Abstract
Several large, randomized, multicenter studies in diabetic and nondiabetic patients with chronic proteinuric nephropathies have clearly demonstrated that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARB) are able to reduce urinary protein excretion and retard renal disease progression. However, the number of patients who reach end-stage renal failure is still considerable and there is a great need to identify therapies that can arrest evolution of kidney damage. Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further increase antiproteinuric and nephroprotective effects of each drug class. However, in order to slow to the greatest extent progression of renal disease, the ideal therapeutic approach for patients with proteinuric nephropathies should be a multimodal strategy including dual RAS blockade, antialdosterone therapy, lipid-lowering agents, smoking cessation, and tight glucose control for diabetes.
| Original language | English |
|---|---|
| Pages (from-to) | 118-124 |
| Number of pages | 7 |
| Journal | Current Hypertension Reports |
| Volume | 11 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2009 |
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ASJC Scopus subject areas
- Internal Medicine
Cite this
Intensified inhibition of renin-angiotensin system : A way to improve renal protection? / Cravedi, Paolo; Ruggenenti, Piero; Remuzzi, Giuseppe.
In: Current Hypertension Reports, Vol. 11, No. 2, 2009, p. 118-124.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Intensified inhibition of renin-angiotensin system
T2 - A way to improve renal protection?
AU - Cravedi, Paolo
AU - Ruggenenti, Piero
AU - Remuzzi, Giuseppe
PY - 2009
Y1 - 2009
N2 - Several large, randomized, multicenter studies in diabetic and nondiabetic patients with chronic proteinuric nephropathies have clearly demonstrated that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARB) are able to reduce urinary protein excretion and retard renal disease progression. However, the number of patients who reach end-stage renal failure is still considerable and there is a great need to identify therapies that can arrest evolution of kidney damage. Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further increase antiproteinuric and nephroprotective effects of each drug class. However, in order to slow to the greatest extent progression of renal disease, the ideal therapeutic approach for patients with proteinuric nephropathies should be a multimodal strategy including dual RAS blockade, antialdosterone therapy, lipid-lowering agents, smoking cessation, and tight glucose control for diabetes.
AB - Several large, randomized, multicenter studies in diabetic and nondiabetic patients with chronic proteinuric nephropathies have clearly demonstrated that angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARB) are able to reduce urinary protein excretion and retard renal disease progression. However, the number of patients who reach end-stage renal failure is still considerable and there is a great need to identify therapies that can arrest evolution of kidney damage. Maximizing renin-angiotensin system (RAS) blockade through combined ACE inhibitor and ARB therapy has been shown to further increase antiproteinuric and nephroprotective effects of each drug class. However, in order to slow to the greatest extent progression of renal disease, the ideal therapeutic approach for patients with proteinuric nephropathies should be a multimodal strategy including dual RAS blockade, antialdosterone therapy, lipid-lowering agents, smoking cessation, and tight glucose control for diabetes.
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UR - http://www.scopus.com/inward/citedby.url?scp=62549163397&partnerID=8YFLogxK
U2 - 10.1007/s11906-009-0022-9
DO - 10.1007/s11906-009-0022-9
M3 - Article
C2 - 19278601
AN - SCOPUS:62549163397
VL - 11
SP - 118
EP - 124
JO - Current Hypertension Reports
JF - Current Hypertension Reports
SN - 1522-6417
IS - 2
ER -