REDEFINING THE TYPE 4 CARDIORENAL SYNDROME: Long-term cardiac reverse remodeling after kidney transplantation

Introduction: The currently available evidence states that 12 months after kidney transplantation (KT), more than half of the patients have severe cardiac structural and functional abnormalities. Objective: To assess the cardiac reverse remodeling using echocardiography in the long-term after KT and its association with fibroblast growth factor-23 (FGF-23), carboxy-terminal propeptide of procollagen type I (PIP), and parathyroid hormone (PTH). Methods: Fifty-three patients with end-stage renal disease were assessed before and 28 months after KT by echocardiography and serum quantification of FGF-23, PIP, and PTH. Results: Thirty men and 23 women, with a mean age of 34±11 years, were included in the study. At 28 months after KT, an increase in functional capacity, complete resolution of the left ventricle (LV) hypertrophy (LV mass:121 ± 48 vs. 65 ± 14 gr/m2), reduction in left atrial volume (46 vs. 30 ml/m2), improvement in LV ejection fraction (53 vs. 63 %), global longitudinal strain (-15.9 vs.-19.4 %), and diastolic function were observed. Multivariate analysis showed that pre-KT LV mass, graft function, hypertension, and post-KT PIP predicted post-KT LV mass (R2=0.65, F=12.1, p=0.001). Logistic regression showed that the pre-KT FGF-23 concentration was the only variable related to hypertension after KT (X2=12.1, R2=0.3, p=0.032). PTH levels were not associated with LV hypertrophy. Conclusions: Long-term follow-up after KT demonstrated that type 4 cardiorenal syndrome is reversible. Myocardial interstitial expansion is a minor component of absolute LV mass and is dominated by cardiomyocyte hypertrophy. FGF-23 plays an important role in persistent hypertension after KT.