ACE (Angiotensin Converting Enzyme) Inhibitors, ACE Antagonists and ACE receptor blockers are the drugs used to treat hypertension. These drugs are widely prescribed for their beneficial effect on other conditions like Heart Failure and proteinuria in chronic kidney disease etc..
A new study published in the PLOS One, associates the use of these drugs with Acute Kidney Injury (AKI) . The study implicates increased use of of ACE inhibitors and ACE Receptor Antagonists, in England, to count for 15% of increased hospital admissions with AKI between 2007 and 2011.
ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This anti-hypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease.
These drugs cause vasodilation of the efferent vessels of glomerulus, the filtering unit of kidney, by disrupting the renin-angiotensin-aldosterone system. This vasodilation leads to sodium excretion and fall in the filtration pressure.
The mechanisms held to be involved in their renoprotective effects, are thought to be responsible for the renal adverse effects, as well.
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.
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.
On 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.
There are certain guidelines for use of these drugs, which is reproduced from the Circulation.
1. ACE inhibitors improve RBF (Renal Blood Flow) and stabilize GFR (Glomerular Filtration Rate) in most patients with CHF (Congestive Heart Failure).
2. ACE inhibitor therapy is indicated in patients with diabetic nephropathy and in patients with nondiabetic nephropathies when protein excretion exceeds 1 g/d.
3. A rise in serum creatinine may occur after initiation of therapy in patients with CHF. This rise usually occurs promptly, is less than 10% to 20%, is not progressive, and is a consequence of the renal hemodynamic changes brought about by ACE inhibitor therapy. Serum creatinine often stabilizes and may decline thereafter.
4. Although there is no serum creatinine level per se that contraindicates ACE inhibitor therapy, greater increases in serum creatinine occur more frequently when ACE inhibitors are used in patients with underlying chronic renal insufficiency.
5. The occurrence of ARF (Acute Renal Failure) should prompt a search for systemic hypotension (MAP, Mean Arterial Pressure<65 mm Hg), ECF (Extra-cellular Fluid) volume depletion, or nephrotoxin administration. An attempt should be made to correct or remove these factors. Consideration should also be given to high-grade bilateral renal artery stenosis or stenosis in a single kidney.
6. ACE inhibitors should be discontinued temporarily while precipitating factors for ARF are corrected; Ang II receptor blockers are not an appropriate substitute under these conditions. Once ARF has resolved with correction of the precipitating factors, ACE inhibitor therapy can be reinstituted.
7. Hyperkalemia is a potential complication of ACE inhibitor therapy, particularly in patients with diabetes or chronic renal failure. Monitoring of serum potassium early after initiation of therapy, appropriate reduction in dietary potassium intake, and avoidance of agents that can aggravate hyperkalemia (eg, potassium-sparing diuretics and NSAIDs) are recommended.
A new study published in the PLOS One, associates the use of these drugs with Acute Kidney Injury (AKI) . The study implicates increased use of of ACE inhibitors and ACE Receptor Antagonists, in England, to count for 15% of increased hospital admissions with AKI between 2007 and 2011.
ACE inhibitors effectively reduce systemic vascular resistance in patients with hypertension, heart failure or chronic renal disease. This anti-hypertensive efficacy probably accounts for an important part of their long term renoprotective effects in patients with diabetic and non-diabetic renal disease.
These drugs cause vasodilation of the efferent vessels of glomerulus, the filtering unit of kidney, by disrupting the renin-angiotensin-aldosterone system. This vasodilation leads to sodium excretion and fall in the filtration pressure.
The mechanisms held to be involved in their renoprotective effects, are thought to be responsible for the renal adverse effects, as well.
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.
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.
On 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.
There are certain guidelines for use of these drugs, which is reproduced from the Circulation.
1. ACE inhibitors improve RBF (Renal Blood Flow) and stabilize GFR (Glomerular Filtration Rate) in most patients with CHF (Congestive Heart Failure).
2. ACE inhibitor therapy is indicated in patients with diabetic nephropathy and in patients with nondiabetic nephropathies when protein excretion exceeds 1 g/d.
3. A rise in serum creatinine may occur after initiation of therapy in patients with CHF. This rise usually occurs promptly, is less than 10% to 20%, is not progressive, and is a consequence of the renal hemodynamic changes brought about by ACE inhibitor therapy. Serum creatinine often stabilizes and may decline thereafter.
4. Although there is no serum creatinine level per se that contraindicates ACE inhibitor therapy, greater increases in serum creatinine occur more frequently when ACE inhibitors are used in patients with underlying chronic renal insufficiency.
5. The occurrence of ARF (Acute Renal Failure) should prompt a search for systemic hypotension (MAP, Mean Arterial Pressure<65 mm Hg), ECF (Extra-cellular Fluid) volume depletion, or nephrotoxin administration. An attempt should be made to correct or remove these factors. Consideration should also be given to high-grade bilateral renal artery stenosis or stenosis in a single kidney.
6. ACE inhibitors should be discontinued temporarily while precipitating factors for ARF are corrected; Ang II receptor blockers are not an appropriate substitute under these conditions. Once ARF has resolved with correction of the precipitating factors, ACE inhibitor therapy can be reinstituted.
7. Hyperkalemia is a potential complication of ACE inhibitor therapy, particularly in patients with diabetes or chronic renal failure. Monitoring of serum potassium early after initiation of therapy, appropriate reduction in dietary potassium intake, and avoidance of agents that can aggravate hyperkalemia (eg, potassium-sparing diuretics and NSAIDs) are recommended.
