COVID-19 infection between March and September 2020 and healthy individuals as a control group (n = 20). The uKIM-1, serum creatinine, cystatin C, spot urine protein, creatinine, and albumin levels of the patients were evaluated again after an average of 21 days. RESULTS: The median (interquartile range) uKIM-1 level at the time of presentation was 246 (141-347) pg/mL in the proteinuric group, 83 (29-217) pg/mL in the non-proteinuric group, and 55 (21-123) pg/mL in the control group and significantly high in the proteinuric group than the others (p < 0.001). Creatinine and cystatin C were significantly higher in the proteinuric group than in the group without proteinuria, but none of the patients met the KDIGO-AKI criteria. uKIM-1 had a positive correlation with PCR, non-albumin proteinuria, creatinine, cystatin C, CRP, fibrinogen, LDH, and ferritin, and a negative correlation with eGFR and albumin (p < 0.05). In the multivariate regression analysis, non-albumin proteinuria (p = 0.048) and BUN (p = 0.034) were identified as independent factors predicting a high uKIM-1 level. After 21 ± 4 days, proteinuria regressed to normal levels in 20 (67%) patients in the proteinuric group. In addition, the uKIM-1 level, albuminuria, non-albumin proteinuria, and CRP significantly decreased. CONCLUSIONS: Our findings support that the kidney is one of the target organs of the COVID-19 and it may cause proximal tubule injury even in patients that do not present with AKI or critical/severe COVID-19 infection.


Subject(s)
Acute Kidney Injury , Biomarkers , COVID-19 , Hepatitis A Virus Cellular Receptor 1/analysis , Noncommunicable Diseases , Urinalysis , Acute Kidney Injury/blood , Acute Kidney Injury/epidemiology , Acute Kidney Injury/etiology , Acute Kidney Injury/urine , Biomarkers/blood , Biomarkers/urine , COVID-19/complications , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/physiopathology , Comorbidity , Correlation of Data , Creatinine/blood , Creatinine/urine , Cystatin C/blood , Female , Humans , Male , Middle Aged , Noncommunicable Diseases/drug therapy , Noncommunicable Diseases/epidemiology , Proteinuria , Reproducibility of Results , SARS-CoV-2 , Severity of Illness Index , Turkey/epidemiology , Urinalysis/methods , Urinalysis/statistics & numerical data
5.
J Am Soc Nephrol ; 32(10): 2517-2528, 2021 10.
Article in English | MEDLINE | ID: covidwho-1259282

ABSTRACT

BACKGROUND: AKI is a complication of coronavirus disease 2019 (COVID-19) that is associated with high mortality. Despite documented kidney tropism of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there are no consistent reports of viral detection in urine or correlation with AKI or COVID-19 severity. Here, we hypothesize that quantification of the viral load of SARS-CoV-2 in urine sediment from patients with COVID-19 correlates with occurrence of AKI and mortality. METHODS: The viral load of SARS-CoV-2 in urine sediments (U-viral load) was quantified by qRT-PCR in 52 patients with PCR-confirmed COVID-19 diagnosis, who were hospitalized between March 15 and June 8, 2020. Immunolabeling of SARS-CoV-2 proteins Spike and Nucleocapsid was performed in two COVID-19 kidney biopsy specimens and urine sediments. Viral infectivity assays were performed from 32 urine sediments. RESULTS: A total of 20 patients with COVID-19 (39%) had detectable SARS-CoV-2 U-viral load, of which 17 (85%) developed AKI with an average U-viral load four-times higher than patients with COVID-19 who did not have AKI. U-viral load was highest (7.7-fold) within 2 weeks after AKI diagnosis. A higher U-viral load correlated with mortality but not with albuminuria or AKI stage. SARS-CoV-2 proteins partially colocalized with the viral receptor ACE2 in kidney biopsy specimens in tubules and parietal cells, and in urine sediment cells. Infective SARS-CoV-2 was not detected in urine sediments. CONCLUSION: Our results further support SARS-CoV-2 kidney tropism. A higher SARS-CoV-2 viral load in urine sediments from patients with COVID-19 correlated with increased incidence of AKI and mortality. Urinary viral detection could inform the medical care of patients with COVID-19 and kidney injury to improve prognosis.


