Hans S S, Hans B A, Dhillon R, Dmuchowski C, Glover J
Department of Surgery, Macomb Hospital Center, Warren, Michigan, USA.
Am Surg. 1998 May;64(5):432-6.
Contrast media-induced nephropathy is one of the leading causes of hospital-acquired renal failure, occurring most frequently in patients with pre-existing renal insufficiency. We prospectively studied 55 patients with chronic renal insufficiency (serum creatinine concentration 1.4 to 3.5 mg/dl) who underwent abdominal aortography and arteriography of the lower extremities. The patients were randomized into two groups. Group 1, 28 patients, received dopamine 2.5 mcg/kg beginning 1 hour before arteriography and continuing for 12 hours. Group 2 received an equal volume of saline for the same period of time. Serum creatinine and 12-hour creatinine clearance were measured before arteriography and for 4 consecutive days afterward. Acute contrast-induced decrease in renal function was defined as increase in the baseline serum creatinine concentration > or = 0.5 mg/dl. On day 1 postarteriography the serum creatinine increased from baseline .193 mg/dl for controls while the dopamine group decreased slightly from baseline .018 mg/dl (p = 0.002). Excepting day 1 postarteriography, there was no statistical difference between groups, and serum levels for both groups increased linearly from baseline across time (dopamine p = 0.028, control p = 0.025). In patients with pre-arteriography baseline serum levels greater than or equal to 2.0 mg/dl, however, the increase in serum creatinine from baseline levels was consistently and significantly greater in the control group through the fourth day (0.012 < or = p < or = 0.049). Creatinine clearance did not change significantly from baseline after arteriography in the dopamine group (baseline versus days 1 through 4, 0.238 < or = p < or = 0.968); however, the control group showed a significant linear decrease in creatinine clearance from baseline through the fourth day after arteriography (p = 0.016). Dopamine infusion prevented a rise in serum creatinine 24 hours after angiography in patients with pre-existing renal insufficiency, and protected against contrast-induced decrease in renal function in patients whose baseline serum creatinine was > or = 2.0 mg/dl.
造影剂肾病是医院获得性肾衰竭的主要原因之一,最常发生于已有肾功能不全的患者。我们前瞻性地研究了55例慢性肾功能不全(血清肌酐浓度1.4至3.5mg/dl)且接受腹部主动脉造影和下肢动脉造影的患者。患者被随机分为两组。第1组28例患者,在动脉造影前1小时开始接受多巴胺2.5mcg/kg,并持续12小时。第2组在相同时间段内接受等量的生理盐水。在动脉造影前及之后连续4天测量血清肌酐和12小时肌酐清除率。急性造影剂所致肾功能下降定义为基线血清肌酐浓度升高≥0.5mg/dl。动脉造影后第1天,对照组血清肌酐较基线升高0.193mg/dl,而多巴胺组较基线略有下降0.018mg/dl(p = 0.002)。除动脉造影后第1天外,两组间无统计学差异,且两组血清水平均随时间从基线呈线性升高(多巴胺组p = 0.028,对照组p = 0.025)。然而,在动脉造影前基线血清水平≥2.0mg/dl的患者中,至第4天对照组血清肌酐较基线水平的升高始终且显著更大(0.012≤p≤0.049)。多巴胺组动脉造影后肌酐清除率与基线相比无显著变化(基线与第1至4天相比,0.238≤p≤0.968);然而,对照组在动脉造影后至第4天肌酐清除率较基线呈显著线性下降(p = 0.016)。多巴胺输注可预防已有肾功能不全患者造影后24小时血清肌酐升高,并可保护基线血清肌酐≥2.0mg/dl的患者免受造影剂所致肾功能下降的影响。