Renal failure related to angiotensin-converting enzyme inhibitors.
The introduction of agents that block the renin-angiotensin system has provided major benefit to patients with hypertension, renal diseases, and congestive heart failure. Some of the therapeutic advantages related to the kidney derive from removing angiotensin II at the efferent arteriole. Under some circumstances when afferent blood supply is compromised, particularly beyond a renal arterial stenosis, use of angiotensin-converting enzyme (ACE) inhibitors can lead to decrements of glomerular filtration rate (GFR) and impaired potassium excretion, which clinicians should be prepared to identify and manage. How often this occurs and when such a decrement poses a hazard to renal parenchymal viability depends on the starting conditions of the renal vasculature and sodium balance. Although these observations have been made primarily with ACE inhibitors, the basic principles apply to other agents interacting with components of the renin-angiotensin system, including angiotensin II antagonists and renin-inhibitors. When promptly identified and treated, changes in kidney function under these conditions represent a modest and acceptable risk worth taking in exchange for major therapeutic benefits.
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Division of Hypertension, Mayo Clinic, Rochester, MN 55905, USA.
D000804:Angiotensin II / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000009:adverse effects*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D011188:Potassium / Q000378:metabolism; D051437:Renal Insufficiency / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology; D012307:Risk Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D000804:Angiotensin II; D011188:Potassium