Abstract
Introduction: Conventional hemodialysis (CHD) is the standard method of dialysis with concomitant changes in the cardiovascular system that may result in left ventricular hypertrophy (LVH). Importantly, increased frequency of dialysis reduces cardiac complications by regulating fluid status. Klotho and Fibroblast Growth Factor 23 (FGF23) has been shown to be expressed in a reciprocal fashion in patients with end-stage renal disease with LVH. Research Questions/Hypothesis: The Klotho/FGF23 axis may be regulated by circulating microRNAs (miRs) in CHD patients that transition to nocturnal hemodialysis (NHD) thereby regulating the development of LV mass. Goals/ Aims: To define alterations in expression of circulating miRs in patients transitioning from CHD to NHD and correlate the miR signatures with alterations in LV mass. Methods/Approach: Total RNA was isolated from serum of patients undergoing CHD and NHD and used to define the differential expression of miRs via microarray analysis. In parallel, circulating levels of Klotho and FGF23 were measured via ELISA analysis. Results/Data: We identified miRs with differential expression patterns in CHD vs NHD that targeted the Klotho/FGF23 axis. In patients with ≥10% increase or decrease of LV mass, a subset of miRs were identified that regulated the Klotho/FGF23 axis, namely let-7 members, miR-200c, miR-1 and miR-30c. There was no significant correlation between Klotho levels and LV mass in ESRD patients (p >0.05). However, we observed an association between FGF23 levels and LV mass in patients who were treated with NHD such that there were increased circulating FGF23 levels with increased LV mass, and vice versa (p=0.008, two-way ANOVA). Conclusion: Our novel findings have identified the differential expression of miRs in patients that transition from CHD to NHD with concomitant alterations in LV mass. Therapeutic delivery of miR antagomirs or mimics may mitigate cardiac hypertrophy in patients with renal disease by regulating the Klotho/FGF23 axis.
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