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Published on: April 12, 2014
Ascorbic acid prevents contrast-mediated nephropathy in patients with renal dysfunction undergoing coronary
Konstantinos Spargias1, Elias Alexopoulos, Stamatis Kyrzopoulos
1Department of Cardiology, Onassis Cardiac Surgery Centre, 356 Syngrou Ave, 176 74, Athens, Greece. spargias@ocsc.gr
Insights
Oral ascorbic acid (vitamin C) may prevent kidney damage in patients undergoing coronary procedures. This antioxidant reduced the incidence of contrast-mediated nephropathy in a randomized trial, suggesting a protective effect against contrast-induced kidney injury.
Area of Science:
- Nephrology
- Cardiology
- Pharmacology
Background:
- Contrast agents can induce renal dysfunction via reactive oxygen species.
- Acetylcysteine has shown potential in preventing contrast-induced nephropathy, but other antioxidants remain uninvestigated.
Purpose of the Study:
- To evaluate the efficacy of ascorbic acid as a prophylactic agent against contrast-mediated nephropathy in patients undergoing coronary angiography or intervention.
Main Methods:
- A randomized, double-blind, placebo-controlled trial involving 231 high-risk patients (serum creatinine > or =1.2 mg/dL).
- Patients received either oral ascorbic acid (3g pre-procedure, 2g post-procedure) or a placebo.
- Contrast-mediated nephropathy was defined as an increase in serum creatinine > or =0.5 mg/dL or > or =25% within 2-5 days post-procedure.
Main Results:
- Contrast-mediated nephropathy occurred in 9% of patients receiving ascorbic acid versus 20% in the placebo group (OR, 0.38; P=0.02).
- The mean increase in serum creatinine was significantly greater in the placebo group compared to the ascorbic acid group (P=0.049).
Conclusions:
- Prophylactic oral ascorbic acid administration may offer protection against contrast-mediated nephropathy in high-risk patients undergoing coronary procedures.
- Ascorbic acid represents a potential therapeutic strategy to mitigate contrast-induced kidney injury.
Background:
Contrast agents can cause a reduction in renal function that may be due to the generation of reactive oxygen species. Conflicting evidence suggests that administration of the antioxidant acetylcysteine prevents this renal impairment. The action of other antioxidant agents has not been investigated.
Methods And Results:
We conducted a randomized, double-blind, placebo-controlled trial of ascorbic acid in 231 patients with a serum creatinine concentration > or =1.2 mg/dL who underwent coronary angiography and/or intervention. Ascorbic acid, 3 g at least 2 hours before the procedure and 2 g in the night and the morning after the procedure, or placebo was administered orally. Contrast-mediated nephropathy was defined by an absolute increase of serum creatinine > or =0.5 mg/dL or a relative increase of > or =25% measured 2 to 5 days after the procedure. Contrast-mediated nephropathy occurred in 11 of the 118 patients (9%) in the ascorbic acid group and in 23 of the 113 patients (20%) in the placebo group (odds ratio [OR], 0.38; 95% confidence interval [CI], 0.17 to 0.85; P=0.02). The mean serum creatinine concentration increased significantly in the placebo group (from 1.36+/-0.50 to 1.50+/-0.54 mg/dL, P<0.001) and nonsignificantly in the ascorbic acid group (from 1.46+/-0.52 to 1.52+/-0.64 mg/dL, P=0.07). The mean increase in serum creatinine concentration was greater in the placebo group than in the ascorbic acid group (difference of 0.09 mg/dL; 95% CI, 0.00 to 0.17; P=0.049).
Conclusions:
Prophylactic oral administration of ascorbic acid may protect against contrast-mediated nephropathy in high-risk patients undergoing a coronary procedure.
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