| Summary: | <p><strong>BACKGROUND:</strong> Chronic kidney disease (CKD) is associated with fluid excess
which can be estimated by bioimpedance spectroscopy. We aimed to assess effects of sodium glucose co-transporter 2 inhibition on bioimpedance-derived “Fluid Overload” and adiposity in a CKD population.</p>
<p><strong>METHODS:</strong> EMPA-KIDNEY was a 6609-participant double-blind placebo-controlled
trial of empagliflozin 10 mg once daily in patients with CKD at risk of progression. In a 660-participant substudy, bioimpedance measurements were added to the main trial procedures at randomization, 2- and 18-month follow-up visits. The substudy’s primary outcome was the study-average difference in absolute “Fluid Overload” (an estimate of excess extracellular water) analyzed using a mixed-model repeated
measures approach.</p>
<p><strong>RESULTS:</strong> The 660 substudy participants were broadly representative of the 6609-
participant trial population. Substudy mean baseline absolute “Fluid Overload” was 0.4±1.7 L. Compared to placebo, the overall mean absolute “Fluid Overload” difference among those allocated empagliflozin was -0.24 L (95%CI -0.38, -0.11), with similar-sized differences at 2- and 18-months, and in pre-specified subgroups. Total body water differences comprised between-group differences in extracellular water of -0.49 L (95%CI -0.69, -0.30, including the -0.24 L “Fluid Overload” difference); and a -0.30 L (95%CI -0.57, -0.03) difference in intracellular water. There was no significant effect of empagliflozin on bioimpedance-derived adipose tissue mass (- 0.28 [95%CI -1.41, 0.85] kg). The between-group difference in weight was -0.7 kg
(95%CI -1.3, -0.1).</p>
<p><strong>CONCLUSIONS:</strong> In a broad range of patients with CKD, empagliflozin resulted in a
sustained reduction in a bioimpedance-derived estimate of fluid overload, with no statistically significant effect on fat mass.</p>
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