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Volume 37: Issue 2: 2007




In  renal  artery  stenosis, GFR  becomes  angiotensin  II-dependent  and therefore sensitive to ACE inhibitor.  However, the effect of ACE inhibitor on SCr in  the  presence  of  RAS  is  complicated  by  several  factors: serum  creatinine  is  a poor  indicator  of  GFR, RAS  can  affect  one  or  both  kidneys, GFR  depends  on systemic blood pressure and ACE inhibitor dose, and other conditions can render GFR ACE  inhibitor-sensitive.

A basic understanding of the mechanism of glomerular filtration allows us to interpret ACE inhibitor-induced changes in SCr, and to decide whether they  warrant  further  investigation  of  the  renal  arteries  or  exclude  the possibility of RAS.