Background: Infective endocarditis (IE) poses significant challenges in cardiovascular medicine, often necessitating valvular surgery to manage severe complications. Postoperative acute kidney injury (AKI) is a notable complication affecting patient outcomes. While clinical and procedural factors have been well studied, the role of radiological renal artery parameters in AKI risk remains underexplored. Methods: This retrospective study analyzed 80 patients with IE who underwent valvular surgery from 2013 to 2021, focusing on postoperative AKI as defined by the Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Radiological parameters, including renal artery calcification, renal ostial calcification, the presence of renal infarctions, and additional arteries, were assessed using preoperative computed tomography (CT). Statistical analyses included binary logistic and linear regression models, Kaplan–Meier survival curves, and Cox proportional hazard regression to explore associations between these parameters and AKI incidence, creatinine levels, and mortality. Results: Out of 80 patients, 31 (38.8%) developed AKI. No significant differences were found in baseline characteristics or radiological parameters between the AKI+ and AKI− groups. Binary logistic and linear regression analyses revealed no substantial relationship between anatomical factors and AKI risk or creatinine levels. However, Cox regression identified “additional renal artery” as a significant predictor of 1-month mortality (HR: 1.747, 95% CI: 1.024–2.979, p = 0.041) but not for 6- or 12-month mortality. Conclusions: Radiological anatomical factors, including calcifications and additional arteries, did not significantly impact AKI risk in IE patients undergoing valvular surgery. However, the presence of additional arteries was associated with increased short-term mortality. These findings suggest the need for further research to elucidate factors contributing to AKI and mortality in this context.

Background: Lipoprotein(a) [Lp(a)] has emerged as a key mediator of calcific aortic valve disease and is strongly linked to the development and progression of aortic stenosis (AS). Whether elevated Lp(a) influences disease severity, long-term prognosis, or both in patients undergoing transcatheter aortic valve implantation (TAVI) remains uncertain. Methods: This multicenter study included 213 patients with severe symptomatic AS undergoing TAVI between 2016 and 2018. Pre-procedural Lp(a) concentrations were measured using a standardized immunoturbidimetric assay. Associations with long-term all-cause mortality were evaluated using Kaplan–Meier analyses and Cox proportional hazards models. The relationship between Lp(a) and AS severity was assessed using correlation analyses, multivariable linear regression models, and restricted cubic spline analyses. Anatomical and hemodynamic measures included aortic valve calcium score (AVCS), peak aortic jet velocity (AV Vmax), and transvalvular pressure gradients. Results: During a median follow-up of 7.58 years (IQR 4.33–8.66 years), Lp(a) was not associated with all-cause mortality, irrespective of whether it was analyzed as a continuous variable, according to established clinical thresholds, or across quartiles. In contrast, higher Lp(a) concentrations were associated with greater valvular calcification and more severe hemodynamic obstruction. These associations remained significant after adjustment for age, sex, diabetes mellitus, and renal function. Restricted cubic spline analyses suggested predominantly linear associations without evidence of significant non-linearity. Conclusions: Elevated Lp(a) concentrations were associated with greater anatomical and hemodynamic severity of AS but not with long-term mortality after TAVI. These findings suggest that elevated Lp(a) is associated with greater anatomical and hemodynamic severity of calcific aortic valve disease but was not linked to long-term mortality after TAVI.