Systemic reserve dysfunction and contrast-associated acute kidney injury following percutaneous coronary intervention

被引:0
作者
Kim, Mi-Jeong [1 ,2 ,3 ]
Jeon, Doo Soo [1 ,2 ,3 ]
Ahn, Youngchul [1 ]
Byeon, Jaeho [1 ]
Lee, Dongjae [1 ]
Choi, Ik Jun [1 ]
机构
[1] Catholic Univ Korea, Incheon St Marys Hosp, Dept Cardiol, Incheon, South Korea
[2] Catholic Univ Korea, Coll Med, Dept Cardiol, Seoul, South Korea
[3] Catholic Univ Korea, Catholic Res Inst Intractable Cardiovasc Dis, Coll Med, Seoul, South Korea
关键词
GELATINASE-ASSOCIATED LIPOCALIN; 2011 ACCF/AHA/SCAI GUIDELINE; ACUTE HEART-FAILURE; INDUCED NEPHROPATHY; AMERICAN-COLLEGE; RISK; PREDICTORS; EXPRESSION; DIALYSIS; OUTCOMES;
D O I
10.1371/journal.pone.0299899
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background Developing contrast-associated acute kidney injury (CA-AKI) following percutaneous coronary intervention (PCI) is closely related to patient-related risk factors as well as contrast administration. The diagnostic and prognostic roles of neutrophil gelatinase-associated lipocalin (NGAL) in CA-AKI following PCI are not well established. Methods Consecutive patients undergoing PCI were enrolled prospectively. CA-AKI was defined as an increase in the serum creatinine level >= 0.3 mg/dL within 48 hours or >= 1.5 times the baseline within 7 days after PCI. Serum NGAL concentrations were determined immediately before and 6 hours after PCI. The participants were classified into four NGAL groups according to the pre- and post-PCI NGAL values at 75th percentile. Results CA-AKI occurred in 38 (6.4%) of 590 patients. With chronic kidney disease status (hazard ratio [HR] 1.63, 95% confidence interval [CI]: 1.06-2.52), NGAL groups defined by the combination of pre- and 6 h post-PCI values were independently associated with the occurrence of CA-AKI (HR 1.69, 95% CI: 1.16-2.45). All-cause mortality for 29-month follow-ups was different among NGAL groups (log-rank p<0.001). Pre-PCI NGAL levels significantly correlated with baseline cardiac, inflammatory, and renal markers. Although post-PCI NGAL levels increased in patients with larger contrast administration, contrast media made a relatively limited contribution to the development of CA-AKI. Conclusion In patients undergoing PCI, the combination of pre- and post-PCI NGAL values may be a useful adjunct to current risk-stratification of CA-AKI and long-term mortality. CA-AKI is likely caused by systemic reserve deficiency rather than contrast administration itself.
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