AST-120 to target protein-bound uremic toxins improves cardiac output and kidney oxygenation in experimental chronic kidney disease.

Kidney and Blood Pressure Research

Abstract

Introduction Chronic kidney disease (CKD) is a global health problem with increasing incidence which is closely associated with cardiac dysfunction. In CKD uremic toxins accumulate as kidney function declines. Additionally, high salt intake is a growing health issue worldwide which can exacerbate kidney disease. In this study, we investigated the effect of reducing plasma levels of protein bound uremic toxins in a rat model of CKD, challenged with high salt intake and compared the effects to that of conventional treatment using an angiotensin converting enzyme inhibitor (ACEI). Methods In rats, the right kidney and 2/3 of the left kidney were surgically removed (5/6 nephrectomy). Animals were fed a normal salt diet and randomized to either no treatment (control) or chronic treatment with either the oral absorbent AST-120 to reduce plasma levels of protein bound uremic toxins; or the ACEI enalapril to inhibit angiotensin II signaling for five weeks. Following treatment, kidney function was measured before and after a week of high salt intake. Cardiac output and markers of oxidative stress was measured at the end of the study period. Results Treatment with AST-120 resulted in decreased levels of the uremic toxin indoxyl sulfate, improved cardiac output (ml/min: AST-120 44.9±5.4 compared to control 26.6±2.0; P

The Author(s). Published by S. Karger AG, Basel

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