Does Renin-Angiotensin Aldosterone System Blockade Exacerbate Contrast-Induced Nephropathy in Patients with Chronic Kidney Disease? A Prospective 50-month Mayo Clinic Study

Onuigbo, Macaulay; Onuigbo, Nnonyelum

doi:10.1080/08860220701742153

Cited by 30 publications

(35 citation statements)

References 26 publications

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“…In the last 5 years, we have published several reports from our single-center experience describing sometimes reversible AKI in CKD patients associated with concurrent RAAS blockade [55,56,71,72,73,74,75,76,95]. The clinical circumstances under which we described worsening renal failure associated with concurrent RAAS blockade include the absence of any identifiable so-called precipitating risk factor [72], in association with multiple varied risk factors such as infections, heart failure exacerbation, hypotension and dehydration [70,72], in association with renal artery stenosis [75,76], in hospitalized patients [95], and in association with contrast-induced nephropathy [73,96].…”

Section: The Association Of Aki With Raas Blockade In Generalmentioning

confidence: 99%

“…These RCTs have several design flaws, and questions abound regarding the general applicability of the trial findings from these RCTs to the general CKD population, more so the older (>65-year-old) CKD patients [55,56,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80]. The several limitations and concerns raised regarding the veracity of the claims of these RCTs as well as doubts regarding the general applicability of the recommendations of the large RAAS blockade RCTs to especially the older CKD patient population include the following:…”

Section: A Brief Critique Of the Evidence Base For Renoprotection Witmentioning

confidence: 99%

“…The clinical circumstances under which we described worsening renal failure associated with concurrent RAAS blockade include the absence of any identifiable so-called precipitating risk factor [72], in association with multiple varied risk factors such as infections, heart failure exacerbation, hypotension and dehydration [70,72], in association with renal artery stenosis [75,76], in hospitalized patients [95], and in association with contrast-induced nephropathy [73,96]. What is more, recently, sustained increases in estimated GFR (eGFR) were demonstrated from 16.4 to 26.6 ml/min/1.73 m 2 body surface area, in 52 patients, mean age 73 years, following the discontinuation of ACEIs and/or ARBS [97,98].…”

Section: The Association Of Aki With Raas Blockade In Generalmentioning

confidence: 99%

“…Many of the published large RAAS blockade randomized controlled trials (RCTs), upon which current evidence-based practice for the increasing use of the ACEIs and ARBs for renoprotection derived from, have strong deficiencies that have been highlighted over the years [55,56,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80]. These RCTs have several design flaws, and questions abound regarding the general applicability of the trial findings from these RCTs to the general CKD population, more so the older (>65-year-old) CKD patients [55,56,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80].…”

Section: A Brief Critique Of the Evidence Base For Renoprotection Witmentioning

confidence: 99%

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Can ACE Inhibitors and Angiotensin Receptor Blockers Be Detrimental in CKD Patients?

Onuigbo

2011

Nephron Clin Pract

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Current epidemiological data from the USA, Europe, Asia and the Indian subcontinent, Africa, the Far East, South America, the Middle East and Eastern Europe all point to the increasing incidence of renal failure encompassing acute kidney injury (AKI), chronic kidney disease (CKD) and end-stage renal disease (ESRD). While the explanations for these worldwide epidemics remain speculative, it must be acknowledged that these increases in AKI, CKD and ESRD, happening worldwide, have occurred despite the universal application of strategies of renoprotection over the last 2 decades, more especially the widespread use of angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). We note that many of the published large renin-angiotensin-aldosterone system (RAAS) blockade randomized controlled trials, upon which current evidence-based practice for the increasing use of ACEIs and ARBs for renoprotection derived from, have strong deficiencies that have been highlighted over the years. From reports in the literature, there is an increasing association of exacerbations of renal failure with ACEIs and ARBs, more so in the older hypertensive patient, >65 years old. The biological plausibility for ACEI and ARB to protect the kidneys against a background of potential multiple pathogenetic pathways to account for CKD progression appears to be not very defensible. We reviewed the literature along these lines and submit that ACEIs and ARBs often cause unrecognized significant worsening renal failure in CKD patients, sometimes irreversible, and that more caution is required regarding their use, especially in the older hypertensive patients, with likely ischemic hypertensive nephropathy. Given the increasing association of concomitant RAAS blockade with worsening renal failure following exposure to iodinated contrast, during acute illness, in the perioperative period and following lower bowel preparations prior to colonoscopy, we submit that, preferably, ACEIs and ARBs be withheld for 2–4 days prior to or during these clinical scenarios. This represents the concept of renoprevention.

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Section: The Association Of Aki With Raas Blockade In Generalmentioning

confidence: 99%

Section: A Brief Critique Of the Evidence Base For Renoprotection Witmentioning

confidence: 99%

Section: The Association Of Aki With Raas Blockade In Generalmentioning

confidence: 99%

Section: A Brief Critique Of the Evidence Base For Renoprotection Witmentioning

confidence: 99%

See 2 more Smart Citations

Can ACE Inhibitors and Angiotensin Receptor Blockers Be Detrimental in CKD Patients?

