Does urine alkalinization prevent contrast-induced acute kidney injury?

The findings led researchers to conclude that urinary pH is not a mediator but a marker of CI-AKI as bicarbonate did not reduce the incidence of CI-AKI.

Contrast-induced acute kidney injury is useful for prognosis in invasive cardiological and radiological procedures. The administration of sodium bicarbonate has controversial effects. There is a hypothesis that bicarbonate is ineffective when it cannot achieve adequate urine alkalinization. Considering this, Marco Lombardi, Institute of Cardiology, G. d'Annunzio University, Chieti, Italy, and colleagues tested the hypothesis that alkaline urine status with oral or intravenous (i.v.) bicarbonate on top of hydration alone prevents CI-AKI.

For this purpose, the researchers compared the parameters in a prospective, randomized, parallel-group, open-label trial: 1) i.v. Bicarbonate (n=82); 2) saline hydration alone (n=81); and oral bicarbonate (n=78) in chronic kidney disease patients scheduled for the intra-arterial administration of contrast medium. The study's primary endpoint was the incidence of CI-AKI in accordance with the alkaline urine status achieved immediately before angiography. Secondary endpoints include the incidence of CI-AKI in the three groups and the mean change of urine pH up to the time of angiography.

The study led to the following findings:

• The incidence of CI-AKI was not remarkably 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).
• 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 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.

"Urinary pH before contrast medium administration is an inverse correlate of CI-AKI incidence, and bicarbonate is superior to hydration alone in achieving urinary alkalinization," the researchers wrote.

Since bicarbonate did not reduce the risk of CI-AKI, the researchers conclude that urinary pH is a marker and not a mediator of CI-AKI.

Reference:

"The study titled "Urine alkalinization to prevent contrast-induced acute kidney injury: the prospective, randomized, controlled, open-label TEATE trial" was published in the journal EuroIntervention.

DOI: 10.4244/EIJ-D-22-00010