Orris

Why ace inhibitors are contraindicated in bilateral renal artery stenosis

Reading File
Reading File
Finding Sources
Searching PubMed

"renal artery stenosis" AND "angiotensin-converting enzyme inhibitors"

Searching the Web

bilateral renal artery stenosis ACE inhibitors mechanism acute kidney injury authoritative

ACE inhibitors are contraindicated in bilateral renal artery stenosis because both kidneys become dependent on angiotensin II to maintain glomerular filtration pressure.
  • Renal artery narrowing reduces renal perfusion pressure.
  • In response, the kidneys activate RAAS and produce angiotensin II.
  • Angiotensin II preferentially constricts the efferent arteriole. This raises pressure inside the glomerular capillaries and helps preserve GFR despite low incoming blood flow.
  • An ACE inhibitor blocks angiotensin II formation, so the efferent arteriole dilates.
  • Intratubular glomerular pressure then falls sharply in both kidneys, causing a major fall in GFR, rising creatinine, oliguria, and potentially acute kidney injury.
Why bilateral disease matters: in unilateral stenosis, the unaffected kidney can usually maintain overall GFR. With bilateral severe stenosis, or stenosis of an artery supplying a solitary functioning kidney, there is no adequately perfused kidney to compensate.
This is a hemodynamic, often reversible form of acute kidney injury after stopping the ACE inhibitor and restoring renal perfusion. The textbook library lists bilateral renal artery stenosis among ACE-inhibitor contraindications. A review of renal artery stenosis pathophysiology describes the potential for abrupt GFR reduction and AKI with ACE inhibitor or ARB therapy in severe bilateral disease.

Spironolactone is commonly used in cirrhosis with ascites

Reading File
Finding Sources
Searching PubMed

cirrhosis ascites spironolactone

Searching the Web

AASLD ascites cirrhosis spironolactone aldosterone sodium retention guideline

Yes. Spironolactone is a first-line diuretic for ascites due to cirrhosis because cirrhosis produces secondary hyperaldosteronism.

Why aldosterone is high in cirrhosis

Portal hypertension causes splanchnic vasodilation, so the body senses a low effective arterial blood volume despite total-body fluid excess. This activates RAAS:
Renin → angiotensin II → aldosterone
Aldosterone increases sodium reabsorption in the distal nephron. Water follows sodium, worsening edema and ascites.

How spironolactone helps

Spironolactone blocks the mineralocorticoid (aldosterone) receptor, leading to:
  • Increased urinary sodium excretion (natriuresis)
  • Loss of excess water
  • Reduced ascites and peripheral edema
  • Potassium retention
It targets the primary sodium-retaining mechanism in cirrhotic ascites, which is why it is more appropriate than loop-diuretic monotherapy. The AASLD outpatient cirrhosis guidance identifies aldosterone antagonists and loop diuretics as the principal drugs for this condition.
Usually it is paired with furosemide, commonly in a 100 mg spironolactone : 40 mg furosemide ratio, to augment diuresis and help balance potassium effects. Monitor body weight, serum potassium, sodium, creatinine, and blood pressure. Hyperkalemia, acute kidney injury, severe hyponatremia, or encephalopathy may require reducing or stopping diuretics.
This is a shared conversation. Sign in to Orris to start your own chat.