Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

Aurelio, Andrea; Durante, Alessandro

doi:10.1159/000358042

Cited by 46 publications

(47 citation statements)

References 103 publications

(162 reference statements)

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“…In suspended rabbit tubular epithelial cells [164] or isolated proximal tubule segments [165] RCM toxicity was observed only with concomitant ischemia [18]. Furthermore, in different tubular cell cultures RCM induced mitochondrial swelling [65] and DNA fragmentation and/or apoptosis [46, 163, 166–169]. Also, in human CI-AKI patients, tubular cells were found in the urine [170].…”

Section: Further Pathological Markers Of Ci-akimentioning

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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Section: Further Pathological Markers Of Ci-akimentioning

confidence: 99%

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Kiss

Hamar

2016

BioMed Research International

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“…While the incidence of CIN related to contrast medium use in the outpatient setting is < 5%, it is higher in patients who undergo coronary angiography (10-15%) [9]. The higher incidence in this group may be associated with the high-risk profile of these patients [10]. This rate was determined as 23.3% in our study.…”

Section: Discussionmentioning

confidence: 69%

CHA2DS2-VASc score predicts contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction, who have undergone primary percutaneous coronary intervention

Çiçek¹,

Yıldırım²

2018

Kardiol Pol

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A b s t r a c t Background and aim:We aimed to investigate the predictive value of the CHA 2 DS 2 -VASc score in the development of contrast-induced nephropathy (CIN). Methods:A total of 2972 patients who had been diagnosed with ST elevation myocardial infarction (STEMI) and who had undergone primary coronary angioplasty were included in the study. The patients were divided into three groups according to the CHA 2 DS 2 -VASc score, i.e.: low risk (1 point), intermediate risk (2 points), and high risk (≥ 3 points). The groups were followed with regard to CIN development. Results:The median CHA 2 DS 2 -VASc score was significantly higher in the CIN(+) group compared to the CIN(-) group (3 vs. 2, p < 0.001). The rate of CIN was 3.32-fold higher (OR 3.32, 95% CI 1.98-5.55, p < 0.001) in the high-risk group (CHA 2 DS 2 -VASc ≥ 3) compared to the low-risk group (CHA 2 DS 2 -VASc = 1). Age (OR 1.25, 95% CI 1.14-1.36, p < 0.001), female gender (OR 1.52, 95% CI 1.23-1.89, p < 0.001), hypertension (OR 1.50, 95% CI 1.265-1.78, p < 0.001), peak creatinine kinase-MB (OR 1.15, 95% CI 1.10-1.21, p < 0.001), and the Killip score > 1 (OR 4.25, 95% CI 3.10-5.82, p < 0.001) were found to be independent predictors for CIN development. Conclusions:The CHA 2 DS 2 -VASc score is an independent and strong predictor of CIN development in patients with acute STEMI.

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“…In recent years it became possible, largely thanks to pre-clinical studies, to form a rather comprehensive view on the pathophysiology behind CIN [2,[28][29][30][31]. CIN comes about by concerted action of cytotoxic effects of CM, auto-and paracrine factors which impinge on (intra) renal blood supply and oxygenation, and alterations of rheological properties that affect tubular fluid flow and renal haemodynamics.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

2015

J Urol Nephrol

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Dehydration is a major risk for contrast media (CM) induced acute kidney injury, yet prospective studies in human patients without ample hydration are not feasible. The freely drinking rat can serve as a model for hydropenic humans.We compared the effects of two CM, iso-osmolar iodixanol and lowosmolar iopamidol, on urine flow, urine viscosity and glomerular filtration rate (GFR) in non-hydrated rats, and studied the impact of hydration by saline. In four groups of rats, either iodixanol 320 mg iodine/mL or iopamidol 370 mg iodine/mL was injected as 1.5 mL bolus into the thoracic aorta. Two groups had access to drinking water only and two groups received additional saline infusion (4 mL/hour per kg) starting 60 min before CM injection. Urine was collected (10 min sampling periods), urine viscosity measured, and GFR determined by creatinine clearance. In nonprehydrated rats, iodixanol led to a massive increase in urine viscosity and a transient 50% drop in GFR. Iopamidol had a much stronger diuretic effect than iodixanol, urine viscosity increased much less and GFR was unaffected. Saline infusion blunted the viscosity rise and transient decline in GFR caused by iodixanol. It is concluded that the choice of CM and ample hydration are important elements in the prevention of CM induced kidney injury. Low-osmolar iopamidol has a better renal safety profile than iso-osmolar iodixanol, at least in non-hydrated subjects. Hydration by saline counteracts the renal tubular concentration of CM thereby alleviating the increase in urine viscosity and the decline in GFR.

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Contrast-Induced Nephropathy in Percutaneous Coronary Interventions: Pathogenesis, Risk Factors, Outcome, Prevention and Treatment

Cited by 46 publications

References 103 publications

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

Histopathological Evaluation of Contrast-Induced Acute Kidney Injury Rodent Models

CHA2DS2-VASc score predicts contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction, who have undergone primary percutaneous coronary intervention

Comparison of the Effects of Iodixanol and Iopamidol on Urine Flow, Urine Viscosity, and Glomerular Filtration in Rats

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