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

Abstract

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.