Subject(s)
Acute Kidney Injury/virology , COVID-19/complications , SARS-CoV-2/isolation & purification , Viral Load , Acute Kidney Injury/etiology , Acute Kidney Injury/urine , Adult , Aged , Angiotensin-Converting Enzyme 2/analysis , COVID-19/urine , Female , Humans , Male , Middle Aged , Severity of Illness Index , Urine/virology
6.
Sci Rep ; 11(1): 11134, 2021 05 27.
Article in English | MEDLINE | ID: covidwho-1246397

ABSTRACT

Risk factors associated with severity and mortality attributable to COVID-19 have been reported in different cohorts, highlighting the occurrence of acute kidney injury (AKI) in 25% of them. Among other, SARS-CoV-2 targets renal tubular cells and can cause acute renal damage. The aim of the present study was to evaluate the usefulness of urinary parameters in predicting intensive care unit (ICU) admission, mortality and development of AKI in hospitalized patients with COVID-19. Retrospective observational study, in a tertiary care hospital, between March 1st and April 19th, 2020. We recruited adult patients admitted consecutively and positive for SARS-CoV-2. Urinary and serum biomarkers were correlated with clinical outcomes (AKI, ICU admission, hospital discharge and in-hospital mortality) and evaluated using a logistic regression model and ROC curves. A total of 199 COVID-19 hospitalized patients were included. In AKI, the logistic regression model with a highest area under the curve (AUC) was reached by the combination of urine blood and previous chronic kidney disease, with an AUC of 0.676 (95%CI 0.512-0.840; p = 0.023); urine specific weight, sodium and albumin in serum, with an AUC of 0.837 (95% CI 0.766-0.909; p < 0.001) for ICU admission; and age, urine blood and lactate dehydrogenase levels in serum, with an AUC of 0.923 (95%CI 0.866-0.979; p < 0.001) for mortality prediction. For hospitalized patients with COVID-19, renal involvement and early alterations of urinary and serum parameters are useful as prognostic factors of AKI, the need for ICU admission and death.


Subject(s)
Acute Kidney Injury/mortality , Acute Kidney Injury/urine , COVID-19/mortality , COVID-19/urine , Acute Kidney Injury/complications , Acute Kidney Injury/physiopathology , Adult , Aged , Area Under Curve , Biomarkers/urine , COVID-19/complications , COVID-19/physiopathology , Critical Care , Female , Hospitalization , Humans , Logistic Models , Male , Middle Aged , Observational Studies as Topic , Prognosis , ROC Curve , Retrospective Studies , Risk Factors , Severity of Illness Index , Urine/chemistry
7.
Cytokine ; 146: 155589, 2021 10.
Article in English | MEDLINE | ID: covidwho-1240276

ABSTRACT

BACKGROUND: Acute kidney injury is common in COVID-19 patients admitted to the ICU. Urinary biomarkers are a non-invasive way of assaying renal damage, and so far, urinary cytokines are not fully investigated. The current study aimed to assess urinary cytokine levels in COVID-19 patients. METHODS: Urine was collected from COVID-19 patients (n = 29) in intensive care and compared to a preoperative group of patients (n = 9) with no critical illness. 92 urinary cytokines were analyzed in multiplex using the Olink Target 96 inflammation panel and compared to clinical characteristics, and urinary markers of kidney injury. RESULTS: There were strong correlations between proinflammatory cytokines and between urinary cytokines and urinary kidney injury markers in 29 COVID-19 patients. Several cytokines were correlated to kidney injury, 31 cytokines to AKI stage and 19 cytokines correlated to maximal creatinine. CONCLUSIONS: Urinary inflammatory cytokines from a wide range of immune cell lineages were significantly upregulated during COVID-19 and the upregulation correlated with acute kidney injury as well as urinary markers of kidney tissue damage.


