Exploratory analysis of urine po2 peri-procedural kinetics and ci-aki prognostic abilities in patients undergoing pci.

Novel contrast-induced acute kidney injury (CI-AKI) biomarkers are needed to detect earlier and with greater precision the pathophysiological changes in renal medulla associated with kidney damage. We prospectively assessed the kinetics of urine oxygen tension (PO2) in control healthy individuals, and its prognostic ability for CI-AKI in patients undergoing percutaneous coronary intervention (PCI). We enrolled 202 consecutive patients (78% men, mean age 66±10 years) treated with elective or urgent PCI. PO2 was measured using a point-of-care (POC) standard blood gas analyzer at 3 time points (baseline, post -within 3 hours- PCI and at 24 hours post PCI) in urine samples. CI-AKI was defined as an increase of ≥25% or ≥0.5 mg/dl in pre-PCI serum creatinine at 48 hours post PCI. Between baseline and post-PCI measurements, patients without CI-AKI showed a decrease of -37 (36) mmHg in PO2 urine levels whereas patients with CI-AKI showed a decrease of only -23 (38) mmHg. (P=0.014). Using ROC analysis, percentage change in urine PO2 immediately after PCI relative to baseline levels, significantly predicted CI-AKI (AUC 0.804 95%CI 0.717-0.892). A significant drop in urine oxygen tension appears as a normal response of the kidney medulla to an acute insult (contrast media) immediately post PCI with a recovery to baseline levels 24 hours later. Absence or attenuation of this drop in urine oxygen tension could predict CI-AKI earlier and more precisely.