Regression of cardiac growth in kidney transplant recipients using anti-m-TOR drugs plus RAS blockers: a controlled longitudinal study
1 Department of Nephrology, Carlos Haya University Hospital and IBIMA, Malaga E-29010, Spain
2 Department of Cardiology and Radiology, Carlos Haya University Hospital and IBIMA, Malaga E-29010, Spain
3 Department of Radiology, Carlos Haya University Hospital and IBIMA, Malaga E-29010, Spain
4 Department of Nephrology, Hospital Puerta del Mar, Cadiz E-11009, Spain
BMC Nephrology 2014, 15:65 doi:10.1186/1471-2369-15-65Published: 23 April 2014
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 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.
We 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.
Nineteen 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).
Switching 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.