Subject(s)
Acute Kidney Injury/urine , Biomarkers/urine , COVID-19/urine , Critical Illness , Cytokines/urine , Aged , Albuminuria/urine , COVID-19/diagnosis , COVID-19/virology , Creatinine/blood , Creatinine/urine , Critical Care , Female , Humans , Male , Middle Aged , SARS-CoV-2/physiology
8.
J Am Soc Nephrol ; 32(1): 151-160, 2021 01.
Article in English | MEDLINE | ID: covidwho-1080996

ABSTRACT

BACKGROUND: Early reports indicate that AKI is common among patients with coronavirus disease 2019 (COVID-19) and associated with worse outcomes. However, AKI among hospitalized patients with COVID-19 in the United States is not well described. METHODS: This retrospective, observational study involved a review of data from electronic health records of patients aged ≥18 years with laboratory-confirmed COVID-19 admitted to the Mount Sinai Health System from February 27 to May 30, 2020. We describe the frequency of AKI and dialysis requirement, AKI recovery, and adjusted odds ratios (aORs) with mortality. RESULTS: Of 3993 hospitalized patients with COVID-19, AKI occurred in 1835 (46%) patients; 347 (19%) of the patients with AKI required dialysis. The proportions with stages 1, 2, or 3 AKI were 39%, 19%, and 42%, respectively. A total of 976 (24%) patients were admitted to intensive care, and 745 (76%) experienced AKI. Of the 435 patients with AKI and urine studies, 84% had proteinuria, 81% had hematuria, and 60% had leukocyturia. Independent predictors of severe AKI were CKD, men, and higher serum potassium at admission. In-hospital mortality was 50% among patients with AKI versus 8% among those without AKI (aOR, 9.2; 95% confidence interval, 7.5 to 11.3). Of survivors with AKI who were discharged, 35% had not recovered to baseline kidney function by the time of discharge. An additional 28 of 77 (36%) patients who had not recovered kidney function at discharge did so on posthospital follow-up. CONCLUSIONS: AKI is common among patients hospitalized with COVID-19 and is associated with high mortality. Of all patients with AKI, only 30% survived with recovery of kidney function by the time of discharge.


Subject(s)
Acute Kidney Injury/etiology , COVID-19/complications , SARS-CoV-2 , Acute Kidney Injury/epidemiology , Acute Kidney Injury/therapy , Acute Kidney Injury/urine , Aged , Aged, 80 and over , COVID-19/mortality , Female , Hematuria/etiology , Hospital Mortality , Hospitals, Private/statistics & numerical data , Hospitals, Urban/statistics & numerical data , Humans , Incidence , Inpatients , Leukocytes , Male , Middle Aged , New York City/epidemiology , Proteinuria/etiology , Renal Dialysis , Retrospective Studies , Treatment Outcome , Urine/cytology
9.
Diabetes Metab Syndr ; 15(1): 187-191, 2021.
Article in English | MEDLINE | ID: covidwho-987526

ABSTRACT

BACKGROUND AND AIMS: Renal involvement in Covid-19 infection is varied and can affect glomeruli, tubules, interstitium and can cause acute kidney injury (AKI). AKI is a strong predictor of mortality. Routine urinalysis gives an insight into the renal pathology of the patient. We studied the incidence of urinary abnormalities in hospitalised Covid-19 patients and analysed their impact on development of AKI and mortality. METHODS: Information on 110 hospitalised patients with confirmed Covid-19 was retrospectively collected and analysed. The demographic data such as age, gender, comorbid conditions such as diabetes mellitus, the need for dialysis and laboratory data such as urine for albumin, glucose, RBC and WBC, and serum creatinine were collected. The diagnosis of AKI was based on the KDIGO criteria. The outcomes studied were development of AKI and hospital mortality. RESULTS: Urine abnormalities were seen in 71% of the patients. Proteinuria in 58.2%, haematuria in 17.3%, pyuria in 8.2% of patients and concurrent proteinuria and haematuria was seen in 13.6% of patients. AKI was seen in 28.2% of patients and hospital mortality was 24.5%. AKI was strongly associated with mortality. Proteinuria and haematuria were good predictors of development of AKI, more strongly when they occurred concurrently (p < 0.01). CONCLUSION: Our results suggest that urine analysis is a simple test, which can be used to predict development of AKI and mortality and may be used for risk stratification of Covid-19 patients, especially in low resource settings.


