Additional Antiproteinuric Effect of Ultrahigh Dose Candesartan

Schmieder, Roland E.; Klingbeil, Arnfried U.; Fleischmann, Erwin H.; Veelken, Roland; Delles, Christian

doi:10.1681/asn.2005020138

Cited by 141 publications

(85 citation statements)

References 32 publications

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“…The greater reduction in proteinuria and the slower decline in creatinine clearance and eGFR that were seen in the titration groups provide further evidence of the long-term renal protection that is afforded by this strategy. Although previous clinical studies have shown that titrating an ACEi or an ARB to higher dosages reduces proteinuria more effectively (27)(28)(29)(30), to our knowledge, this is the first study to demonstrate that titration of these therapies against urinary protein excretion provides further benefit not only on proteinuria but also on a renal hard end point.…”

Section: Discussionmentioning

confidence: 75%

Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study

Hou

Xie²,

Zhang³

et al. 2007

Journal of the American Society of Nephrology

224

169

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The Renoprotection of Optimal Antiproteinuric Doses (ROAD) study was performed to determine whether titration of benazepril or losartan to optimal antiproteinuric doses would safely improve the renal outcome in chronic renal insufficiency. . Uptitration was performed to optimal antiproteinuric and tolerated dosages, and then these dosages were maintained. Median follow-up was 3.7 yr. The primary end point was time to the composite of a doubling of the serum creatinine, ESRD, or death. Secondary end points included changes in the level of proteinuria and the rate of progression of renal disease. Compared with the conventional dosages, optimal antiproteinuric dosages of benazepril and losartan that were achieved through uptitration were associated with a 51 and 53% reduction in the risk for the primary end point (P ‫؍‬ 0.028 and 0.022, respectively). Optimal antiproteinuric dosages of benazepril and losartan, at comparable BP control, achieved a greater reduction in both proteinuria and the rate of decline in renal function compared with their conventional dosages. There was no significant difference for the overall incidence of major adverse events between groups that were given conventional and optimal dosages in both arms. It is concluded that uptitration of benazepril or losartan against proteinuria conferred further benefit on renal outcome in patients who did not have diabetes and had proteinuria and renal insufficiency.

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Section: Discussionmentioning

confidence: 75%

Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study

Hou

Xie²,

Zhang³

et al. 2007

Journal of the American Society of Nephrology

224

169

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“…[3][4][5] Conversely, the 600 mg daily dose of aliskiren is known to have incremental antihypertensive efficacy, but also to significantly increase the incidence of gastrointestinal adverse events, compared with lower doses.…”

Section: Harikrishna Makani Sripal Bangalore and Franz H Messerlimentioning

confidence: 99%

Optimal renin–angiotensin system blockade—wishful thinking?

2013

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“…The greatest antiproteinuric efficacy of RAAS blockers is often observed at the highest tested dosage, which is frequently the upper end of their BP-dosing range. 92,93 However, the optimal renoprotective doses of these agents has not yet been clearly established and is the subject of ongoing investigation. 93 When initiating either an ACE inhibitor or an ARB-especially in patients with renal impairment-it is important that several safety considerations are addressed and that patients are monitored closely for adverse effects.…”

Section: Optimal Dosing and Safety Considerations With The Use Of Raamentioning

confidence: 99%

Evidence for renoprotection by blockade of the renin–angiotensin–aldosterone system in hypertension and diabetes

Karalliedde

Viberti

2006

J Hum Hypertens

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The incidence of end-stage renal disease (ESRD) is rising worldwide, accompanied by corresponding increases in the risk of morbidity and mortality. Underlying this trend are increasing rates of hypertension and diabetes mellitus, the two most common causes of ESRD. In addition to the adverse haemodynamic effects of hypertension on the kidney, elevated blood pressure (BP) can activate components of the renin-angiotensinaldosterone system (RAAS), which, in turn, activate mediators of inflammation, oxidative stress, cell growth, and matrix accumulation. Lowering BP reduces the risk of cardiovascular events and renal damage. Accumulating evidence from clinical and laboratory studies suggests that interrupting the RAAS with therapies such as angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and aldosterone receptor blockers can interfere with the mechanisms that promote diabetic and non-diabetic renal damage. Moreover, clinical trials of RAAS blockade have demonstrated reductions in microalbuminuria, a predictor of increased cardiorenal risk and overt nephropathy in patients with and without diabetes and/or hypertension. In this way, agents that block the RAAS should be considered the drugs of first choice as they provide enhanced renoprotection compared with other classes of antihypertensive agents such as calcium channel blockers and b-blockers.

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Additional Antiproteinuric Effect of Ultrahigh Dose Candesartan

Cited by 141 publications

References 32 publications

Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study

Renoprotection of Optimal Antiproteinuric Doses (ROAD) Study

Optimal renin–angiotensin system blockade—wishful thinking?

Evidence for renoprotection by blockade of the renin–angiotensin–aldosterone system in hypertension and diabetes

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