Abstract

Introduction: Cardiovascular disease is a leading cause of mortality in patients with end-stage renal disease, even undergoing transplantation. Left ventricular hypertrophy (LVH) is the most common feature and an independent risk factor for cardiac complications in kidney transplant recipients. The aim of this study was to identify cardiac alteration after kidney transplantation and analyze predictors of the post-transplant LVH. Methods: Among 2957 kidney transplant recipients in a multicenter cohort from 1997 to 2012, a total of 206 patients who conducted echocardiography before and one year after transplantation were enrolled in this study. Echocardiographic findings and clinical parameters were evaluated. Results: Kidney transplantation significantly reduced mean left ventricular mass index (LVMI) from 128.8±47.2g/m<sup style=“font-family: ‘Times New Roman’, serif; line-height: 150%; text-indent: 6pt;”>2[/sup] to 106.4±33.0g/m<sup style=“font-family: ‘Times New Roman’, serif; line-height: 150%; text-indent: 6pt;”>2 [/sup](p<0.001).Figure: No Caption available.The ejection fraction was improved (59.4±8.0% vs. 62.1±6.7%, p<0.001). The prevalence of LVH by echocardiography significantly decreased (62.6% vs. 46.1%, p=0.001). The prevalence of diastolic dysfunction, mitral and tricuspid regurgitation, and pulmonary hypertension also decreased. Pre-transplant lower hemoglobin level (OR 0.74, 95% CI 0.56-0.96, p=0.026) and pre-transplant higher LVMI (OR 1.02, 95% CI 1.01-1.02, p<0.001) were independently associated with persistent LVH after kidney transplantation. On the other hand, ejection fraction, diastolic dysfunction, underlying renal disease, albumin or cholesterol level, blood pressure, rejection, and allograft function were not correlated with post-transplant LVH. Conclusions: Cardiac morphology and function were significantly improved by kidney transplantation. Treatment of anemia might be crucial in regression and prevention of persistent LVH in kidney transplant recipients.

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