ACE Inhibitors and the Kidney

Abstract

ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This antihypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease. The renal mechanisms underlying the renal adverse effects of ACE inhibitors--intrarenal efferent vasodilation with a consequent fall in filtration pressure--are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to long term renoprotection. The former is suggested by the positive correlation between the fall in filtration fraction and the reduction in proteinuria found during ACE inhibition. The latter is suggested by the correlation between the (slight) reduction in glomerular filtration rate at onset of therapy and a more favourable course of renal function in the long term. Such a fall in filtration rate at the onset of ACE inhibitor treatment is reversible after withdrawal, and can be considered the trade-off for long term renal protection in patients with diabetic and nondiabetic chronic renal disease. In conditions in which glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibition can induce acute renal failure, which is reversible after withdrawal of the drug. Systemic and renal haemodynamic effects of ACE inhibition, both beneficial and adverse, are potentiated by sodium depletion. Consequently, sodium repletion contributes to the restoration of renal function in patients with ACE inhibitor-induced acute renal failure. Our the other hand, co-treatment with diuretics and sodium restriction can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients at the greatest risk for renal adverse effects (those with heart failure, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monitoring of renal function and serum potassium levels.

Prevalence and predictors of chronic kidney disease among Ghanaian patients with hypertension and diabetes mellitus: A multicenter cross‐sectional study

“…The concomitant use of other medications such as herbal medications that may be worsening their renal functions cannot be ruled out. ACE‐I or ARBs have also been associated with acute kidney injury . The use of ACE‐I and or ARBs can also be associated with CKD by decreasing glomerular filtration rate more especially with the concomitant use of NSAIDs which are very common in the cohort as most patients are prescribed NSAIDS for the musculoskeletal pains or buy them over the counter.…”

“…ACE-I or ARBs have also been associated with acute kidney injury. 41 The use of ACE-I and or ARBs can also be associated with CKD by decreasing glomerular filtration rate more especially with the concomitant use of NSAIDs which are very common in the cohort as most patients are prescribed NSAIDS for the musculoskeletal pains or buy them over the counter. ACE inhibitors can also cause CKD in a short run as a nephrotoxin and may account for the non-protection in our cohort.…”

Dual Effects of Lisinopril on Puromycin Aminonucleoside Nephrosis in Unilaterally Nephrectomized Rats.

“…ACEI-induced renal dysfunction is pre sumed to be caused by the reduction of intraglomerular blood pressure originating from predominant vasodilata tion of the renal efferent artery in humans (23). Ca 2+-chan nel blockers are known to act as vasodilators of the renal afferent artery and to subsequently increase renal blood flow.…”

Renin angiotensin aldosterone inhibition in the treatment of cardiovascular disease

“…It is well established that RAAS blockage presents a particular risk-benefit analysis in regards to renal impairment [137], and that such risks are amplified in the setting of salt-restriction/dehydration [138–140], in the elderly [141], or in patients with diabetes, heart or renal disease [142]. Because Ang II has divergent activities on promoting hypertension and disease as well as maintaining essential renal homeostatic mechanisms, the conflicting results obtained to-date underscore the need to better understand the role of intrarenal RAAS.…”