Fenoldopam for the prevention of contrast-induced nephropathy (CIN)—do we need more trials? A meta-analysis

Naeem, Muhammad; McEnteggart, Gregory E.; Murphy, Timothy P.; Prince, Ethan A.; Ahn, Sun Ho; Soares, Gregory M.

doi:10.1016/j.clinimag.2015.02.003

Cited by 16 publications

(9 citation statements)

References 26 publications

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“…Em metanálise recente, fenoldopam intravenoso não foi superior à salina ou N-acetilcisteína. 20 Rosuvastatina e atorvastatina são drogas promissoras que se mostraram eficientes em prevenir NIC em metanálise baseada em estudos clínicos randomizados. 21 Em nosso estudo, a presença de NIC não se associou nem à mortalidade nem a adventos adversos no curto prazo (72 horas).…”

Section: Resultsunclassified

Contrast-induced nephropathy after primary angioplasty for acute myocardial infarction

Santos¹,

Neto²,

Arcanjo³

et al. 2015

Jornal Brasileiro De Nefrologia

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Nefropatia induzida por contraste após angioplastia primária no infarto agudo do miocárdio Contrast-induced nephropathy after primary angioplasty for acute myocardial infarctionIntrodução: A prevenção da nefropatia induzida por contraste (NIC) é difícil nas situações de emergência, tornando essenciais estudos sobre NIC em pacientes submetidos à angioplastia de urgência. Objetivo: Determinar a incidência e fatores associados à NIC em pacientes com infarto agudo do miocárdio (IAM) submetidos à angioplastia nas primeiras 12 horas após início dos sintomas. Métodos: Foram estudados 201 casos consecutivos de IAM com supradesnivelamento do segmento ST com menos de 12 horas de evolução. Todos os pacientes foram submetidos ao mesmo protocolo de angioplastia. A NIC foi definida como elevação absoluta da creatinina de pelo menos 0,5 mg/dL e/ou aumento relativo da creatinina de 25% em relação ao valor basal no período entre 48 e 72 horas após a administração do contraste. As variáveis que diferiram entre os pacientes com e sem NIC na análise univariada foram analisadas por regressão logística. Resultados: A amostra foi formada por 135 (67,2%) homens e 66 (32,8%) mulheres com idade média de 66,6 ± 11,7 anos. A incidência de NIC foi de 23,8%. Na análise univariada os pacientes com NIC eram mais idosos e com maior frequência de fração de ejeção do ventrículo esquerdo ≤ 40% e da classificação Killip ≥ 2. Na análise multivariada não foram encontrados preditores independentes de NIC. Conclusão: A NIC acomete ¼ dos pacientes com IAM submetidos à angioplastia sem variáveis preditoras. Esse resultado ressalta a necessidade de medidas preventivas para NIC após uso de contraste em angioplastia de urgência. ResumoPalavras-chave: angioplastia coronária com balão; infarto do miocárdio; lesão renal aguda; meios de contraste. Introduction:The prevention of contrastinduced nephropathy (CIN) is difficult in emergency situations, making it essential to study CIN in patients submitted to urgent angioplasty. Objective: To determine the incidence and associated factors to CIN in patients with myocardial infarction (MI) submitted to primary angioplasty in the first 12 hours after onset of symptoms. Methods: We studied 201 consecutive cases of MI with ST-segment elevation with less than 12 hours of evolution. All patients were submitted to the same angioplasty protocol. CIN was defined as an absolute increase of creatinine of at least 0.5 mg/ dL and/or a relative increase of creatinine of 25% in relation to baseline in a period between 48 and 72 hours after contrast administration. The variables that differed between patients with and without CIN in univariate analysis were analyzed by logistic regression. Results: The sample was formed by 135 (67.2%) men and 66 (32.8%) women, with mean age of 66.6 ± 11.7 years. The incidence of CIN was 23.8%. In univariate analysis the patients with CIN were older and had higher frequency of left ventricular ejection fraction ≤ 40% and Killip classification ≥ 2. In multivariate analysis, we did not find independe...

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Section: Resultsunclassified

Contrast-induced nephropathy after primary angioplasty for acute myocardial infarction

Santos¹,

Neto²,

Arcanjo³

et al. 2015

Jornal Brasileiro De Nefrologia

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“… Conflicting or negative evidence. Fenoldopam, 102 dopamine, 103 calcium channel blockers, 104 L-arginine, 105 furosemide without matched hydration, 106 mannitol, 107 endothelin receptor antagonists. 108 CIN, contrast-induced nephropathy; RCT, randomised controlled trial; RR, relative risk; SCr, serum creatinine.…”

Section: Novel Preventative Measuresmentioning

confidence: 99%

“… Fenoldopam, 102 dopamine, 103 calcium channel blockers, 104 L-arginine, 105 furosemide without matched …”

Section: Novel Preventative Measuresmentioning

confidence: 99%

Contrast-induced nephropathy following angiography and cardiac interventions

Rear

Bell

Hausenloy

2016

Heart

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175

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“…Although contrast enhanced X-ray is the most common indication of RCM use (Figure 1), percutaneous coronary angiography (in the USA: 1.4–1.3 million/year between 1997 and 2010 [12]) is the primary cause of CI-AKI [4, 5]. Although hydration is considered to be the most effective preventive measure [13, 14], CI-AKI may develop in 3–25% of patients despite appropriate hydration [15] and further preventive measures such as antioxidants [2, 16] or statins [4, 17]. However, the affected patient population is much larger considering subclinical cases [9].…”

Section: Introductionmentioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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Contrast-induced acute kidney injury (CI-AKI) can occur in 3–25% of patients receiving radiocontrast material (RCM) despite appropriate preventive measures. Often patients with an atherosclerotic vasculature have to receive large doses of RCM. Thus, animal studies to uncover the exact pathomechanism of CI-AKI are needed. Sensitive and specific histologic end-points are lacking; thus in the present review we summarize the histologic appearance of different rodent models of CI-AKI. Single injection of RCM causes overt renal damage only in rabbits. Rats and mice need an additional insult to the kidney to establish a clinically manifest CI-AKI. In this review we demonstrate that the concentrating ability of the kidney may be responsible for species differences in sensitivity to CI-AKI. The most commonly held theory about the pathomechanism of CI-AKI is tubular cell injury due to medullary hypoxia. Thus, the most common additional insult in rats and mice is some kind of ischemia. The histologic appearance is tubular epithelial cell (TEC) damage; however severe TEC damage is only seen if RCM is combined by additional ischemia. TEC vacuolization is the first sign of CI-AKI, as it is a consequence of RCM pinocytosis and lysosomal fusion; however it is not sensitive as it does not correlate with renal function and is not specific as other forms of TEC damage also cause vacuolization. In conclusion, histopathology alone is insufficient and functional parameters and molecular biomarkers are needed to closely monitor CI-AKI in rodent experiments.

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Fenoldopam for the prevention of contrast-induced nephropathy (CIN)—do we need more trials? A meta-analysis

Cited by 16 publications

References 26 publications

Contrast-induced nephropathy after primary angioplasty for acute myocardial infarction

Contrast-induced nephropathy after primary angioplasty for acute myocardial infarction

Contrast-induced nephropathy following angiography and cardiac interventions

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

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