Abstract
BackgroundLeft ventricular hypertrophy (LVH) is common in kidney transplant (KT) recipients. LVH is associated with a worse outcome, though m-TOR therapy may help to revert this complication. We therefore conducted a longitudinal study to assess morphological and functional echocardiographic changes after conversion from CNI to m-TOR inhibitor drugs in nondiabetic KT patients who had previously received RAS blockers during the follow-up.MethodsWe undertook a 1-year nonrandomized controlled study in 30 non-diabetic KT patients who were converted from calcineurin inhibitor (CNI) to m-TOR therapy. A control group received immunosuppressive therapy based on CNIs. Two echocardiograms were done during the follow-up.ResultsNineteen patients were switched to SRL and 11 to EVL. The m-TOR group showed a significant reduction in LVMi after 1 year (from 62 ± 22 to 55 ± 20 g/m2.7; P = 0.003, paired t-test). A higher proportion of patients showing LVMi reduction was observed in the m-TOR group (53.3 versus 29.3%, P = 0.048) at the study end. In addition, only 56% of the m-TOR patients had LVH at the study end compared to 77% of the control group (P = 0.047). A significant change from baseline in deceleration time in early diastole was observed in the m-TOR group compared with the control group (P = 0.019).ConclusionsSwitching from CNI to m-TOR therapy in non-diabetic KT patients may regress LVH, independently of blood pressure changes and follow-up time. This suggests a direct non-hemodynamic effect of m-TOR drugs on cardiac mass.
Highlights
Left ventricular hypertrophy (LVH) is common in kidney transplant (KT) recipients
reninangiotensin system (RAS) blockers are frequently used in KT recipients as cardio-protective and reno-protective drugs and, their use has been associated with regression of LVH after KT [9,10]
A higher baseline 24-hour urinary protein excretion was observed in the Mammalian target of rapamycin (m-TOR) inhibitor group because chronic allograft dysfunction was present in 16 patients prior to conversion
Summary
Left ventricular hypertrophy (LVH) is common in kidney transplant (KT) recipients. LVH is associated with a worse outcome, though m-TOR therapy may help to revert this complication. We conducted a longitudinal study to assess morphological and functional echocardiographic changes after conversion from CNI to m-TOR inhibitor drugs in nondiabetic KT patients who had previously received RAS blockers during the follow-up. A randomized controlled study demonstrated that the use of everolimus (EVL) plus a reduced exposure of cyclosporine (CsA) proved effective in regressing LVH in KT recipients [8]. None of these studies included patients who had received reninangiotensin system (RAS) blockers together with the m-TOR inhibitors during the first post-conversion year. Angiotensin II leads to prolonged diastolic filling [12], and changes in diastolic function might be expected when both RAS blockers and m-TOR inhibitors concur in these patients
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