Subject(s)
Acute Kidney Injury/epidemiology , Acute Kidney Injury/urine , COVID-19/epidemiology , COVID-19/urine , Acute Kidney Injury/diagnosis , Adult , Aged , COVID-19/diagnosis , Female , Hospitalization/trends , Humans , India/epidemiology , Male , Middle Aged , Predictive Value of Tests , Proteinuria/diagnosis , Proteinuria/epidemiology , Proteinuria/urine , Retrospective Studies , Urinalysis/trends
10.
Acta Anaesthesiol Scand ; 65(3): 364-372, 2021 03.
Article in English | MEDLINE | ID: covidwho-944614

ABSTRACT

BACKGROUND: Acute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate and/or reduced urine flow associated with mortality in corona virus disease 2019 (COVID-19). AKI is often associated with renal tissue damage, which may lead to chronic kidney disease. Biomarkers of tissue damage may identify patients of particular risk. METHODS: In a prospective observational study of 57 patients admitted to intensive care, AKI incidence and characteristics was evaluated according to KDIGO criteria and related to days after admission. Urinary albumin, Neutrophil Gelatinase-Associated Lipocalin (NGAL), Kidney Injury Molecule 1 (KIM-1) and Plasma Tissue Inhibitor of MetalloProteinase 2 (TIMP-2) were analysed in 52 patients at admission. The majority (n = 51, 89%) of patients developed AKI, and 27 (47%) patients had predominantly oliguric AKI where oliguria was more severe than plasma Creatinine increase. Severe oliguria within first 2 days after admission was common (n = 37, 65%), whereas stage 2 and 3 AKI due to Creatinine occurred later than day 2 in 67% (12/18) of cases. Renal replacement therapy was started in 9 (16%) patients, and 30-day mortality was 28%. Urinary biomarkers were increased in a majority of patients, but did not robustly predict KDIGO stage. Most patients had microalbuminuria, and severe albuminuria (albumin Creatinine ratio > 30 mg/mmol) was found in n = 9 (17%) patients. CONCLUSIONS: A majority of patients with COVID-19 admitted to the ICU develop AKI. The functional deficit is often low urinary volume, and initial levels of biomarkers are generally increased without clear relation to final AKI stage.


Subject(s)
Acute Kidney Injury/etiology , COVID-19/complications , Critical Care/methods , Oliguria/etiology , Acute Kidney Injury/therapy , Acute Kidney Injury/urine , Biomarkers/urine , COVID-19/urine , Female , Humans , Intensive Care Units , Male , Middle Aged , Oliguria/therapy , Oliguria/urine , Prospective Studies , Renal Replacement Therapy/methods , SARS-CoV-2
11.
Kidney Blood Press Res ; 45(6): 1018-1032, 2020.
Article in English | MEDLINE | ID: covidwho-917826

