Background: Chronic kidney disease (CKD) is a prevalent clinical condition affecting 15.1% of the general population according to recent published. CKD type 4 is characterized by an underlying CKD condition leading to impairment of cardiac function and to a 10-20 fold increased risk for major cardiovascular events, leading to disease progression to cardiorenal syndrome- CRS.
Objectives: Assess whether the pathological changes that occur in the heart in the setting of CKD involve enhanced cell death of cardiac cells.
Methods: We established a rat model for CKD, for acute myocardial infarction (acute MI), left ventricular dysfunction (LVD) and sham (control arms). We measured the cardiac to body weight as well as kidney to body weight ratios to validate that renal and cardiac hypertrophy take place as part of disease progression to CRS. Cardiac cells were then isolated following digestion with collagenase II 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 using anti-cleaved caspase-3 antibody.
Results: CKD, as well as acute MI and LVD, resulted in a 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.
Conclusions: Our data demonstrate that while CKD induces pathological changes in the heart, this clinical setting per se does not induce cardiac cell death.
