Abstract Background and Aims Right ventricular dysfunction (RVD) has been shown to predict mortality in patients with kidney failure. It has been proposed that RVD in these patients is mediated by inflammatory and fibrotic mechanisms, which may be enhanced by hemodialysis (HD). The present study aimed to investigate the potential associations between RVD and circulating biomarkers of myocardial inflammation and fibrosis with all-cause mortality in HD patients. Method We performed a retrospective single-centre cohort study of prevalent patients admitted in a chronic HD program for more than 3 months. Clinical characteristics and echocardiographic parameters were assessed in all patients. Pre-dialysis blood samples for measurement of inflammatory (e.g., C reactive protein, interleukin-1, interleukin-18) and fibrotic (e.g., soluble suppression of tumorigenesis-2 [sST2], galectin-3, C-terminal pro-peptide of procollagen type I and N-terminal pro-peptide of procollagen type III) biomarkers were collected. Right ventricular dysfunction (RVD) was defined using tricuspid annular plane systolic excursion (TAPSE) <1.7 cm or pulsed Doppler peak annular velocity (S´) <9.5 cm/s. The ability of sST2 to discriminate between mortality was assessed using AuROC curve. Results We enrolled 48 patients (mean age 74 [64–79] years, 62.5% males) followed over a period of 1.4 years. Mortality was higher 45.5% (log-rank, p=0.003) in patients with RVD as diagnosed by S' than in patients without RVD. No difference in mortality was observed for RVD defined by TAPSE. There were no differences in the morphology and function parameters of the left ventricle between patients with and without RVD. From all biomarkers measured only sST2 was associated with RVD. Indeed, an age- and sex-adjusted analyses showed that doubling of sST2 was inversely associated with a decreased in S´ (estimate=-2.03, 95% CI [-3.04 to -1.00] cm/s; P=0.002). Mortality was increased in patients with sST2 ≥40.45 ng/mL compared to patients with sST2 <40.45 ng/mL (66.7% vs. 18.9%, log-rank; p=0.004). Crude analysis showed that patients presenting with S’ <9.5 cm/s and sST2 ≥40.45 ng/mL exhibited higher mortality (log-rank; p=0.001) than patients with S’ >9.5 cm/s and sST2 <40.45pg/mL. Conclusion Albeit preliminary these findings suggest that an excess of sST2 may be involved in RVD and on its effect on mortality in HD patients. The myocardial pro-remodeling effect of sST2 among HD patients with RVD warrants further investigation.