MO925VALVULAR HEART DISEASE EVOLUTION IN KIDNEY TRANSPLANT RECIPIENTS AND RELATED RISK FACTORS

Abstract

Abstract Background and Aims Cardiovascular diseases remains the leading cause of death in recipients of kidney transplantation (KT). Valvular heart disease (VHD) is not an exclusion criteria for KT, however it’s repercussion on KT follow-up has been less studied. Our objective was to analyse the impact of VHD in KT recipients and related risk factors of VHD progression (VHDp). Method Observational retrospective cohort study of all patients who underwent KT at Hospital del Mar (Barcelona, Spain) between January 1980 and December 2018. VHD was defined as presence of aortic stenosis (AS), aortic regurgitation, mitral stenosis, mitral regurgitation, tricuspid stenosis, tricuspid regurgitation or double valve injury of any degree diagnosed by echocardiography. We analysed the VHDp, defined as worsening of the initial valvular degree on heart ultrasound after KT, risk factors related with VHDp, recipients and graft survival. Results During the study period, 1422 patient underwent KT and 48 of them (3.4%) had VHD diagnosed prior to KT. In the median time of follow-up of 56.3 months (IQR25-75 17.7-119 month), 17 patients (35.4%) presented VHDp and 31 patients did not (64.6%). Figure 1 shows the primary outcome in the different types of VHD, AS was the valve with more VHDp after KT. Statistical evaluation revealed that recipients with VHDp had a higher body mass index (BMI) (27.4 ± 6.3 vs 24.3 ± 3.8 kg/m2, p=0.04) and worse PTH control (427.0 ± 309.3 vs 186.2 ± 140.6 pg/ml, p=0.02) at the moment of the KT. Also, patients with VHDp reached a worse nadir glomerular filtration rate (GFR) (44.1 ± 17.5 vs 56.0 ± 13.9 ml/min/1.73m2, p=0.01) during the follow-up, needed more time to reach their nadir GFR (4 [2-13] vs 1.2 [1.0-4.7] months, p<0.001) and required more furosemide dose at that time (72.7 ± 21.7 vs 15.8 ± 5.6 mg/day, p=0.02). At the end of follow-up, 213 KT recipients had died, 16 with preKT-VHD (33.3% of all patients with VHD) and 197 without preKT-VHD (14.3% of all cases without VHD). There was a statistical significant association between preKT-VHD status and all-cause mortality after KT (log rank < 0.001). However, there wasn’t statistical association between preKT-VHD status and death-censored graft survival (log rank = 0.2). Conclusion VHD has a significant impact on increased pos-KT mortality but it is not associated with graft survival. More than one third of recipients with preKT-VHD presented deterioration after KT. We found that increased preKT BMI and PTH, nadir GFR after KT, time to reach this nadir GFR and diuretic dose at that time are related with VHD progression.