The clinical utility of plasma neutrophil gelatinase-associated lipocalin in acute kidney injury

血浆中性粒细胞明胶酶相关脂质运载蛋白在急性肾损伤中的临床应用

阅读:6
作者:John W Pickering, Zoltan H Endre

Aim

Neutrophil gelatinase-associated lipocalin (NGAL) is derived from the distal tubule and is both reabsorbed and filtered and also shed into the urine after tubular injury. Plasma NGAL is unique amongst the candidate biomarkers of acute kidney injury (AKI) since elevated concentrations may reflect either a change in renal glomerular function or in structural tubular injury or both. In this study, we compared the performance of plasma NGAL in the diagnosis of functional changes and in the diagnosis of structural injury.

Conclusion

Increased plasma NGAL reflects both decreased filtration and structural injury. For patients at a low calculated risk, the addition of NGAL reduced the risk, and for those at a higher risk, NGAL correctly assigned patients to even a higher risk.

Methods

Plasma and urine samples from 528 patients were collected on entry to an intensive care unit (ICU) as well as 12 and 24 h later. Plasma NGAL diagnostic performance was independently assessed for Functional-AKI and Structural-AKI. Functional-AKI was defined by changes in plasma creatinine, whereas Structural-AKI was defined by elevations in urinary NGAL.

Results

On ICU entry, the area under the curve (AUC) for the diagnosis of Functional-AKI was 0.74 (95% CI: 0.69-0.79), and for Structural-AKI it was 0.79 (0.74-0.83). Plasma NGAL also predicted the need for dialysis (0.79; 0.66-0.81), but not for death. A principal component analysis demonstrated that the maximum plasma NGAL in 24 h reflected structural injury marginally more than functional changes. Plasma NGAL added value to an AKI diagnostic model comprising plasma creatinine, sepsis, age, and APACHE II score (integrated discrimination improvement: 0.073; 0.034-0.12).

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。