Phenotyping of Acute Kidney Injury: Beyond Serum Creatinine

被引:131
作者
Moledina, Dennis G. [1 ]
Parikh, Chirag R. [2 ]
机构
[1] Yale Sch Med, Dept Internal Med, Sect Nephrol, Program Appl Translat Res, New Haven, CT USA
[2] VA Connecticut Healthcare Syst, West Haven, CT USA
基金
美国国家卫生研究院;
关键词
AKI; biomarkers; creatinine; cystatin C; NGAL; IL-18; KIM-1; L-FABP; IL-6; furosemide; urine microscopy; urinary casts; LONG-TERM SURVIVAL; URINARY BIOMARKERS; DIFFERENTIAL-DIAGNOSIS; GENE-EXPRESSION; ISCHEMIC-INJURY; POOR OUTCOMES; CYSTATIN C; AKI; DEFINITIONS; MORTALITY;
D O I
10.1016/j.semnephrol.2017.09.002
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Acute kidney injury (AKI) is a common complication in hospitalized patients and is associated with adverse short- and long-term outcomes. AKI is diagnosed by serum creatinine (SCr)-based consensus definitions that capture an abrupt decrease in glomerular filtration rate associated with AKI. However, SCr-based AKI definitions lack sensitivity and specificity for diagnosing structural kidney injury. Moreover, AKI is a heterogeneous condition consisting of distinct phenotypes based on its etiology, prognosis, and molecular pathways, and that may potentially require different therapies. SCr-based AKI definitions provide no information on these AKI phenotypes. This review highlights traditional and novel tools that overcome the limitations of SCr-based AKI definitions to improve AKI phenotyping. (C) 2017 Elsevier Inc. All rights reserved.
引用
收藏
页码:3 / 11
页数:9
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