The verapamil versus amlodipine in nondiabetic nephropathies treated with trandolapril (VVANNTT) study

Boero, R; Rollino, Cristiana; Massara, Carlo; Berto, I M; Perosa, Paolo Maurizio; Vagelli, G; Lanfranco, Giacomo; Quarello, F

doi:10.1016/s0272-6386(03)00410-4

Cited by 28 publications

(21 citation statements)

References 23 publications

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“…43,50,[81][82][83][84][85][86][87][88] In a placebo-controlled trial, 3 years of benazepril therapy reduced the risk of the primary composite end point (doubling of serum creatinine or need for dialysis) by 53% compared with placebo (Po0.001). 50 A greater risk reduction was seen in patients with mild renal insufficiency (71%) compared with patients with moderate renal insufficiency (46%).…”

Section: Clinical Evidence Of Benefits Of Raas Inhibition In Non-diabmentioning

confidence: 99%

“…43 In subjects with overt proteinuria at baseline, the mean decline in GFR after 3 years was 36% slower in the ramipril group than in the amlodipine group (P ¼ 0.006). 83 In the Verapamil Versus Amlodipine in Nondiabetic Nephropathies Treated With Trandolapril (VVANNTT) study, 87 treatment with trandolapril significantly decreased proteinuria (P ¼ 0.018) vs baseline, but the addition of either amlodipine or verapamil did not provide any further decrease in proteinuria. REIN Evidence for renoprotection by blockade of the RAAS J Karalliedde and G Viberti…”

Section: Clinical Evidence Of Benefits Of Raas Inhibition In Non-diabmentioning

confidence: 99%

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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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Section: Clinical Evidence Of Benefits Of Raas Inhibition In Non-diabmentioning

confidence: 99%

Section: Clinical Evidence Of Benefits Of Raas Inhibition In Non-diabmentioning

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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“…In the randomized phase, there was a slight reduction in proteinuria in both groups without significant differences within and between treatments. [96] Furthermore, it has been reported that verapamil may improve renal function in hypertensive patients when it has been impaired by the previous use of ACE inhibitors. [97,98] As a conclusion, in spite of the promising initial results, verapamil has not shown any special ability to reduce proteinuria when compared with renin-angiotensin axis blocking drugs.…”

Section: Non-dihydropyridine Calcium Antagonistsmentioning

confidence: 99%

Calcium Antagonists and Renal Failure Progression

Robles

2008

Renal Failure

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Although tighter blood pressure control is considered the main mechanism for preventing the progression of chronic renal failure, angiotensin-converting enzyme inhibitors and angiotensin receptors blockers seem to have an additional organ protective role. The effects of calcium antagonists in renal disease are not so clearly defined. Calcium antagonists have pleiotropic effects that might contribute to protect the kidney, such as attenuating mesangial entrapment of macromolecules, countervailing the mitogenic effect of platelet-derived growth factors and platelet-activating factors, and suppressing mesangial cell proliferation. They could also act as free radical scavengers and inhibit the renal effects of endothelin. Some evidence has been accumulated demonstrating that certain new dihydropyridinic calcium antagonists may affect postglomerular as well as preglomerular vessels, resulting in decreased filtration fraction and nephroprotective effect as renin-angiotensin axis-blocking drugs. Though there are few reports on the clinical renal effects of new calcium antagonists, they have rendered promising results. Manidipine does not increase proteinuria as do some classic calcium antagonists, and lercanidipine combined with renin-angiotesin axisblocking drugs reduce proteinuria. Both drugs have been shown to decrease microalbuminuria when administered alone.

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“…In addition, a rise in serum creatinine of more than 35% above baseline or the emergence of hyperkalemia may be a reason to withhold first-line ACEI or ARB therapy [176, 177]. CCBs are among the most commonly used classes of antihypertensive drugs in patients with kidney disease [178]. However, evidence for any renoprotective effects of calcium antagonists is equivocal.…”

Section: Calcium Channel Blockersmentioning

confidence: 99%

Diabetic Nephropathy: The Proteinuria Hypothesis

Williams¹

2005

Am J Nephrol

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Background/Aims: Proteinuria, nearly a universal finding in progressive kidney disease, has been the subject of frequent recent analyses in the renal literature. Proteinuria is a hallmark of diabetic nephropathy: microalbuminuria is the principal early predictor for progression of diabetic glomerulopathy, and proteinuria may be viewed as a measure of the severity and promoter of progression of nephropathy. Methods: This article critically reviews for the first time the full scope of diabetic proteinuria – complex molecular mechanisms, natural history, and analysis of treatment trials – in order to address the validity of ‘the proteinuria hypothesis’, i.e., that diabetic proteinuria is a modifiable determinant of renal progression. This hypothesis is analyzed in detail, including recent studies on the primary therapy of diabetic nephropathy, renin-angiotensin blockade. Results: As fully developed, this hypothesis consists of three postulates: that higher amounts of proteinuria predict progressive loss of function, that proteinuria reduction correlates with slowing progression, and that proteinuria is a surrogate endpoint for clinical trials. The latter postulate has not before been adequately linked to growing information about the first two postulates as they apply to diabetic kidney disease. Conclusion: While diabetic nephropathy is a disease model for the potential use of proteinuria as a surrogate marker for renal progression, this shift in perspective will require prospective data from additional clinical trials, particularly of non-renin-angiotensin blocking drugs, to be complete.

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The verapamil versus amlodipine in nondiabetic nephropathies treated with trandolapril (VVANNTT) study

Cited by 28 publications

References 23 publications

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

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

Calcium Antagonists and Renal Failure Progression

Diabetic Nephropathy: The Proteinuria Hypothesis

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