title: Cardiac Hypertrophy and Cardiac Cell Death in Chronic Kidney Disease.
abstract: BACKGROUND
  Chronic kidney disease (CKD) is a prevalent clinical condition affecting 15% of the general population. Cardiorenal syndrome (CRS) type 4 is characterized by an underlying CKD condition leading to impairment of cardiac function and increased risk for major cardiovascular events. To date, the mechanisms leading from CKD to CRS are not completely understood. In particular, it is unclear whether the pathological changes that occur in the heart in the setting of CKD involve enhanced cell death of cardiac cells.
  
  
  OBJECTIVE
  To assess whether CKD may mediate loss of cardiac cells by apoptosis.
  
  
  METHODS
  We established rat models for CKD, acute myocardial infarction (acute MI), left ventricular dysfunction (LVD), and sham. We measured the cardiac-to-body weight as well as kidney-to-body weight ratios to validate that renal and cardiac hypertrophy occur as part of disease progression to CRS. Cardiac cells were then isolated and the percent of cell death was determined by flow cytometry following staining with annexin-FITC and propidium iodide. In addition, the levels of caspase-3-dependent apoptosis were determined by Western blot analysis using an anti-cleaved caspase-3 antibody.
  
  
  RESULTS
  CKD, as well as acute MI and LVD, resulted in significant cardiac hypertrophy. Nevertheless, unlike the increased levels of cell death observed in the acute MI group, in the CKD group, cardiac hypertrophy was not associated with induction of cell death of cardiac cells. Caspase-3 activity was even slightly reduced compared to sham-operated controls.
  
  
  CONCLUSIONS
  Our data show that while CKD induces pathological changes in the heart, it does not induce cardiac cell death.
authors.forename: May-Tal
authors.initials: MT
authors.lastname: Rofe
authors.forename: Ran
authors.initials: R
authors.lastname: Levi
authors.forename: Einat
authors.initials: E
authors.lastname: Hertzberg-Bigelman
authors.forename: Pavel
authors.initials: P
authors.lastname: Goryainov
authors.forename: Rami
authors.initials: R
authors.lastname: Barashi
authors.forename: Jeremy
authors.initials: J
authors.lastname: Ben-Shoshan
authors.forename: Gad
authors.initials: G
authors.lastname: Keren
authors.forename: Michal
authors.initials: M
authors.lastname: Entin-Meer
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D059347:Cardio-Renal Syndrome / Q000209:etiology / Q000503:physiopathology*; D006332:Cardiomegaly / Q000209:etiology* / Q000503:physiopathology; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005434:Flow Cytometry; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology; D032383:Myocytes, Cardiac / Q000473:pathology*; D051381:Rats; D011917:Rats, Inbred Lew; D051436:Renal Insufficiency, Chronic / Q000150:complications* / Q000503:physiopathology; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology
chemical_list: D053148:Caspase 3