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. 2021 Mar;7(2):143-155.
doi: 10.1159/000510455. Epub 2020 Sep 30.

Drug-Induced Hospital-Acquired Acute Kidney Injury in China: A Multicenter Cross-Sectional Survey

Affiliations

Drug-Induced Hospital-Acquired Acute Kidney Injury in China: A Multicenter Cross-Sectional Survey

Chen Liu et al. Kidney Dis (Basel). 2021 Mar.

Abstract

Introduction: Drug-induced acute kidney injury (D-AKI) is one of the important types of AKI. The incidence of D-AKI in China has rarely been studied.

Objective: This study aims to explore the disease burden, related drugs, and risk factors of D-AKI.

Methods: A nationwide cross-sectional survey was conducted in adult patients from 23 academic hospitals in 17 provinces in China. Suspected AKI was screened based on serum creatinine changes in accordance with the 2012 Kidney Disease: Improving Global Outcomes Clinical Practice Guideline for AKI, patients who met the diagnosis of hospital-acquired AKI in January and July of 2014 were defined. Suspected AKI was firstly evaluated for the possibility of D-AKI by pharmacists using the Naranjo Scale and finally defined as D-AKI by nephrologists through reviewing AKI clinical features.

Results: Altogether 280,255 hospitalized patients were screened and 1,960 cases were diagnosed as hospital-acquired AKI, among which 735 cases were defined as having D-AKI (37.50%, 735/1,960) with an in-hospital mortality rate of 13.88% and 54.34% of the survivors did not achieve full renal recovery. 1,642 drugs were related to AKI in these patients. Anti-infectives, diuretics, and proton pump inhibitors were the top 3 types of drugs relevant to D-AKI, accounting for 66.63% cumulatively. Besides age, AKI staging, severe disease, hypoalbuminemia, plasma substitute, and carbapenem related D-AKI were independent risk factors for in-hospital mortality of D-AKI patients.

Conclusion: In China, D-AKI has caused a substantial medical burden. Efforts should be made to pursue nephrotoxic drug stewardship to minimize attributable risk and improve the prevention, diagnosis, and treatment of D-AKI.

Keywords: Drug-induced acute kidney injury; Hospital-acquired acute kidney injury.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Fig. 1
Fig. 1
Flowchart of the total research process. AKI, acute kidney injury; D-AKI, drug-induced acute kidney injury; SCr, serum creatinine.
Fig. 2
Fig. 2
With the increase in the number of AKI-related drugs used, the SCr peak value increased, but the difference did not reach statistical significance (p = 0.06). AKI, acute kidney injury; SCr, serum creatinine.
Fig. 3
Fig. 3
Different types of drugs were associated with various clinical features of D-AKI. The time interval between drug administration and AKI diagnosis was 3 (2, 6) days. Contrast agents, plasma substitutes, NSAIDs, and neuropsychiatric drugs caused the fastest AKI occurrence, that is, 2 (1, 6) days. The occurrence of AKI induced by anticoagulant and antiplatelet drugs was the slowest, that is, 5 (2, 8) days. Peak SCr levels were the highest in RASI-induced D-AKI (202 [165, 275] μmol/L) and the lowest in antitumor drug-induced AKI (114.3 [89, 159] μmol/L) and NSAID-induced AKI (117 [97, 160] μmol/L). D-AKI, drug-induced acute kidney injury; SCr, serum creatinine; NSAIDs, nonsteroidal anti-inflammatory drugs; RASIs, renin-angiotensin system inhibitors.
Fig. 4
Fig. 4
Patients with D-AKI relevant to plasma substitutes had the highest in-hospital death rate (19.72%) and the highest percentage of survivors failed to renal recover (50.88%). Those who had D-AKI associated with NSAIDs presented the lowest mortality (5.97%) and the lowest rate of kidney failure to recover (20.63%). D-AKI, drug-induced acute kidney injury; NSAIDs, nonsteroidal anti-inflammatory drugs.

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