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Original Articles

Platelet count as a new biomarker for acute kidney injury induced by hemorrhagic shock

, , , , , , , , , & show all
Pages 94-102 | Received 18 Nov 2018, Accepted 20 Jan 2019, Published online: 27 Feb 2019
 

Abstract

The aim of this study was to investigate the association between nadir platelet count and acute kidney injury (AKI) or 28-day all-cause mortality induced by hemorrhagic shock (HS), and to determine the cutoff value of nadir platelet count in HS clinical practice. This retrospective study included hospitalized patients enrolled in a tertiary-care teaching hospital from January 1, 2010 to December 31, 2015. Clinical data from HS admitted to the intensive care unit (ICU) were evaluated. Nadir platelet count was defined as the lowest values in the first 48 h. Multivariate logistic regression and Cox proportional hazards regression were used to assess the correlation between nadir platelet count and AKI or 28-day all-cause mortality induced by HS, respectively; the area under receiver operating characteristic (AU-ROC) and Youde’s index were used to determine the optimal cutoff value of nadir platelet count. Kaplan-Meier’s method and log-rank test were assessed for the 28-day all-cause mortality in AKI and non-AKI groups. Of 1589 patients screened, 84 patients (mean age,37.1 years; 58 males) were included in the primary analysis in which 30 patients with AKI. Multiple logistic results indicated that nadir platelet count was a risk factor of AKI (OR = 0.71,95% confidence interval [CI] 0.54–0.93, P < 0.05). Cox regression analysis revealed that nadir platelet count was independent risk factors for 28-day all-cause mortality (Hazard ratios [HR]0.89,95%CI 0.76–0.99, P < 0.05). Kaplan-Meier curve showed that 28-day all-cause mortality was significantly higher in patients with AKI than non-AKI (P < 0.001).These results suggest that nadir platelet count in the first 48 h is a new biomarker for AKI and 28-day all-cause mortality induced by HS. Moreover, the risk for AKI and 28-day all-cause mortality in HS patients decreased by 29% and 11%, respectively, for every 10 × 109/L increase in platelet count. Additional studies are needed to investigate whether elevation of nadir platelet count reduces the risk in different genders.

Consent for publication

All authors agree with the content of this manuscript.

Acknowledgement

The authors acknowledge all staff who helped perform this study. and particularly acknowledge Xinglin Chen, Ph.D., who works in Empower Stats software, for providing advice regarding the data analysis.

Ethics approval and consent to participate

The ethics committee of the Second People’s Hospital of Shenzhen approved this study (Ethical Number: 20160115004), and the consent was obtained from each patient or their next of kin.

Disclosure Statement

The authors have no conflicts of interest to declare.

Author Contributions

Ming Wu, Yong-ming Yao, and Yong-wen Feng contributed to the study conception and design. All authors performed the research. Jun-fu Lu collected and analyzed the data. Ming Wu, and Ying-yi Luan wrote the manuscript.

Additional information

Funding

This study was supported, in part, by grants from the National Natural Science Foundation (Nos. 81130035, 81272090, 81372054), Medical Science and Technology Research Foundation of Guangdong Province (No. A2016353), Sanming Project of Medicine in Shenzhen (SZSM20162011), the Beijing Nova Program of China (No. Z171100001117113), Shenzhen Science and Technology Planning Project (No. JCYJ20160425103130218, JCYJ20170306091335008). and (SZLY2017007)the National Natural Science Foundation of China [81130035, 81272090,81372054];the Beijing Nova Program [Z171100001117113].

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