Searched over 200M research papers
10 papers analyzed
Some studies suggest ACE inhibitors can worsen kidney damage, cause atrophy, and reduce renal function in renal artery stenosis, while other studies indicate they may improve renal blood flow and reduce chronic kidney disease progression.
20 papers analyzed
Angiotensin-converting enzyme (ACE) inhibitors are widely used in the treatment of hypertension, heart failure, and chronic kidney disease. However, their use in patients with renal artery stenosis (RAS) has been a subject of considerable debate due to potential adverse effects on renal function.
Research indicates that ACE inhibitors can exacerbate kidney damage in the presence of renal artery stenosis. This is primarily due to the reduction in renal perfusion pressure, which is critical for maintaining kidney function in these patients . Studies in animal models, such as the two-kidney, one-clip (2K-1C) rat model, have shown that ACE inhibitors like enalapril can worsen lesions in the clipped kidney, leading to increased proteinuria and decreased renal function.
Clinical evidence supports the notion that ACE inhibitors can induce acute renal failure in patients with RAS. This is particularly evident in cases where renal perfusion pressure is highly dependent on angiotensin II, such as in bilateral RAS or stenosis of a single functioning kidney . In a study involving dogs with induced renal artery stenosis, ACE inhibitors led to significant reductions in glomerular filtration rate (GFR) and renal blood flow (RBF), highlighting the risk of acute renal failure.
Long-term use of ACE inhibitors in patients with unilateral RAS can lead to atrophy and functional loss of the stenosed kidney. Experimental studies in rats have shown that chronic ACE inhibition results in significant interstitial fibrosis and tubular atrophy in the affected kidney, with a marked reduction in kidney weight and function. This suggests that prolonged ACE inhibitor therapy may lead to irreversible kidney damage in the stenosed kidney.
Patients with pre-existing conditions such as chronic heart failure, diabetes, and volume depletion are at higher risk of developing acute renal failure when treated with ACE inhibitors. It is crucial to monitor renal function closely in these patients, especially during the initiation and titration of ACE inhibitor therapy.
In cases where ACE inhibitors pose a significant risk, alternative treatments such as calcium channel blockers may be considered. However, these alternatives also have their own set of complications. For instance, calcium channel blockers have been shown to worsen lesions in the clipped kidney in animal models, although they may have different effects on the unclipped kidney.
Given the limited efficacy of ACE inhibitors in preventing the progression of renal failure in RAS, revascularization procedures such as percutaneous angioplasty and stenting have been explored. However, these interventions have shown only modest benefits in blood pressure control and renal function preservation. Therefore, a more effective strategy may involve focusing on cardiovascular health to prevent cardiovascular death, which is a more common outcome in patients with atherosclerotic RAS.
The use of ACE inhibitors in patients with renal artery stenosis requires careful consideration due to the potential for worsening renal function and inducing acute renal failure. While alternative therapies and revascularization procedures offer some benefits, the primary focus should be on comprehensive cardiovascular management to improve overall outcomes. Close monitoring and individualized treatment plans are essential to mitigate the risks associated with ACE inhibitor therapy in this patient population.
Most relevant research papers on this topic