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Heart failure (HF) remains a significant public health issue, with heart transplantation (HT) being the gold standard treatment for end-stage HF. The increasing use of mechanical circulatory support, particularly left ventricular assist devices (LVADs), as a bridge to transplant (BTT), presents new perspectives for increasingly complex clinical scenarios. This study aimed to compare long-term clinical outcomes in patients in heart failure with reduced ejection fraction (HFrEF) receiving an LVAD as BTT to those undergoing direct-to-transplant (DTT) without mechanical support, focusing on survival and post-transplant complications.

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Background: Long-term renal allograft acceptance has been achieved in macaques using a transient mixed hematopoetic chimerism protocol, but similar regimens have proven unsuccessful in heart allograft recipients unless a kidney transplant was performed simultaneously. Here, we test whether a modified protocol based on targeting CD154, CD2, and CD28 is sufficient to prolong heart allograft acceptance or promote the expansion of regulatory T cells.

Methods: Eight macaques underwent heterotopic allo-heart transplantation from major histocompatibility complex-mismatched donors.

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Characteristic alterations in the urinary microbiome, or urobiome, are associated with renal transplant pathology. To date, there has been no direct study of the urobiome during acute allograft rejection. The goal of this study was to determine if unique urobiome alterations are present during acute rejection in renal transplant recipients.

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Renal fibrosis is a leading cause of chronic allograft nephropathy. While renal biopsy remains the gold standard for diagnosing fibrosis, it is an invasive procedure with potential for severe complications. Elastography, an emerging ultrasound imaging technique, appears to be a valuable tool for quantifying tissue stiffness, which correlates with fibrosis.

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Donor-derived cell-free DNA in chronic lung allograft dysfunction phenotypes: a pilot study.

Front Transplant

December 2024

Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of CHROMETA, KU Leuven, Leuven, Belgium.

Long-term survival after lung transplantation is limited due to chronic lung allograft dysfunction (CLAD), which encompasses two main phenotypes: bronchiolitis obliterans syndrome (BOS) and restrictive allograft syndrome (RAS). Donor-derived cell-free DNA (dd-cfDNA) is a biomarker for (sub)clinical allograft injury and could be a tool for monitoring of lung allograft health across the (pre)clinical spectrum of CLAD. In this proof-of-concept study, we therefore assessed post-transplant plasma dd-cfDNA levels in 20 CLAD patients (11 BOS and 9 RAS) at three consecutive time points free from concurrent infection or acute rejection, during stable condition, preclinical CLAD, and established CLAD ( = 3 × 20 samples).

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