Prevention of contrast induced nephropathy with urine alkalinization: the final results of the TEATE study

Abstract Aims Contrast-induced acute kidney injury (CI-AKI) after coronary angiography and percutaneous interventions (PCI) impacts on hospitalization duration and mortality. Pre-procedural hydration is the sole strategy currently recommended for preventing CI-AKI. The role of sodium bicarbonate (SB) although attractive, since urine alkalinization suppresses the production of reactive oxygen species, is still controversial, and the optimal dosing to attain adequate urine alkalinization is still undefined. The PrevenTion of contrast-inducEd nephropathy with urine alkalinization (TEATE) study was a prospective 3-centre 3-arm single-blind randomized controlled trial testing the hypothesis that adequate urine alkalinization is associated with CI-AKI prevention. Secondary endpoints were the efficacy of SB vs. saline in achieving adequate urine alkalinization and reducing the incidence of CI-AKI compared with saline. Methods and results Patients candidate to coronary angiography and/or PCI with moderate-to-severe chronic kidney disease [eGFR of 15–60 ml/min/1.73 m2, by the Modification of Diet in Renal Disease Study equation (MDRD)] were randomly assigned to saline hydration (control), oral SB or i.v. SB. The study protocol was registered (ClinicalTrials.gov NCT02980003). We evaluated urinary pH at the time of hospitalization, immediately before coronary angiography and 24–48 h after angiography. According to urine pH immediately before the procedure, patients were divided in two groups above or below a pH cut-off of 6. We enrolled a total of 241 patients: 81 were randomly assigned to the control group, 82 to i.v. SB and 78 to oral SB. Patients achieving a urinary pH > 6 before angiography had a lower incidence of CI-AKI (46%) than patients with urinary pH ≤ 6 (54%) [OR = 0.48 (95% CI: 0.25–0.9), P = 0.023]. The number of patients with urine pH > 6 was higher in both the i.v. (71%) and the oral SB (65%) groups compared to the hydration-only group (44%, P = 0.004). We found however no difference in the incidence of CI-AKI in the three treatment arms (20% in hydration alone, 21% in oral SB group and 22% in i.v. SB group) (P = 0.94). Subgroup analyses according to basal urine pH and eGFR ranges failed to identify statistically significant differences in the development of CI-AKI according to treatment allocation. Conclusions Urinary pH before the administration of contrast medium is an inverse correlate of CI-AKI incidence, and SB is superior to hydration alone in achieving urinary alkalinization. Since, however, SB did not reduce the incidence of CI-AKI, we conclude that urinary pH is a marker and not a mediator of CI-AKI.