| Objectives: Contrast-induced nephropathy (CIN) is defined as new-onset or an exacerbation renal dysfunction after contrast medium administration in the absence of other causes. The condition is marked by an increase of >25% or an absolute increase of >0.5mg/dL in baseline serum creatinine. Symptoms occur 24–48 hours after contrast medium exposure, with creatinine peaking 3-5days later and normalizing within 7 days in most cases. The exact pathogenesis of CIN is still unclear. Several injury pathways have been proposed. The main mechanism by which contrast medium causes nephropathy are renal medulla ischemia, direct toxicity to tubular epithelial cells and activate oxyradical. Contrast medium induces initial transient renal vasodilatation followed by a sunstained vasoconstriction. The changes of renal hemodynamics lead medulla ischemic and anoxyaemia. Subsequent reperfusion injury may increase free radical formation and create oxidative stress. Besides the high viscosity and osmolality of contrast medium lead renal blood flow low and vessel embolism which aggravate the injury of renal. Although contrast-induced nephropathy is usually self-limited, it may cause permanent renal injury and even lead to long-term dialysis in patients with the risk factors of CIN. Cardiologists have pay much attention to prevent CIN.Strategies to prevent CIN including prophylactic hydration, administration of N-acetylcysteine, bicarbonate and so on, were proposed to be effective. But, there are con?icted results except hydration and control risk factors. Furosemide, a loop diuretic, is believed to act by inhibiting sodium reabsorption and decreasing the metabolic demand (oxygen consumption) of the renal tubular cells in the medullary portion of the kidney. Furosemide also transiently increases global renal plasma ?ow without increasing glomerular filtration rate. At relatively high concentrations, furosemide has prostaglandin-independent relaxing effects on renal vasculature. Lowing renal vascular resistance and increasing renal blood could relieve renal injury. For this reason, the scholar assumed to use furosemide reducing renal injury, but the result was not satisfied. Recently, it is found that hydration plays a very important role for preventing CIN by the study. Using furosemide without adequate hydration or with high dose could lead renal medullary hypoperfusion which was the main reason for treatment failure. The purpose of present study was to observe the effects of low dose furosemide on preventing contrast-induced nephropathy at the basic of adequate hydration.Methods: 759 patients who were performed coronary angiography and (or) percutaneous coronary intervention (PCI)in catheterization room of cardiology department were enrolled between September 2009 and February 2011. There were 545 males and 214 females, with a mean age of 58.00(14.00) years and the average weight was 71.00(13.00) Kg. Ultravist (370) was administrated for all the patients, with a mean dose of 60.00(40.00) ml. All patients were randomly assigned to furosemide group or control group. Serum creatinine concentration was measured before angiography. And according to the Modification of Diet in Renal Disease (MDRD) to estimate glomerular filtration rate(GFR). Creatinine clearance rate was estimated according to the Cockcroft-Gault formula. GFR (ml/min/1.73m2) = 186 x (Serum creatinine [mg/dL])-1.154 x (Age)-0.203 x (0.742 if female). Creatinine clearance rate (ml/min) = (140-age) x Body Weight [kg] x (0.85 if female) / (72×Scr). All the patients received 0.9 percent saline intravenously at a rate of 1 ml per kilogram of body weight per hour beginning 4 hours before the scheduled angiography. The furosemide group was given furosemide 20mg immediately after angiography, control group given nothing. All the patients continued to receive 0.9 percent saline intravenously at the same rate for 20 hours after angiography and were encouraged to drink if thirsty. Serum creatinine was measured 48 hours later. Glomerular filtration rate and Serum creatinine clearance were estimated. Contrast-induced nephropathy was defined as anincrease of >25% or an absolute increase of >0.5mg/dL in baseline serum creatinine within 48 hours after the adminstration of contrast medium. Categorical Continuous variables were expressed as the mean value±standard deviation (SD) or median(inter-quartile range); categorical variables were summarized as percentages. The comparison of serum creatinine concentration, creatinine clearance rate,GFR between two groups were evaluated by repeated measures engineered variance analysis. Paired t test or rank-sum test was performed to compare the marks in every group at different time. The incidence of CIN was compared by the chi-square test. The risk factors of CIN were selected by logistic regression analysis. A P value of <0.05 was considered statistically significant.Results: The baseline characteristics such as age, body weight body height and gender were not significantly different between the two groups (P>0.05). The patients who were administrated with the drug of statins in control group was more than that of furosemide group (P<0.05). The serum creatinine concentration were higher and creatinine clearance rate,GFR were lower 48 hours later after coronary angiography both in the control group (P<0.05) and furosemide group (P>0.05). The changes in control group were more significantly than that of furosemide group (P<0.05); the incidence of CIN in the control group was higher than that of furosemide group (14.24% VS 8.06%, P<0.05). The results of logistic analysis indicated that furosemide was benefit for preventing CIN and female, acute myocardial infarction,receiving the drug of ACEI are the risk factors of CIN.Conclusions: At basic of adequate hydration, low dose furosemide could reduce the injury of renal induced by contrast medium and decrease the incidence of CIN.
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