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ORIGINAL RESEARCH article

Front. Nephrol.
Sec. Kidney Transplantation
Volume 4 - 2024 | doi: 10.3389/fneph.2024.1455036

ROLE OF KIDNEY TRANSPLANTATION IN LONG-TERM CARDIAC REVERSE REMODELING AND INTERCONNECTING MECHANISMS IN TYPE 4 CARDIORENAL SYNDROME

Provisionally accepted
Jose Luis Salas-Pacheco Jose Luis Salas-Pacheco 1,2Jose Manuel Arreola Guerra Jose Manuel Arreola Guerra 1RICARDO MARQUEZ VELASCO RICARDO MARQUEZ VELASCO 3Sergio Casarez-Alvarado Sergio Casarez-Alvarado 3*Israel Pérez Torres Israel Pérez Torres 3Giovanny Fuentevilla-Alvarez Giovanny Fuentevilla-Alvarez 3Verónica Guarner-Lans Verónica Guarner-Lans 3Randall Cruz-Soto Randall Cruz-Soto 3*Maria Elena Soto-Lopez Maria Elena Soto-Lopez 3,4*
  • 1 Centenario Hospital Miguel Hidalgo, Aguascalientes, Mexico
  • 2 National Autonomous University of Mexico, México City, México, Mexico
  • 3 National Institute of Cardiology Ignacio Chavez, Mexico, México, Mexico
  • 4 Centro Médico ABC, Mexico City, México, Mexico

The final, formatted version of the article will be published soon.

    Background. Type 4 cardiorenal syndrome (CRS) involves cardiovascular alterations caused by chronic kidney disease (CKD). Fibroblast growth factor-23 (FGF23), carboxy-terminal propeptide of procollagen type I (PIP), and parathyroid hormone (PTH) have been proposed as biomarkers of pathological cardiac remodeling in CKD. In contrast, it has been suggested that MicroRNA 221 has a cardioprotective role. Available evidence shows that, 12 months after kidney transplantation (KT), type 4 CRS reverts in only half of the patients. Objective. To assess long-term cardiac reverse remodeling after KT and its association with FGF23, PIP, and PTH levels. Methods. Patients with end-stage renal disease were assessed before and 28 months after KT using FGF23, PIP, and PTH serum concentrations and transthoracic echocardiography. Results. Fifty-three patients were followed for 28 months after KT. All the patients showed cardiac abnormalities upon inclusion. A follow-up assessment showed a reduction in left ventricle (LV) mass (121 ± 48 vs. 65 ± 14 gr/m2) and left atrial volume (46 vs. 30 ml/m2). The LV ejection fraction (53 vs. 63%), LV global longitudinal strain (-15.9 vs.-19.4%), and LV diastolic function improved. miR-221 expression increased after KT (8.73 RIQ= 3.7-25 vs. 40.16 RIQ= 24-223, p=0.001) and was correlated with the Ee´ratio (r= -0.32, p= 0.02). Multivariate analysis showed that post-KT LV mass was determined by pre-KT LV mass, serum Cr level, post-KT PIP, and hypertension (R2=0.65, F=12.1, p=0.001). Conclusions. Contrary to other evidence, this study demonstrated that type 4 CRS is reversible over the long term. This is a paramount finding because KT normalizes cardiac structure and function independently of the severity of basal cardiac abnormalities.

    Keywords: cardiorenal syndrome, Left ventricle hypertrophy, Reverse cardiac remodeling, kidney tranplantation, Echocadiography, Fibroblast growth facctor-23, microRNA

    Received: 26 Jun 2024; Accepted: 15 Nov 2024.

    Copyright: © 2024 Salas-Pacheco, Arreola Guerra, MARQUEZ VELASCO, Casarez-Alvarado, Pérez Torres, Fuentevilla-Alvarez, Guarner-Lans, Cruz-Soto and Soto-Lopez. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Sergio Casarez-Alvarado, National Institute of Cardiology Ignacio Chavez, Mexico, 14080, México, Mexico
    Randall Cruz-Soto, National Institute of Cardiology Ignacio Chavez, Mexico, 14080, México, Mexico
    Maria Elena Soto-Lopez, National Institute of Cardiology Ignacio Chavez, Mexico, 14080, México, Mexico

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