Vol. 5, Issue 1, Part A (2023)

In individuals suffering from chronic renal illness, heart failure, or hypertension, ACE inhibitors efficiently lower systemic vascular resistance. A significant portion of their long-term renoprotective effects in patients with diabetes and non-diabetic renal illness are likely explained by their antihypertensive efficacy.
ACE inhibition can cause acute renal failure, which is reversible after the drug is stopped, in situations where glomerular filtration is critically dependent on angiotensin II-mediated efferent vascular tone. Sodium depletion increases the positive and negative effects of ACE inhibition on systemic and renal hemodynamic. Consequently, in patients with acute renal failure brought on by ACE inhibitors, sodium repletion helps to restore renal function. Conversely, in individuals whose blood pressure or proteinuria do not respond adequately to treatment, co-treatment with diuretics and salt restriction can increase therapeutic efficacy.