title: Fisher-Lewis kidney transplantation model as a tool for investigation of transplantation-induced cardiomyopathy.
abstract: BACKGROUND
  Cardiovascular disease is a major cause of death after kidney transplantation; thus, cardiovascular protection is a major concern in transplant recipients. Data about cardiac characteristics from animal models after kidney transplantation are lacking. Therefore, we investigated cardiac structure and function in a model of chronic allograft injury.
  
  
  METHODS
  Kidneys from Fisher 344 rats were orthotopically transplanted into Lewis rats. Eight recipient rats were treated with placebo or an angiotensin II type-1 receptor blocker (AT1RB; candesartan cilexitil, 5 mg/kg/d) for 24 weeks posttransplantation, and 8 untreated matched Lewis rats were used as healthy controls. Echocardiography was performed at 24 weeks posttransplantation to measure ejection fraction, fractional shortening, and left ventricular mass, in triplicate. Proteinuria at 24 hours was determined, and after harvesting, the heart weight-body weight ratio (HW/BW) was measured.
  
  
  RESULTS
  At 24 weeks posttransplantation, renal transplant-recipient rats demonstrated a significantly decreased ejection fraction (mean [SD], 58.9% [3.2%] vs 70.7% [2.1%]) and fractional shortening (29.8% [2.0%] vs 38.3% [2.0%]) and increased HW/BW and left ventricular mass (7.7 [0.2] cm(3) vs 6.7 [0.2] cm(3)) compared with healthy control rats. The HW/BW and left ventricular mass were significantly ameliorated by AT1RB compared with placebo-treated transplant-recipient rats (6.8 [0.2] cm(3) vs 7.7 [0.2] cm(3)). In addition, decreased proteinuria was evident after AT1RB.
  
  
  CONCLUSIONS
  The Fisher-Lewis rat kidney transplantation model resulted in cardiac hypertrophy and decreased cardiac function. AT1RB normalized cardiac hypertrophy without improving function. These findings demonstrate that the Fisher-Lewis rat renal transplantation model can be used to investigate transplantation-induced cardiomyopathy.
authors.affiliation: Department of Nephrology, Technical University Munich, Munich, Germany. marcus.baumann@lrz.tum.de
authors.forename: M
authors.initials: M
authors.lastname: Baumann
authors.forename: J
authors.initials: J
authors.lastname: Chang
authors.forename: K
authors.initials: K
authors.lastname: Thürmel
authors.forename: M
authors.initials: M
authors.lastname: Roos
authors.forename: M
authors.initials: M
authors.lastname: von Eynatten
authors.forename: D
authors.initials: D
authors.lastname: Sollinger
authors.forename: J
authors.initials: J
authors.lastname: Lutz
authors.forename: U
authors.initials: U
authors.lastname: Heemann
mesh_terms: D000818:Animals; D001835:Body Weight; D009202:Cardiomyopathies / Q000209:etiology* / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000401:mortality; D016572:Cyclosporine / Q000627:therapeutic use; D004195:Disease Models, Animal; D004452:Echocardiography; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016030:Kidney Transplantation / Q000009:adverse effects*; D008297:Male; D009392:Nephrectomy; D009929:Organ Size; D011507:Proteinuria / Q000453:epidemiology / Q000209:etiology; D051381:Rats; D011916:Rats, Inbred F344; D011917:Rats, Inbred Lew; D013599:Systole; D014184:Transplantation, Homologous
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine