Renal resistive index changes in a murin acute heart failure model

Abstract

Heart failure (HF) affects more than 10% of people over the age of 651. Regardless the etiology, kidney injury is common during HF1. Correlation between the evolution, severity and mortality of HF and increase of renal resistance index (RRI) has been shown. The objective of this study is to describe the evolution of RRI in a mice acute heart failure (AHF) model. The local ethics committee approved the study (S84/CNREEA#9). AHF was induced by subcutaneous injections of isoproterenol 3 and defined by a 10% decrease in the shortening fraction (SF) compared to baseline in C57Bl6 wild type male mice. The RRI was assessed by echography, after induction of AHF or in sham mice, as follow: RRI = (peak systolic velocity–end diastolic peak)/peak systolic velocity. RRI were compared by a Wilcoxon test (R software v3.4.4). A P value < 0.05 was considered significant. A total of 13 C57Bl6 mice were included (7 in sham group, 6 in AHF group). AHF mice had a lower SF and heart rate (HR) compared to sham mice (respectively 47 ± 1.7 vs. 62 ± 0.9, P < 0.05, and 432 ± 24 vs. 626 ± 12, P < 0.01). Cardiac output decreased in AHF group (15 ± 2.3 vs. 22.65 ± 2.3, P = 0.051). RRI was higher in AHF mice compared to sham mice (0.74 ± 0.05 vs. 0.54 ± 0.03, P < 0.05) and renal mean velocity was decreased (6.09 ± 0.8 vs. 9.20 ± 1.13, P = 0.051). In our study, RRI increased in AHF mice and renal mean velocity decreased, suggesting a kidney injury induced by AHF. For the first time in a mice preclinical model, we showed the availability of a new tool in small animal to assess renal hemodynamic. Further studies are needed to confirm the validity of this marker during AHF, especially regarding kidney injury biomarkers.