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Published on: February 2, 2021
Systemic reserve dysfunction and contrast-associated acute kidney injury following percutaneous coronary intervention
Mi-Jeong Kim1,2,3, Doo Soo Jeon1,2,3, Youngchul Ahn1
1Department of Cardiology, Incheon St. Mary's Hospital, The Catholic University of Korea, Incheon, Republic of Korea.
Insights
Neutrophil gelatinase-associated lipocalin (NGAL) levels before and after percutaneous coronary intervention (PCI) can help predict contrast-associated acute kidney injury (CA-AKI). This NGAL combination also indicates long-term mortality risk in PCI patients.
Area of Science:
- Nephrology
- Cardiology
- Biomarkers
Background:
- Contrast-associated acute kidney injury (CA-AKI) is a complication of percutaneous coronary intervention (PCI).
- Risk factors include patient characteristics and contrast media administration.
- The role of neutrophil gelatinase-associated lipocalin (NGAL) in CA-AKI post-PCI is not well understood.
Purpose of the Study:
- To investigate the diagnostic and prognostic value of NGAL in CA-AKI following PCI.
- To assess the association between NGAL levels and long-term mortality in these patients.
Main Methods:
- Prospective enrollment of patients undergoing PCI.
- CA-AKI defined by serum creatinine increase within 48-7 days post-PCI.
- Serum NGAL measured pre-PCI and 6 hours post-PCI.
- Patients grouped based on NGAL levels relative to the 75th percentile.
Main Results:
- CA-AKI occurred in 6.4% of patients.
- Combined pre- and post-PCI NGAL levels were independently associated with CA-AKI occurrence.
- NGAL groups showed significant differences in all-cause mortality over 29 months.
- Contrast administration had a limited role in CA-AKI development.
Conclusions:
- Combined pre- and post-PCI NGAL levels can aid in risk-stratifying CA-AKI and long-term mortality.
- Systemic reserve deficiency, not contrast alone, likely drives CA-AKI.
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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