Challenges of targeting vascular stability in acute kidney injury.
Acute kidney injury following folate administration is characterized by a vascular remodeling that is initially proliferative but subsequently results in vascular endothelial loss. Interventions directed toward promoting endothelial growth may preserve vascular structure and therefore renal function. However, angiopoietin-1 therapy in the setting of folate-induced acute kidney injury resulted in an expanded fibrotic response despite apparent preservation of the vasculature, indicating that renal repair responses are complex and vascular-directed therapies should be approached with caution.
Basile
David P
DP
Department of Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA. dpbasile@iupui.edu
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D042683:Angiopoietin-1 / Q000627:therapeutic use; D000818:Animals; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology; D005355:Fibrosis / Q000517:prevention & control; D005492:Folic Acid / Q000009:adverse effects; D006801:Humans; D018919:Neovascularization, Physiologic / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects*
D042683:Angiopoietin-1; D005492:Folic Acid