Contrast-Induced Acute Kidney Injury(CIAKI) was defined as an absolute increase in serum creatinine of more than or equal to 0.3mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline) within 48 hours of intravascular contrast administration in the absence of any alternative causes, or a reduction in urine output documented oliguria of less than 0.5 ml/kg per hour for more than six hours. It is the common cause of new hospital-acquired renal insufficiency. The occurrence of CIAKI may be influenced by pre-existing renal insufficiency, diabetic nephropathy, dehydration, congestive heart failure, concurrent administration of nephrotoxic drugs, or the dose and type of contrast media used. Previous studies have shown the independent effectiveness of several agents in preventing CIAKI. Even now, hydration is crucial for preventing CIAKI. Since CIAKI is presumed to be caused by free radical generation, N-Acetylcysteine, which is a potent free radical scavenger, is shown to be effective in preventing nephropathy. At the same time, because free radical formation is promoted by an acidic environment, bicarbonate, which alkalinizes renal tubular fluid, has been shown to reduce renal involvement. These days, some studies have shown that hydration with sodium bicarbonate plus N-Acetylcysteine was effective and safe in the prevention of CIAKI. In these studies, bicarbonate was used for both alkalinizing renal tubular fluid and hydration. However, if we want to do hydration, we can use saline and if we want to alkalinize renal tubular fluid, we might use bicarbonate by bolus injection. Actually, bicarbonate for hydration is prepared at sterile preparation room in a hospital, which is very cumbersome procedure and increase in cost. This is one of the reasons that bicarbonate for hydration use does not become common with wide clinical application. In past issues, though it differs depending on the level of the renal dysfunction, the probability of CIAKI was 8-33% when hydration was administered, 5-15% when hydration and N-Acetylcysteine were administered, and 1.8-1.9% when bicarbonate and N-Acetylcysteine were administered. Thus, we can hypothesize the combination of N-Acetylcysteine and bicarbonate will play a complementary role in preventing contrast-induced nephropathy. This is the rational for this study.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
NONE
Enrollment
458
All patients receive N-Acetylcysteine(NAC) and sodium chloride. NAC is given orally at a dose of 700mg twice daily, on the day before and on the day of administration of the contrast media, for a total of two days. 154mEq/L of sodium chloride is given intravenously. The initial intravenous bolus is 3ml/kg per hour for 1 hour immediately before contrast injection. And then, patients receive the same fluid at 1ml/kg per hour during the contrast exposure and for 6 hours after the procedure. In addition, intervention arms receive sodium bicarbonate.1000mEq/L of sodium bicarbonate is given intravenously twice at a dose of 40ml immediately before the contrast exposure and immediately after the procedure.
Sapporo Higashi Tokushukai Hospital
Sapporo, Hokkaido, Japan
Development of contrast-induced acute kidney injury
Contrast-Induced Acute Kidney Injury(CIAKI) was defined as an absolute increase in serum creatinine of more than or equal to 0.3mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline) within 48 hours of intravascular contrast administration in the absence of any alternative causes, or a reduction in urine output documented oliguria of less than 0.5 ml/kg per hour for more than six hours.
Time frame: within 48 hours
Requirement of dialysis
Time frame: 6 months
Requirement of hospitalization and death
Time frame: 6 months
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