Onuigbo

2011

Nephron Clin Pract

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“…They recommended not withholding ACEIs prior to contrast exposure. However a recent report from Mayo clinic suggests withdrawal of RAAS blocker usage 24-48 hour before elective interventions, relying on their own clinical experience and also an earlier literature data (17,18). Chronic ACEI administration was investigated by Cirit et al (5).…”

Section: Discussionmentioning

confidence: 99%

The effects of chronic usage of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on contrast-induced nephropathy in low-risk patients

Barış¹,

Özpelit²,

Doğan³

et al. 2012

Anadolu Kardiyol Derg

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Objective: There is conflicting data about the role of renin-angiotensin-aldosterone system (RAAS) blockers in contrast-induced nephropathy (CIN) pathophysiology. In this study, we aimed to investigate the effects of chronic usage of RAAS blocker drugs on development of CIN in low risk patients. Methods: Study was designed as a prospective cohort study. A total of 295 patients were enrolled in the study. Study population was consisted of three subgroups according to prior usage of RAAS blockers: no RAAS blocker group (n=95), angiotensin-converting enzyme inhibitor (ACEI) group (n=106), angiotensin receptor blocker (ARB) group (n=94). CIN was defined as an increase of ≥25% in creatinine over the baseline value or 0.5 mg/dL rise within 48-72 h of angiography. Mehran score was calculated for each patient. Baseline variables and percentage of CIN were compared with ANOVA, Mann-Whitney U, Kruskal-Wallis and Pearson Chi-square tests between groups. In order to determine the independent predictors of CIN, binary logistic regression analyses were performed. Results: CIN occurred in 18 patients (17.0%) in the ACEI group, 17 patients (18.1%) in ARB group and 7 patients (7.4%) in the no RAAS group. CIN occurrence was significantly higher in RAAS than no RAAS group (17.5% vs. 7.4%, p=0.01). Chronic RAAS blocker administration was an independent predictor of CIN (OR=2.69; 95% CI: 1.025-7.067; p=0.04). Mehran score was the only other independent predictor for CIN (OR=1.15; 95% CI: 1.019-1.310; p=0.02).

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Kontrastmittel-induzierte Nephropathie

Hörl

2009

Wien Klin Wochenschr

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Contrast media induced nephropathy is a common complication, particularly in high risk patients, such as patients with chronic kidney disease (CKD) and diabetes. The majority of studies show an increased in-hospital mortality and an unfavourable long-term prognosis after manifestation of contrast media induced nephropathy. The course and the potential risk factors of this type of acute renal failure are known. Therefore, an effective prophylaxis should allow to prevent this complication. In low risk patients oral or intravenous volume expansion is probably sufficient combined with the withdrawal of non-steroidal anti-inflammatory drugs. In high risk patients additional prophylactic measures are needed but their efficacy is not clearly defined. Therefore, heterogeneous recommendations exist. Hydration reduces (afferent) renovasoconstriction, the tubuloglomerular feedback, the tubulotoxic effects of contrast media (via dilution) and the oxygen radical formation. The optimal composition, timing and amount of fluid which should be administered to the patients remain unclear. Most studies show that intravenous administration of volume is more effective than oral fluid intake. The majority of studies found a benefit of isotonic sodium bicarbonate in comparison to isotonic saline solutions, even if meta-analyses displayed only a positive trend for sodium bicarbionate due to the heterogeneity of the data. Controversies exist for N-acetylcysteine, vitamin C, fenoldopam, theophylline or statins. Due to low cost and low side effects, N-Acetylcysteine is widely used. Theophyllin (given intravenously 30 minutes before contrast media injection) is renoprotective, particularly in intensive care unit patients. Very important is the reduction of contrast media volume (if possible <30 ml for diagnostic procedures and <100 ml for interventions). Iso-osmolar and low-osmolar contrast media may have a comparable low risk for the induction of contrast media induced nephropathy. This risk is probably higher after intra-arterial as compared to intravenous administration of contrast media. Controversies exist with respect to the reduction of contrast media induced nephropathy and mortality by prophylactic hemodialysis or hemofiltration. A possible benefit of these procedures consists probably for patients with advanced chronic kidney disease (stage 5). With the further increase of investigations using contrast media, with the further increase in vascular interventions, in age and comorbidities of the patients one may suggest that the problem of contrast media induced nephropathy will further increase, despite all prophylactic procedures so far recommended.

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Does Renin-Angiotensin Aldosterone System Blockade Exacerbate Contrast-Induced Nephropathy in Patients with Chronic Kidney Disease? A Prospective 50-month Mayo Clinic Study

Cited by 30 publications

References 26 publications

Can ACE Inhibitors and Angiotensin Receptor Blockers Be Detrimental in CKD Patients?

Can ACE Inhibitors and Angiotensin Receptor Blockers Be Detrimental in CKD Patients?

The effects of chronic usage of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on contrast-induced nephropathy in low-risk patients

Kontrastmittel-induzierte Nephropathie

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