Coronary interventions

Urine alkalinisation to prevent contrast-induced acute kidney injury: the prospective, randomised, controlled, open-label TEATE trial

EuroIntervention 2022;18:562-573. DOI: 10.4244/EIJ-D-22-00010

Marco Lombardi
Marco Lombardi1, MD; Michela Molisana1, MD; Eugenio Genovesi1, MD; Carlo De Innocentiis1, MD; Ugo Limbruno2, MD; Leonardo Misuraca2, MD; Luciano Moretti †3, MD; Luca Di Vito3, MD; Giulia Renda1, MD, PhD; Marco Zimarino1, MD, PhD; Marta Di Nicola4, PhD; Raffaele De Caterina5,6, MD, PhD
1. Institute of Cardiology, G. d’Annunzio University, Chieti, Italy; 2. Cardiology Department, Azienda USL Toscana Sud-Est, Grosseto, Italy; 3. Ospedale Mazzoni, Ascoli Piceno, Italy; 4. Department of Medical, Oral and Biotechnological Sciences, G. d’Annunzio University, Chieti, Italy; 5. University Cardiology Division, Pisa University Hospital, Pisa, Italy; 6. Fondazione Villa Serena per la Ricerca, Città Sant'Angelo, Pescara, Italy

Background: Contrast-induced acute kidney injury (CI-AKI) is prognostically relevant in invasive cardiological and radiological procedures. The administration of sodium bicarbonate has controversial effects. It has been hypothesised that bicarbonate is ineffective when unable to achieve adequate urine alkalinisation.

Aims: We tested the hypothesis that alkaline urine status with oral or intravenous (i.v.) bicarbonate on top of hydration alone prevents CI-AKI.

Methods: In a prospective, randomised, parallel-group, open-label trial, we compared 1) saline hydration alone (n=81); 2) i.v. bicarbonate (n=82); and 3) oral bicarbonate (n=78), in patients with chronic kidney disease (CKD) scheduled for the intra-arterial administration of contrast medium. The primary endpoint was the incidence of CI-AKI according to alkaline urine status achieved immediately before angiography. Secondary endpoints were the mean change of urine pH up to the time of angiography and the incidence of CI-AKI in the three groups.

Results: The incidence of CI-AKI was not significantly different in the three treatment arms (20% in the hydration group, 21% in the oral bicarbonate group and 22% in the i.v. bicarbonate group; p=0.94). Patients achieving a pH >6 before angiography (n=145) had a significantly lower incidence of CI-AKI compared with the others (n=96; odds ratio [OR] 0.48, 95% confidence interval [CI]: 0.25-0.90; p=0.023, primary study hypothesis). The proportion of patients achieving a pH >6 was higher in the i.v. and oral bicarbonate groups compared with hydration alone.

Conclusions: Urinary pH before administration of contrast medium is an inverse correlate of CI-AKI incidence, and bicarbonate is superior to hydration alone in achieving urinary alkalinisation. Since, however, bicarbonate did not reduce the incidence of CI-AKI, we conclude that urinary pH is a marker and not a mediator of CI-AKI (ClinicalTrials.gov: NCT02980003).

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contrast-induced nephropathymiscellaneousrenal insufficiency
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