ACE-I/ARB Therapy prior to Contrast Exposure: What Should the Clinician Do?

Kalyesubula, Robert; Bagasha, Peace; Perazella, Mark A.

doi:10.1155/2014/423848

Cited by 19 publications

(14 citation statements)

References 31 publications

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“…Among reported cases, it is interesting to observe that a great percentage of cases reported risk factors. As for b-blockers, the increased risk with concomitant use of ACE-I and CM is still debated and it is not clear whether the treatment with ACE-I should be continued or discontinued 3 days prior to use of CM in order to reduce CM-induced renal toxicity risk [45]. In our case, for this patient, no renal toxicity was reported.…”

Section: Discussionmentioning

confidence: 75%

Suspected adverse reactions to contrast media in Campania Region (Italy): results from 14 years of post-marketing surveillance

Sessa

Rossi

Mascolo

et al. 2015

Expert Opinion on Drug Safety

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Section: Discussionmentioning

confidence: 75%

Suspected adverse reactions to contrast media in Campania Region (Italy): results from 14 years of post-marketing surveillance

Sessa

Rossi

Mascolo

et al. 2015

Expert Opinion on Drug Safety

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“…In diabetic patients, metformin introduction must be canceled 48 h before and limited 48 h after CM injection. ACE inhibitors and angiotensin receptor blockers, due to possible harm and inadequate data on their positive effects on renal hemodynamics and GFR, should be excluded from therapy 1 day before the study, although, under the KDIGO consensus, this allegation has not been fully proved [13,72].…”

Section: Prophylaxismentioning

confidence: 99%

Contrast-induced Acute Kidney Injury: A Contemporary Review

Khilchuk¹,

Власенко²,

Scherbak³

et al. 2018

Int J Ren Dis Ther

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Clinically significant Contrast-Induced Acute Kidney Injury (CIAKI) is a severe complication of interventional contrast-based procedures of all kinds. It involves high morbidity, mortality, social and financial losses. Acute renal damage after coronary angiography or percutaneous coronary intervention may occur in 1-2% of cases in the general population or 50+% of cases with high CIAKI exposure. It is essential to detect high-risk patients with renal damage as a major and frequent CIAKI predisposing factor. There are novel biomarkers with rapid or nearly instant response to acute subclinical contrast-induced renal damage, which are highly valuable in CIAKI diagnosis and for this reason desire deeper clinical research. Despite a number of controversies, prophylactic and therapeutic measures are practically the same in a vast majority of guidelines. An intravenous 0.9% NaCl solution remains the only proven measure in CIAKI prophylaxis and treatment, while the use of other pharmacological approaches still needs more relevant prospective clinical research. The aim of this paper was to review contemporary evidencebased CIAKI data.

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“…ACE is a zinc-dependent metallopeptidase with broad substrate specificity, but it was first described for its catalytic properties in two vasoactive peptides: angiotensin I and bradykinin (Kalyesubula et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

Evangelista¹,

Rios²,

Ribeiro³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Recent studies have shown an association between thrombosis and factor VII (FVII), tissue factor (TF), and angiotensinconverting enzyme (ACE). This suggests that individuals with FVII-402 G/A, FVII-401 G/T, TF+5466 A/G, and ACE-287 insertion/ deletion (I/D) polymorphisms present an increased risk of venous thrombosis, heart disease, and ischemic stroke compared with controls. In this study, we investigated the frequencies of these polymorphisms and their association with arterial and venous thrombosis. For the FVII-402 G/A polymorphism, there were 57.3% heterozygote (HT) genotypes and 8.3% homozygote (HM) genotypes in the patients, and 45.2% HT genotypes and 15.4% HM genotypes in the controls. For the FVII-401 G/T polymorphism, there were 37.5% HT genotypes and 3.1% HM genotypes in the patients, and 32.7% HT genotypes and 4.8% HM genotypes in the controls. The polymorphism TF+5466 A/G was not found in any of the samples analyzed. For the ACE-287 I/D polymorphism, there were 43 (40.6%) HT genotypes and 63 (59.4%) HM genotypes in the controls and 28 (45.2%) HT genotypes and 34 (54.8%) HM genotypes in the patients. No significant difference was observed by comparing patients and controls. In this study, no association was found between the presence of the evaluated polymorphisms and the occurrence of thrombotic events.

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ACE-I/ARB Therapy prior to Contrast Exposure: What Should the Clinician Do?

Cited by 19 publications

References 31 publications

Suspected adverse reactions to contrast media in Campania Region (Italy): results from 14 years of post-marketing surveillance

Suspected adverse reactions to contrast media in Campania Region (Italy): results from 14 years of post-marketing surveillance

Contrast-induced Acute Kidney Injury: A Contemporary Review

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

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