Acute kidney injury in<scp>C</scp>hina

Fang, Yi; Teng, Jie; Ding, Xiaoqiang

doi:10.1111/hdi.12193

Cited by 26 publications

(19 citation statements)

References 49 publications

(116 reference statements)

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“…AKI is one of the most serious complications with a reported mortality rate of 15% in hospitalized patients [15]. Our meta-analysis showed that HUA is a critical and potential risk factor for the incidence of AKI, not only in preoperative patients as reported previously but also in all hospitalized patients.…”

Section: Discussionsupporting

confidence: 64%

“…A current meta analysis found that the incidence of AKI after cardiac surgery was 22.3% around the world (95% CI 19.8-25.1) [2]. The incidence of PCI-induced AKI has been estimated between 2% and 30% depending mainly on baseline renal function, which is increasing along with the higher prevalence of CHD year by year [15, 29]. Our results suggest that higher pre-PCI SUA increased risk of AKI.…”

Section: Discussionmentioning

confidence: 68%

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Hyperuricemia increases the risk of acute kidney injury: a systematic review and meta-analysis

Song

et al. 2017

BMC Nephrol

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BackgroundMounting evidence indicated that the elevated serum uric acid level was associated with an increased risk of acute kidney injury (AKI). Our goal was to systematically evaluate the correlation of serum uric acid (SUA) level and incidence of AKI by longitudinal cohort studies.MethodsWe searched electronic databases and the reference lists of relevant articles. 18 cohort studies with 75,200 patients were analyzed in this random-effect meta-analysis. Hyperuricemia was defined as SUA levels greater than 360-420 μmol/L (6–7 mg/dl), which was various according to different studies. Data including serum uric acid, serum creatinine, and incidence of AKI and hospital mortality were summarized using random-effects meta-analysis.ResultsThe hyperuricemia group significantly exerted a higher risk of AKI compared to the controls (odds ratio OR 2.24, 95% CI 1.76-2.86, p < 0.01). Furthermore, there is less difference of the pooled rate of AKI after cardiac surgery between hyperuricemia and control group (34.3% vs 29.7%, OR 1.24, 95% CI 0.96-1.60, p = 0.10), while the rates after PCI were much higher in hyperuricemia group than that in control group (16.0% vs 5.3%, OR 3.24, 95% CI 1.93-5.45, p < 0.01). In addition, there were significant differences in baseline renal function at admission between hyperuricemia and control groups in most of the included studies. The relationship between hyperuricemia and hospital mortality was not significant. The pooled pre-operative SUA levels were higher in AKI group than that in the non-AKI group.ConclusionsElevated SUA level showed an increased risk for AKI in patients and measurements of SUA may help identify risks for AKI in these patients.

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Section: Discussionsupporting

confidence: 64%

Section: Discussionmentioning

confidence: 68%

Hyperuricemia increases the risk of acute kidney injury: a systematic review and meta-analysis

Song

et al. 2017

BMC Nephrol

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“…The mortality rate of the AKI patients in our study was 16.5%, consistent with other studies in China [20]. Most studies have consistently reported that the risk factors associated with a poor AKI prognosis include advancing age, cardiovascular disease, AKI stage, and so on [21].…”

Section: Discussionsupporting

confidence: 90%

Risk Factor Analysis for AKI Including Laboratory Indicators: a Nationwide Multicenter Study of Hospitalized Patients

Nie

Feng

et al. 2017

Kidney Blood Press Res

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Background/Aims: Risk factor studies for acute kidney injury (AKI) in China are lacking, especially those regarding non-traditional risk factors, such as laboratory indicators. Methods: All adult patients admitted to 38 tertiary and 22 secondary hospitals in China in any one month between July and December 2014 were surveyed. AKI patients were screened according to the Kidney Disease: Improving Global Outcomes’ definition of AKI. Logistic regression was used to analyze the risk factors for AKI, and Cox regression was used to analyze the risk of in-hospital mortality for AKI patients; additionally, a propensity score analysis was used to reconfirm the risk factors among laboratory indicators for mortality. Results: The morbidity of AKI was 0.97%. Independent risk factors for AKI were advancing age, male gender, hypertension, and chronic kidney disease. All-cause mortality was 16.5%. The predictors of mortality in AKI patients were advancing age, tumor, higher uric acid level and increases in Acute Physiologic Assessment and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores. The hazard ratio (HR) for mortality with uric acid levels > 9.1 mg/dl compared with ≤ 5.2 mg/dl was 1.78 (95% CI: 1.23 to 2.58) for the AKI patients as a group, and was 1.73 (95% CI: 1.24 to 2.42) for a propensity score-matched set. Conclusion: In addition to traditional risk factors, uric acid level is an independent predictor of all-cause mortality after AKI.

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“…Acute kidney injury (AKI) is a deterioration of renal function over a period of hours to days [1, 2]. It will cause severe morbidity if not handled properly [1, 2].…”

Section: Introductionmentioning

confidence: 99%

“…It will cause severe morbidity if not handled properly [1, 2]. Ischemic-hypoxia injury is the major pathological mechanism of AKI [1–4].…”

Section: Introductionmentioning

confidence: 99%

Prolyl hydroxylase 2 (PHD2) inhibition protects human renal epithelial cells and mice kidney from hypoxia injury

et al. 2016

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Prolyl hydroxylase domain protein 2 (PHD2) is a key oxygen sensor, setting low steady-state level of hypoxia-inducible factor-α (HIF-α). Here, we showed that treatment of cobalt chloride (CoCl2), a hypoxia mimic, in HK-2 tubular epithelial cells induced PHD2 and HIF-1/2α expression as well as cell apoptosis and autophagy activation. Three methyladenine (3-MA), the autophagy inhibitor, blocked autophagy and protected HK-2 cells from CoCl2. Significantly, siRNA knockdown of PHD2 also protected HK-2 cells from CoCl2, possibly via increasing HIF-1α expression. Reversely, HIF-1α siRNA knockdown almost abolished cytoprotection by PHD2 siRNA in CoCl2-treated HK-2 cells. In vivo, pretreatment with a PHD inhibitor L-mimosine remarkably attenuated mice renal ischemia-reperfusion injuries. Molecularly, L-mimosine inhibited apoptosis and inflammatory responses in injured mice kidneys. Together, our results suggest that PHD2 silence or inhibition protects human renal epithelial cells and mice kidney from hypoxia injuries.

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Acute kidney injury inChina

Cited by 26 publications

References 49 publications

Hyperuricemia increases the risk of acute kidney injury: a systematic review and meta-analysis

Hyperuricemia increases the risk of acute kidney injury: a systematic review and meta-analysis

Risk Factor Analysis for AKI Including Laboratory Indicators: a Nationwide Multicenter Study of Hospitalized Patients

Prolyl hydroxylase 2 (PHD2) inhibition protects human renal epithelial cells and mice kidney from hypoxia injury

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