Angiotensin II and progressive renal insufficiency.
The inhibition of angiotensin II through angiotensin converting enzyme inhibitors or angiotensin receptor blockers has become the foundation of medical treatment of progressive chronic renal disease. Although these drugs provide a significant improvement over earlier treatments, they only slow the progression of renal disease, implying the need for additional drugs that could be combined with antiangiotensin treatment. Potentially valuable novel drug targets include downstream mediators of angiotensin II such as transforming growth factor-b, plasminogen activator inhibitor-1, and endothelin-1. In addition, recent evidence points to aldosterone as a major player in progressive renal disease, indicating that multiple points of the renin-angiotensin-aldosterone system might have to be targeted. This paper reviews the experimental and clinical evidence indicating that targeting these cytokines and hormones could provide additional benefits to antiangiotensin treatment in chronic renal disease.
Gaedeke
Jens
J
Fibrosis Research Laboratory, Salt Lake City, UT 84108, USA. jens.gaedeke@hsc.utah.edu
Noble
Nancy A
NA
Border
Wayne A
WA
D000450:Aldosterone / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D016232:Endothelins / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000188:drug therapy* / Q000517:prevention & control; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011945:Receptors, Angiotensin / Q000378:metabolism; D016212:Transforming Growth Factor beta / Q000494:pharmacology
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D016232:Endothelins; D017395:Plasminogen Activator Inhibitor 1; D011945:Receptors, Angiotensin; D016212:Transforming Growth Factor beta; D000450:Aldosterone