Background
The novel coronavirus is pandemic around the world. Several researchers have given the evidence of impacts of COVID-19 on the respiratory, cardiovascular and gastrointestinal system. Studies still have debated on kidney injury of COVID-19 patients. The purpose of the meta-analysis was to evaluate the association of kidney impairment with the development of COVID-19.
Methods
The PubMed, Embase and MedRxiv databases were searched until May 1, 2020. We extracted data from eligible studies to summarize the clinical manifestations and laboratory indexes of kidney injury on COVID-19 infection patients and further compared the prevalence of acute kidney injury (AKI) and the mean differences of three biomarkers between in ICU/severe and non-ICU/non-severe cases. Heterogeneity was evaluated using the I2 method.
Results
In the sum of 24 studies with 10180 patients were included in this analysis. The pooled prevalence of AKI, increased serum creatinine (Scr), increased blood urea nitrogen (BUN), increased D-dimer, proteinuria and hematuria in patients with COVID-19 were 16.2%, 8.3%, 6.2%, 49.8%, 50.1% and 30.3% respectively. Moreover, the means of Scr, BUN and D-dimer were shown 6.4-folds, 1.8-folds and 0.67-folds, respectively, higher in ICU/severe cases than in corresponding non-ICU/non-severe patients. The prevalence of AKI was about 30 folds higher in ICU/severe patients compared with the non-ICU/non-severe cases.
Conclusions
Overall, we assessed the incidences of the clinic and laboratory features of kidney injury in COVID-19 patients. And kidney dysfunction may be a risk factor for COVID-19 patients developing into the severe condition. In reverse, COVID-19 can also cause damage to the kidney.
Objective
We aimed to establish a tool for rapid identification of KL49
Acinetobacter baumannii
.
Methods
Based on the capsular polysaccharide (CPS) synthesis genes database, we investigated the distribution of K locus type 49 (KL49) genes in other KL types and established a rapid identification method for KL49. We collected 61 clinical carbapenem-resistant
A. baumannii
(CRAB) strains, identified KL49 by
gtr100
detection, and used whole genome sequencing (WGS) for verification. A mouse pneumonia model was used to confirm the hypervirulence phenotype. We tested the presence of
gtr100
gene in 165 CRAB strains from three provinces in China and evaluated the correlation of
gtr100
carrying CRAB infection with mortality.
Results
The
gtr100
gene is the CPS synthesis gene found only in KL49. We screened out nine WGS-validated KL49 strains from 61 CRAB clinical strains using polymerase chain reaction (PCR) to detect the
gtr100
gene. The survival rates of KL49 strains were significantly lower than nonKL49 strains in a mouse pneumonia model. The survival rates of LAC-4
gtr100
knockout strain decreased significantly. Analysis of phylogenetics showed the worldwide spread of KL49
A. baumannii
. Infection of
gtr100
carrying CRAB is an independent risk for mortality (OR, 10.76; 95%CI: 3.08–37.55;
p
<0.001).
Conclusion
The hypervirulence phenotype of KL49 CRAB and the association with mortality highlight the urgent need for implementing control measures. The rapid identification assay has the potential to facilitate early medical intervention and worldwide surveillance.
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