Renal and cardiac microvascular endothelium: injury and repair

Abstract

Injury to the capillary endothelium can be devastating for renal and cardiac function. To halt the progression of chronic kidney disease (CKD) and heart failure (HF) preservation of the microvascular endothelial cell (EC) function and structure is of great importance.1 Increasing knowledge about microvascular EC function and structure during renal and cardiac injury and repair is needed to develop new therapeutic strategies for CKD, HF and combined injury during cardiorenal syndrome (CRS). Therefore, this thesis studied experimental models of CKD, HF and CRS, without or with a therapeutic intervention. In this thesis we showed the close interaction between renal and cardiac function in health and disease, and their relation to microvascular endothelial function and structure. Using complex preclinical models of CKD and HF, surgical or metabolically induced, allowed us to increase knowledge about complicated processes such as dysfunction, hypertrophy, fibrosis and endothelial responses in kidney and heart. These processes were adversely affected by factors such as systemic hypertension, inflammation and oxidative stress. By non-pharmacological and pharmacological interventions, directly or indirectly targeting the microvascular endothelium, systemic factors, and thereby renal and cardiac function, could be positively affected. In the wide range of experimental models of CKD, HF and cardiorenal (metabolic) syndrome, renal and cardiac endothelial responses were not always consistent. This might be due to the severity of the hits (renal or cardiac) or their sequence. The results of this thesis suggest that proliferation of endothelial cells, and not the influx or incorporation of circulating cells, is an important factor for maintenance and restoration of microvascular endothelium. 1.Kingma JG, Simard D, Rouleau JR. Renocardiac syndromes: physiopathology and treatment stratagems. Canadian Journal of Kidney Health and Disease 2015; 2: 1-10.