Additional Anemia Rises the Risk for Radiocontrast Agent-Induced Nephropathy in Patients with Moderate Chronic Renal Insufficiency.

Objective: Patients with diabetes and underlying renal insufficiency exhibit an increased propensitiy to develop radiocontrast agent-induced nephropathy after receiving radiocontrast agents for diagnostic and interventional procedure. In fact, radiocontrast-agent-induced nephropathy is currently a major leading cause of hospital-acquired renal failure. The underlying mechanisms for radiocontrast agent-induced nephropathy most likely involve the interplay of several factors, including vasoconstrictive forces resulting in medullary ischemia, direct effects on renal tubular cells, and damage caused by oxygen radicals. Data from experimental studies indicate that antioxidants, e.g. acetylcysteine, may prevent radiocontrast-induced nephropathy. Glutathion is an endogenous antioxidant primarily considered to be of importance in the erythrocyte antioxidant defense system function. The purpose of this study was to determine the development of radiocontrast agent-induced nephropathy in patients with moderate chronic renal insufficiency in dependence on their hemoglobin. Patients and Methods: We retrospectively studied 250 patients (age: 66.7 ± 10.1 years) with moderate chronic renal insufficiency (serum-creatinine concentration between 1.4 mg/dl (124 µmol/l) and 3.0 mg/dl (265 µmol/l)) who underwent coronary angiography with or without intervention from 1988 till 1999. Contrast-agent-induced nephropathy was defined by an increase in serum creatinine of 0.5 mg/ dL (44 µmol/l) or more than 25% compared to baseline levels within 48 to 72 hours of contrast-agent administration. First, hemoglobin and change of serum creatinine concentrations were correlated; in addition, patients were classified into two groups according to their hemoglobin (hemoglobin ≤12.0 g/dl group 1 [71 patients], hemoglobin ≥12,0 g/dl group 2 [179 patients]). Results: Hemoglobin (Hb) and change of serum creatinine concentrations (dKrea) were linear inverse correlated with a regression equation dKrea (µmol/l) = 137.2 - 8.887 x Hb, negative slope was significantly different from zero with p < 0.0001. There was no difference of serum creatinine between the two groups at baseline (173.5 ± 30.8 vs. 166.2 ± 31.1 µmol/l), in group 1 contrast-agent-induced nephropathy occurred in 39 of 71 patients (54.9%), in group 2 in 23 of 171 patients (13.5%), with a significant difference (p < 0.001) between the two groups. Also, absolute increase in serum creatinine was significantly differrent among the groups (group 1: 173.5 ± 30.8 → 222.6 ± 78.1 µmol/l; group 2: 166.2 ± 31.1 µmol/l → 173.2 ± 59.0 µmol/l; p < 0.001). Conclusions: In patients with moderate chronic renal insufficiency receiving radiocontrast agent for diagnostic and interventional procedures the presence of additional anemia rises the risk for radiocontrast agent-induced nephropathy. Further studies have to determine to what extent the primary antioxidant defense system of erythrocytes is important in this context. [ABSTRACT FROM AUTHOR]