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Kidney transplantation is a common procedure in end-stage kidney disease, and it is the preferred treatment for kidney failure, affording significant survival and quality of life advantages over long-term dialysis. However, kidney transplant (KT) recipients experience a higher risk of cardiovascular disease outcomes compared with the general population. Increasing numbers of patients requiring a transplant, better identification of cardiac risk is required to prevent premature death with a functioning graft. Previous studies show that some of the conventional values of transthoracic echocardiography (TE) improve after KT. Still, there is less information regarding the right and left ventricular strain which evaluate subclinical myocardial dysfunction.
This is a prospective and longitudinal study of one center. We included all the patients who were eligible for kidney transplant (living donor or deceased donor) from January 2022 to May 2022. All the candidates needed a pre-transplant transthoracic echocardiography and a second one a year later after KT. Patients who lost follow up or suffer a cardiovascular event were excluded. The most representative values for cardiovascular structure and function were evaluated, including longitudinal strain of left and right ventricle.
A total a 17 were included in the study (mean age was 50 and 64.7% were men). The median time spent on dialysis was 2.6 years, 64.7% were on hemodialysis and 29.4% on peritoneal dialysis. A reverse remodeling of the LV was observed following kidney transplant as left venticular mass decreased (101 g vs 82 P = 0.01). End-diastolic volumen (124 ml vs 100 ml P=0.022), end-systolic volume (52 mL vs 30 mL P= 0.031) and ejection fraction (57% vs 61% p=0.06) show and improvement. E to early diastolic mitral annular tissue velocity (E/e’) did not change (9 vs 7.65 P = 0.14). Additionally, there were no statistically significant difference in left and right ventricle strain (18.5 vs 19.4 P=0.191 and 24 vs 24 P=0.55).
Left ventricular mass reduction could be explained by the correction of the precipitating factors. The relevance of these finding is the correlation between LV hypertrophy reduction and the improvement in the cardiovascular prognosis. We did not document any improvement in RVFWS nor LVGLS. We hypothesize that there is an irreversible myocardial remodeling related to fibrosis due to a longer time in RRT. Thus, there is no improvement in myocardial strain after transplantation even though the precipitating factors are corrected