Clinical and experimental evidence for prevention of acute renal failure induced by radiographic contrast media.
Acute renal failure still occurs as a complication after radiographic examination using iodinated radiocontrast medium. The incidence rate of radiocontrast medium-induced nephropathy (radiocontrast nephropathy) is low (2 - 3%) in general. However, the rate is remarkably elevated in patients with pre-existing renal insufficiency. Radiocontrast nephropathy is associated with increased morbidity and mortality, particularly in patients with percutaneous coronary interventions. Although the reduction in renal blood flow and direct toxic action on renal tubular cells are considered to be involved, little is known about the etiology of radiocontrast nephropathy. A number of agents that improve renal circulation have been clinically tested for prevention of radiocontrast nephropathy, but none of them has succeeded. Protection of renal tubular cells against oxidative stress is another approach to avoid radiocontrast nephropathy. Prophylactic effects of antioxidants such as N-acetylcysteine and ascorbic acid have been reported by several investigators, although the effectiveness of these compounds is still a matter of debate. At present, hydration is regarded as the only effective, though incomplete, prophylactic regimen for radiocontrast nephropathy. Recently, we have shown that caspase-dependent apoptosis is an important factor in the pathogenesis of radiocontrast nephropathy and clarified cellular mechanisms underlying the radiocontrast media-induced apoptosis. This review summarizes clinical and experimental evidence for the etiology and prevention of radiocontrast nephropathy.
Itoh
Yoshinori
Y
Department of Pharmacy, Kyushu University Hospital, Fukuoka, Japan. yositou@st.hosp.kyushu-u.ac.jp
Yano
Takahisa
T
Sendo
Toshiaki
T
Oishi
Ryozo
R
D000111:Acetylcysteine / Q000494:pharmacology; D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000503:physiopathology / Q000517:prevention & control*; D000241:Adenosine / Q000037:antagonists & inhibitors; D000527:Alprostadil / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001205:Ascorbic Acid / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000494:pharmacology; D003287:Contrast Media / Q000633:toxicity*; D004232:Diuretics / Q000494:pharmacology; D016232:Endothelins / Q000037:antagonists & inhibitors; D011464:Epoprostenol / Q000031:analogs & derivatives / Q000494:pharmacology; D018818:Fenoldopam / Q000494:pharmacology; D005440:Fluid Therapy; D017583:Hemodiafiltration; D006440:Hemofiltration; D006801:Humans; D007457:Iodine Radioisotopes; D007684:Kidney Tubules / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008954:Models, Biological; D006435:Renal Dialysis; D012307:Risk Factors
D003287:Contrast Media; D004232:Diuretics; D016232:Endothelins; D007457:Iodine Radioisotopes; C048081:beraprost; D009320:Atrial Natriuretic Factor; D011464:Epoprostenol; D000527:Alprostadil; D018818:Fenoldopam; D000241:Adenosine; D001205:Ascorbic Acid; D000111:Acetylcysteine