Evidence‐based treatment of hypertension in patients with diabetes mellitus

Onuigbo, Macaulay; Weir, Matthew R.

doi:10.1046/j.1463-1326.2003.00222.x

Cited by 17 publications

(28 citation statements)

References 88 publications

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“…These observations are without prejudice to current guidelines, which recommend that small but non-progressive increases in baseline serum creatinine, up to 30%, following the initiation of an ACEI or an ARB should not warrant drug discontinuation. [1,45] From our study experience, we recommend that RAAS blockade be up-titrated more slowly, particularly in the older patients with close monitoring of eGFR. Such pre-emptive preventative measures would help reduce iatrogenic renal failure in CKD patients on RAAS blockade and will only further optimize both renal and patient outcomes.…”

Section: Discussionmentioning

confidence: 98%

“…As noted earlier, there is a strong evidence-based consensus for renoprotection by RAAS blocking strategies in both diabetic and nondiabetic hypertensives, with and without proteinuria, beyond blood pressure lowering [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] (see Table 2). We have observed that in the large randomized placebo-controlled RAAS blockade trials, the patients were relatively younger, in their 50s and 60s, with near normal baseline serum creatinine (1-1.3 mg/dL), fairly preserved GFR, and on less than 25-50% of maximum recommended drug doses (see Table 2).…”

Section: Discussionmentioning

confidence: 99%

“…[23] Furthermore, in the CHARM trials, surveillance Table 2 A critical appraisal of the large randomized RAAS blockade trials. [1][2][3][4][5] blood safety analyses available in 2743 North American patients revealed that even though serum creatinine changed slightly between baseline and 6 weeks, serum creatinine had doubled in 82 (6%) of 1263 candesartan patients and 47 (4%) of 1279 placebo patients with surveillance laboratory assessments (p = 0.002) [14] From our findings, and cognizant of these previous observations in the literature, [14,23] we submit that in certain susceptible older hypertensive diabetic CKD patients, renal failure including ESRD could result from RAAS blockade, despite normal renal arteries and without precipitating factors, even years after starting RAAS blockade. Microvascular RAS is presumed to explain this potentially reversible syndrome.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Several large multi-center randomized placebo controlled trials have shown renoprotection with RAAS blockade, beyond blood pressure lowering, in CKD patients with diabetic nephropathy [3,7,[9][10][11][12] and in nondiabetic CKD patients with hypertension. [4] As a result, the last two decades have witnessed an escalating use of RAAS blocking agents in clinical medicine.…”

Section: Introductionmentioning

confidence: 99%

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Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Onuigbo

Onuigbo²

2008

Renal Failure

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Architect/Data Base Analyst/Programmer, NT Systems, Eau Claire, Wisconsin, USA Despite proven renoprotection from RAAS blockade and its increased application since the early 1990s, we have experienced an increasing CKD/ESRD epidemic, especially among U.S. diabetics. Consequently, some concerns regarding iatrogenic azotemia from RAAS blockade have surfaced. We hypothesized that susceptible CKD patients with normal renal arteries on conventional angiography, including MRA, but who have microvascular arteriolar narrowing in the renal circulation-mimicking large vessel renal artery stenosis, even without precipitating risk factors-could experience worsening azotemia after periods of time exceeding three months on stable doses of RAAS blockade. Between September 2002 and February 2005, as part of a larger prospective study of renal failure in CKD patients on RAAS blockade, we studied five patients with >25% higher serum creatinine and normal MRA without precipitating factors. RAAS blockade was discontinued. eGFR by MDRD was monitored. Five Caucasians (M:F = 1:4; age 68 years) were enrolled and followed-up at 29.6 months. The duration of RAAS blockade at enrollment was 34.6 months. The baseline eGFR had decreased from 28.4 ± 7.1 to 17.0 ± 7.4 ml/min/1.73 m 2 BSA (p < 0.001) at enrollment. One required temporary hemodialysis; no deaths occurred. eGFR increased from 17.0 ± 7.4 to 24.6 ± 9.5 ml/min/ 1.73 m 2 BSA (p=0.009), 29.6 (20-43) months after stopping the RAAS blockade. We conclude that worsening azotemia occurs in susceptible CKD patients on stable doses of RAAS blockade after long periods of time, despite normal renal arteries without precipitating risk factors. We submit that microvascular renal arteriolar narrowing is the pathophysiologic mechanism. These observations call for further study.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Onuigbo

Onuigbo²

2008

Renal Failure

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“…Since the mid 1990s, an evidence-based consensus has emerged of enhanced renoprotection with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), beyond blood pressure (BP) lowering, in diabetic and nondiabetic nephropathies, with and without hypertension [1] (table 1). As a result, the last 2 decades have witnessed an escalating use of renin-angiotensin-aldosterone system (RAAS) blocking agents in clinical medicine [2].…”

Section: Introductionmentioning

confidence: 99%

Analytical Review of the Evidence for Renoprotection by Renin-Angiotensin-Aldosterone System Blockade in Chronic Kidney Disease – A Call for Caution

Onuigbo¹

2009

Nephron Clin Pract

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Despite reported renoprotection with angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs), and notwithstanding their increased use, we continue to experience an epidemic of acute renal failure (ARF)/chronic kidney disease/end-stage renal disease. Consequently, concerns about iatrogenic renal failure have resurfaced. Different analysis of these trials revealed flaws such as recruitment of relatively younger patients with preserved baseline renal function, common utilization of lower end doses of ACEIs/ARBs, high drug discontinuation rates, excessive use of surrogate endpoints, inadequate reporting of adverse effects, and short duration studies. Again, lower 24-hour ambulatory blood pressure among patients in the ramipril arm of the micro-HOPE (Heart Outcomes Prevention Evaluation) study raises doubts of renoprotection beyond blood pressure lowering. The disappointing results from the ONTARGET (Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial) study only compounded these doubts. We demonstrated significant renal salvage after ACEI/ARB was discontinued in chronic kidney disease patients recruited with increasing ARF while on ACEI/ARB. Apart from our reports, there are increasing reports incriminating the use of ACEI/ARB with ARF exacerbations. We conclude that close and indefinite monitoring of estimated glomerular filtration rate is an absolute must in these patients. The treating physician must be ready to consider trial discontinuation of ACEI/ARB, promptly. Combination ACEI + ARB therapy should be the exception, rather than the rule. Temporary withdrawal of ACEI/ARB before certain exposures, ‘renoprevention’, would only further improve the results of renoprotection.

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Lapane

Cooke²

2012

Arch Intern Med

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ROC curve" term as well. This might be a weakness in our current study methodology; however, we do not expect additional articles to be systematically different to the ones included in our review and thus do not expect to alter our conclusions. Our search did not aim to identify all studies on predictive tools for mortality, but to generate a large enough representative sample that would help in understanding the status of this field. This is why we already restricted searches to a single year of publication, since searches without restrictions may have yielded several thousands of articles 4 (testimony to the highly prolific nature and low translational efficiency of this literature) without improving much the informativeness of our project. We agree with the authors that multivariable information might be important in predicting future mortality, but our data have shown that most of the available tools have modest accuracy to predict death and high heterogeneity between populations and settings.

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Evidence‐based treatment of hypertension in patients with diabetes mellitus

Cited by 17 publications

References 88 publications

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Late Onset Azotemia from RAAS Blockade in CKD Patients with Normal Renal Arteries and No Precipitating Risk Factors

Analytical Review of the Evidence for Renoprotection by Renin-Angiotensin-Aldosterone System Blockade in Chronic Kidney Disease – A Call for Caution

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