BioMed Research International · 2015 · 26 citations · 20 references
MedicineCardiologyPharmacologyEarly DetectionInterventional CardiologyRenal PathophysiologyAcute Kidney InjuryRenal AssessmentRenal DiseaseRenal Function TestingRenal Function TestsRenal ImpairmentAcute Kidney Injury AssessmentAcute Kidney Injury DetectionBiomarker-based Early DetectionContrast Agent AdministrationContrast-induced Kidney InjuryContrast-induced NephropathyCystatin CSerum Creatinine Assessment
We tested the hypothesis whether midkine could represent an early biomarker of contrast-induced acute kidney injury (CIAKI) in 89 patients with normal serum creatinine undergoing PCI. Midkine, serum and urinary NGAL, and cystatin C were evaluated before and 2, 4, 8, 24, and 48 hours after PCI using commercially available kits. Serum creatinine was assessed before and 24 and 48 hours after PCI. We found a significant rise in serum midkine as early as after 2 hours (P < 0.001) when compared to the baseline values. It was also significantly higher 4 hours after PCI and then returned to the baseline values after 24 hours and started to decrease after 48 hours. When contrast nephropathy was defined as an increase in serum creatinine by >25% of the baseline level 48 hours after PCI, the prevalence of CIN was 10%. Patients with CIN received significantly more contrast agent (P < 0.05), but durations of PCI were similar. Midkine was significantly higher 2, 4, and 8 hours after PCI in patients with CIN. Since the "window of opportunity" is narrow in CIAKI and time is limited to introduce proper treatment after initiating insult, particularly when patients are discharged within 24 hours after the procedure, midkine needs to be investigated as a potential early marker for renal ischemia and/or nephrotoxicity.
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