ABSTRACT

INTRODUCTION: Acute kidney injury (AKI) is strongly associated with poor outcomes in hospitalized patients with coronavirus disease 2019 (COVID-19), but data on the association of proteinuria and hematuria are limited to non-US populations. In addition, admission and in-hospital measures for kidney abnormalities have not been studied separately. METHODS: This retrospective cohort study aimed to analyze these associations in 321 patients sequentially admitted between March 7, 2020 and April 1, 2020 at Stony Brook University Medical Center, New York. We investigated the association of proteinuria, hematuria, and AKI with outcomes of inflammation, intensive care unit (ICU) admission, invasive mechanical ventilation (IMV), and in-hospital death. We used ANOVA, t test, χ2 test, and Fisher's exact test for bivariate analyses and logistic regression for multivariable analysis. RESULTS: Three hundred patients met the inclusion criteria for the study cohort. Multivariable analysis demonstrated that admission proteinuria was significantly associated with risk of in-hospital AKI (OR 4.71, 95% CI 1.28-17.38), while admission hematuria was associated with ICU admission (OR 4.56, 95% CI 1.12-18.64), IMV (OR 8.79, 95% CI 2.08-37.00), and death (OR 18.03, 95% CI 2.84-114.57). During hospitalization, de novo proteinuria was significantly associated with increased risk of death (OR 8.94, 95% CI 1.19-114.4, p = 0.04). In-hospital AKI increased (OR 27.14, 95% CI 4.44-240.17) while recovery from in-hospital AKI decreased the risk of death (OR 0.001, 95% CI 0.001-0.06). CONCLUSION: Proteinuria and hematuria both at the time of admission and during hospitalization are associated with adverse clinical outcomes in hospitalized patients with COVID-19.


Subject(s)
Acute Kidney Injury/urine , Acute Kidney Injury/virology , COVID-19/urine , Hematuria/virology , Proteinuria/virology , Acute Kidney Injury/mortality , Aged , COVID-19/mortality , COVID-19/virology , Cohort Studies , Female , Hematuria/mortality , Humans , Male , Middle Aged , New York/epidemiology , Proteinuria/mortality , Retrospective Studies , SARS-CoV-2/isolation & purification , Survival Analysis
14.
Crit Care ; 24(1): 356, 2020 06 18.
Article in English | MEDLINE | ID: covidwho-603793

ABSTRACT

BACKGROUND: The aim of this study is to assess the prevalence of abnormal urine analysis and kidney dysfunction in COVID-19 patients and to determine the association of acute kidney injury (AKI) with the severity and prognosis of COVID-19 patients. METHODS: The electronic database of Embase and PubMed were searched for relevant studies. A meta-analysis of eligible studies that reported the prevalence of abnormal urine analysis and kidney dysfunction in COVID-19 was performed. The incidences of AKI were compared between severe versus non-severe patients and survivors versus non-survivors. RESULTS: A total of 24 studies involving 4963 confirmed COVID-19 patients were included. The proportions of patients with elevation of sCr and BUN levels were 9.6% (95% CI 5.7-13.5%) and 13.7% (95% CI 5.5-21.9%), respectively. Of all patients, 57.2% (95% CI 40.6-73.8%) had proteinuria, 38.8% (95% CI 26.3-51.3%) had proteinuria +, and 10.6% (95% CI 7.9-13.3%) had proteinuria ++ or +++. The overall incidence of AKI in all COVID-19 patients was 4.5% (95% CI 3.0-6.0%), while the incidence of AKI was 1.3% (95% CI 0.2-2.4%), 2.8% (95% CI 1.4-4.2%), and 36.4% (95% CI 14.6-58.3%) in mild or moderate cases, severe cases, and critical cases, respectively. Meanwhile, the incidence of AKI was 52.9%(95% CI 34.5-71.4%), 0.7% (95% CI - 0.3-1.8%) in non-survivors and survivors, respectively. Continuous renal replacement therapy (CRRT) was required in 5.6% (95% CI 2.6-8.6%) severe patients, 0.1% (95% CI - 0.1-0.2%) non-severe patients and 15.6% (95% CI 10.8-20.5%) non-survivors and 0.4% (95% CI - 0.2-1.0%) survivors, respectively. CONCLUSION: The incidence of abnormal urine analysis and kidney dysfunction in COVID-19 was high and AKI is closely associated with the severity and prognosis of COVID-19 patients. Therefore, it is important to increase awareness of kidney dysfunction in COVID-19 patients.


Subject(s)
Acute Kidney Injury/epidemiology , Acute Kidney Injury/virology , Betacoronavirus , Coronavirus Infections/epidemiology , Pneumonia, Viral/epidemiology , Acute Kidney Injury/urine , COVID-19 , Coronavirus Infections/urine , Humans , Pandemics , Pneumonia, Viral/urine , Prevalence , SARS-CoV-2
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