title: Regression of cardiac growth in kidney transplant recipients using anti-m-TOR drugs plus RAS blockers: a controlled longitudinal study.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Nephrology, Carlos Haya University Hospital and IBIMA, Malaga E-29010, Spain. domingohernandez@gmail.com.
authors.forename: Domingo
authors.initials: D
authors.lastname: Hernández
authors.forename: Pedro
authors.initials: P
authors.lastname: Ruiz-Esteban
authors.forename: Daniel
authors.initials: D
authors.lastname: Gaitán
authors.forename: Dolores
authors.initials: D
authors.lastname: Burgos
authors.forename: Auxiliadora
authors.initials: A
authors.lastname: Mazuecos
authors.forename: Rocío
authors.initials: R
authors.lastname: Collantes
authors.forename: Eva
authors.initials: E
authors.lastname: Briceño
authors.forename: Eulalia
authors.initials: E
authors.lastname: Palma
authors.forename: Mercedes
authors.initials: M
authors.lastname: Cabello
authors.forename: Miguel
authors.initials: M
authors.lastname: González-Molina
authors.forename: Manuel
authors.initials: M
authors.lastname: De Mora
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000008:administration & dosage*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000008:administration & dosage*; D004359:Drug Therapy, Combination; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology* / Q000517:prevention & control*; D007166:Immunosuppressive Agents / Q000008:administration & dosage; D016030:Kidney Transplantation / Q000009:adverse effects*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D047428:Protein Kinase Inhibitors / Q000008:administration & dosage*; D058570:TOR Serine-Threonine Kinases / Q000037:antagonists & inhibitors*; D016896:Treatment Outcome
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D007166:Immunosuppressive Agents; D047428:Protein Kinase Inhibitors; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases
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