Acute hyperglycemia exacerbates ischemic injury of the brain and heart (1,2). Renal contrast agents are nephrotoxic, largely due to acute ischemia secondary to renal artery vasoconstriction (3). Historically, diabetic patients have been identified as a high-risk group for the development of contrast-induced nephropathy following cardiac catheterization; however, the mechanism for this increased risk is unclear (4). The purpose of this study was to determine whether acute hyperglycemia is an independent risk factor for the development of contrast-induced nephropathy after cardiac catheterization procedures.
A prospective, observational study was performed on all patients with diabetes (insulin dependent and independent) or any patient with a baseline serum creatinine ≥1.2 mg/dl receiving a cardiac catheterization procedures in a university-affiliated cardiac catheterization facility between June 2001 and January 2002. Patients with a diagnosis of acute renal failure or patients on dialysis were excluded. Patients were divided into two groups, hyperglycemic (AHG) (serum glucose ≥150 mg/dl) and nonhyperglycemic (NHG) (serum glucose <150 mg/dl), at the time of cardiac catheterization procedures. Contrast-induced nephropathy was defined as an increase in serum creatinine ≥0.3 mg/dl or >25% above the patient’s baseline, determined 3–5 days following cardiac catheterization procedures.
The mean age, baseline creatinine, presence or absence of diabetes, hydration status, type and dose of contrast agent received, and use of specific medications, including acetylcysteine, were not different between groups. The percentage of inpatients was greater in the AHG group (74%) than in the NHG (26%), P = 0.049. Ventricular function, as measured by left ventricular end-diastolic pressure, was the same between groups (AHG = 17 ± 10 mmHg vs. NHG = 13 ± 3 mmHg, P = 0.21), and left ventricular ejection fraction was significantly lower in the AHG group (AHG = 45 ± 13% vs. NHG = 59 ± 14%, P = 0.023). A total of 38 patients were studied, including 33 diabetic subjects (87%). One-half of the study group (19 patients) was found to have hyperglycemia at the time of their cardiac catheterization procedure. Mean serum glucose was 217 ± 78 mg/dl for the AHG group vs. 124 ± 15 mg/dl for the NHG group, P < 0.001. The incidence of contrast-induced nephropathy for the entire study population was 24% (9 of 38). The incidence of contrast-induced nephropathy in the AHG group was 42% (8 of 19) and was significantly greater than that for the NHG group, 5.3% (1 of 19), P = 0.01.
Acute hyperglycemia is a potential independent risk factor for the development of contrast-induced nephropathy in diabetic patients undergoing cardiac catheterization procedures. The glucose molecule has been shown to be a potential cytotoxin in the context of hyperglycemia (5). Acute hyperglycemia in patients with or without diabetes can detract from clinical outcomes in cardiovascular disease (1). The mechanism by which acute hyperglycemia worsens ischemic myocardial injury is currently under study. Conceivably, hyperglycemia may exacerbate acute renal ischemia associated with administration of radiographic contrast agents. The observational design of this study limits the relationship between acute hyperglycemia and contrast-induced nephropathy to that of a temporal association and does not address causality. Confounding variables, such as the slightly worse left ventricular ejection fraction in the AHG group, may have contributed to the development of contrast-induced nephropathy; however, the hyperglycemia in the AHG group may have contributed to poorer ventricular function. The relationship between acute hyperglycemia and contrast-induced nephropathy reported here will require a randomized controlled clinical trial for definitive characterization. This report suggests that a temporal association exists between acute hyperglycemia and contrast-induced nephropathy at the time of cardiac catheterization procedures in diabetic patients with mild renal dysfunction, and this topic bears further study.
