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.
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