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 PS210. The Potential for Ascorbic Acid Mediated Nephroprotection in an Animal Model of Contrast-induced Nephropathy Following Endovascular Aneurysm Repair

​Katie E. Rollins1, Ayesha Noorani1, Lucie Janeckova2, Meryl Griffiths3, Matthew Baker2, Jonathan Boyle1
1Department of Vascular Surgery, Addenbrookes Hospital, Cambridge, United Kingdom; 2Antitope Ltd., Babraham Research Campus, United Kingdom; 3Addenbrookes Hospital  ̶ Department of Histopathology, Cambridge, United Kingdom.

OBJECTIVES: The nephroprotective effect of ascorbic acid in humans receiving intravenous contrast in percutaneous coronary interventions is beginning to be established. Currently there is no data from either clinical or in vivo models assessing the potential of ascorbic acid as a nephroprotective agent in patients undergoing Endovascular Aneurysm Repair.
We used an in vivo murine model to evaluate the potential therapeutic effect and appropriate dosage of vitamin C to prevent contrast induced nephropathy (CIN).

METHODS: A total of 24 mice were divided into 4 groups, mice from all groups (except the negative control) received Omnipaque and were then treated with; low or high dose ascorbic acid or saline positive and negative controls. Urine was collected and pooled from each group before and after the various treatments then centrifuged and analyzed for NGAL (neutrophil gelatine associated lipoprotein). At the end of the study kidneys from each mouse were explanted and frozen. One kidney per mouse was analyzed by histopathology and immunohistochemical staining for hematoxylin-eosin (HE), caspase-3, NGAL and TUNEL (transferase mediated dUTP nick-end labelling). The remaining kidney was lysed and analyzed for expression of NGAL by ELISA.

RESULTS: Kidney lysate NGAL ELISA analysis demonstrated a 50% reduction in renal damage in animals receiving low dose following contrast administration, although this degree of protection was not observed in the high dose group. There was no significant difference in the degree of renal injury seen between groups by HE staining, however initial immunohistochemistry for markers of early apoptosis showed a decrease in caspase-3 expression in both low and high dose ascorbic acid groups compared to the positive control.

CONCLUSIONS: Our mouse model suggests that one mechanism for acute renal injury induced by contrast media may involve caspase-dependent apoptosis, and that ascorbic acid administration can prevent CIN. Further work is suggested in human subjects on this topic.

AUTHOR DISCLOSURES: M. Baker, Nothing to disclose; J. Boyle, Nothing to disclose; M. Griffiths, Nothing to disclose; L. Janeckova, Nothing to disclose; A. Noorani, Nothing to disclose; K. E. Rollins, Nothing to disclose.

Posted April 2012

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