Background. Intrarenal resistive index (RI) ≥ 0.80 predicts renal outcomes in proteinuric chronic kidney disease (CKD). However, this evidence in non-proteinuric patients with CKD of unknown etiology is lacking. In this study, we assessed the effect of intrarenal RI on renal function and all-cause mortality in non-proteinuric patients with CKD of unknown etiology despite an extensive diagnostic work-up. Methods. Non-proteinuric CKD patients were evaluated in a retrospective longitudinal study. Progression of renal disease was investigated by checking serum creatinine levels at 1, 3, and 5 years and defined by a creatinine level increase of at least 0.5 mg/dL. The discrimination performance of intrarenal RI in predicting the 5-year progression of renal disease was assessed by calculating the area under the receiver operating characteristic curve (AUROC). Results. One-hundred-thirty-one patients (76 ± 9 years, 56% males) were included. The median follow-up was 7.5 years (interquartile range 4.3–10.5) with a cumulative mortality of 53%, and 5-year renal disease progression occurred in 25%. Patients with intrarenal RI ≥ 0.80 had a faster increase of serum creatinine levels compared to those with RI < 0.80 (+0.06 mg/dL each year, 95% CI 0.02–0.10, p < 0.010). Each 0.1-unit increment of intrarenal RI was an independent determinant of 5-year renal disease progression (odds ratio 4.13, 95% CI 1.45–12.9, p = 0.010) and predictor of mortality (hazards ratio 1.80, 95% CI 1.05–3.09, p = 0.034). AUROCs of intrarenal RI for predicting 5-year renal disease progression and mortality were 0.66 (95% CI 0.57–0.76) and 0.67 (95% CI 0.58–0.74), respectively. Conclusions. In non-proteinuric patients with CKD of unknown etiology, increased intrarenal RI predicted both a faster decline in renal function and higher long-term mortality, but as a single marker, it showed poor discrimination performance.

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Funding Acknowledgements Type of funding sources: None. Introduction. Aortic stenosis (AS) is one of the most common valvular heart diseases; however, the association between left ventricular (LV) myocardial deformation and hemodynamic forces (HDFs) is still mostly  unexplored. Purpose. This study aimed to assess the differences in LV myocardial deformation and HDFs in a large cohort of patients with aortic stenosis retrospectively. Methods. Two-hundred fifty-four subjects (median age 77 years, 50% women) with preserved LV ejection fraction (LVEF), and mild (n = 87), moderate (n = 92) or severe (n = 75) AS, were included in the study. The 2D LV global longitudinal strain (GLS), circumferential strain (GCS), and HDFs were measured with new software that allowed us to calculate all these values and parameters from the three apical views. Results. When comparing severe AS to mild AS, LV mass appeared increased while the LV hypertrophy phenotype was concentric (p &lt;0.0001). Along with the progression of the AS, LVEF was decreased. All GLS, GCS, and HDFs parameters were uniformly reduced in severe AS compared to mild AS (p &lt;0.0001), in the same way, LV longitudinal force, LV longitudinal systolic force, and LV impulse have proven to be accurate on ROC curves (AUC 70%, 73% and 73% respectively). Conclusion. The integrated approach of deformation and cardiac mechanics allows the description of pathophysiological changes during the progression of mild to severe aortic stenosis. Abstract Figure. Strain parameters and aortic stenosis