***TASK*** the task is to summarize an input biomedical literature in six sentences 
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    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: BACKGROUND Low-dose dopamine is commonly administered to critically ill patients in the belief that it reduces the risk of renal failure by increasing renal blood flow . However , these effects have not been established in a large r and omised controlled trial , and use of dopamine remains controversial . We have done a multicentre , r and omised , double-blind , placebo-controlled study of low-dose dopamine in patients with at least two criteria for the systemic inflammatory response syndrome and clinical evidence of early renal dysfunction ( oliguria or increase in serum creatinine concentration ) . METHODS 328 patients admitted to 23 participating intensive-care units ( ICUs ) were r and omly assigned a continuous intravenous infusion of low-dose dopamine ( 2 microg kg(-1 ) min(-1 ) ) or placebo administered through a central venous catheter while in the ICU . The primary endpoint was the peak serum creatinine concentration during the infusion . Analyses excluded four patients with major protocol violations . FINDINGS The groups assigned dopamine ( n=161 ) and placebo ( n=163 ) were similar in terms of baseline characteristics , renal function , and duration of trial infusion . There was no difference between the dopamine and placebo groups in peak serum creatinine concentration during treatment ( 245 [ SD 144 ] vs 249 [ 147 ] micromol/L ; p=0.93 ) , in the increase from baseline to highest value during treatment ( 62 [ 107 ] vs 66 [ 108 ] micromol/L ; p=0.82 ) , or in the numbers of patients whose serum creatinine concentration exceeded 300 micromol/L ( 56 vs 56 ; p=0.92 ) or who required renal replacement therapy ( 35 vs 40 ; p=0.55 ) . Duration s of ICU stay ( 13 [ 14 ] vs 14 [ 15 ] days ; p=0.67 ) and of hospital stay ( 29 [ 27 ] vs 33 [ 39 ] days ; p=0.29 ) were also similar . There were 69 deaths in the dopamine group and 66 in the placebo group . INTERPRETATION Administration of low-dose dopamine by continuous intravenous infusion to critically ill patients at risk of renal failure does not confer clinical ly significant protection from renal dysfunction Kidney  failure after heart transplantation still remains a crucial problem , especially when cyclosporine is used for early postoperative immunosuppressive therapy . To preserve good renal function during immunosuppression with cyclosporine , urodilatin ( CDD/ANP-95 - 126 ) , the kidney-born analogue to the circulating cardiac peptide hANP ( CDD/ANP-99 - 126 ) , was given for the first time as a long-term , low-dose infusion in addition to the usual drug therapy immediately after heart transplantation . From November 1990 to January 1992 , 47 patients ( 44 men and three women ; mean age , 51 years ) were treated by a 20 ng/kg body weight/min infusion for 96 hours after heart transplantation . Renal function and hemodynamic parameters of these patients were compared with a group of 40 patients ( 34 male and six female ; mean age , 50 years ) as controls , who underwent heart transplantation from May 1990 to November 1991 . Both groups did not differ significantly with respect to age , sex , indication for heart transplantation , and preoperative renal function . With urodilatin treatment , renal function was significantly improved with lower peak plasma creatinine ( 1.83 + /- 0.1 versus 2.47 + /- 0.19 mg/dl ; p = 0.003 ) , lower peak serum urea ( 118 + /- 7 versus 178.3 + /- 10.3 mg/dl ; p = 0.0036 ) and absence of hemodialysis ( 0 % versus 10 % ; p = 0.026 ) . Additionally , adequate diuresis was maintained although furosemide was reduced by more than 50 % ( p = 0.005 ) on each day of urodilatin treatment . Mean central venous pressure was significantly lower ( -2 mm Hg ; p = 0.02 ) during application of urodilatin , despite reduction of vasodilator therapy with nitroglycerin by about 50 % ( p = 0.02 ) . Because of the significantly improved renal function and beneficial hemodynamic effects , the recommendation is therefore to introduce urodilatin in the postoperative treatment protocol after heart transplantation BACKGROUND The majority of patients undergoing surgical treatment for ST-elevation myocardial infa rct ion receive antifibrinolytic therapy to limit blood loss . This approach appears counterintuitive to the accepted medical treatment of the same condition -- namely , fibrinolysis to limit thrombosis . Despite this concern , no independent , large-scale safety assessment has been undertaken . METHODS In this observational study involving 4374 patients undergoing revascularization , we prospect ively assessed three agents ( aprotinin [ 1295 patients ] , aminocaproic acid [ 883 ] , and tranexamic acid [ 822 ] ) as compared with no agent ( 1374 patients ) with regard to serious outcomes by propensity and multivariable methods . ( Although aprotinin is a serine protease inhibitor , here we use the term antifibrinolytic therapy to include all three agents . ) RESULTS In propensity-adjusted , multivariable logistic regression ( C-index , 0.72 ) , use of aprotinin was associated with a doubling in the risk of renal failure requiring dialysis among patients undergoing complex coronary-artery surgery ( odds ratio , 2.59 ; 95 percent confidence interval , 1.36 to 4.95 ) or primary surgery ( odds ratio , 2.34 ; 95 percent confidence interval , 1.27 to 4.31 ) . Similarly , use of aprotinin in the latter group was associated with a 55 percent increase in the risk of myocardial infa rct ion or heart failure ( P<0.001 ) and a 181 percent increase in the risk of stroke or encephalopathy ( P=0.001 ) . Neither aminocaproic acid nor tranexamic acid was associated with an increased risk of renal , cardiac , or cerebral events . Adjustment according to propensity score for the use of any one of the three agents as compared with no agent yielded nearly identical findings . All the agents reduced blood loss . CONCLUSIONS The association between aprotinin and serious end-organ damage indicates that continued use is not prudent . In contrast , the less expensive generic medications aminocaproic acid and tranexamic acid are safe alternatives OBJECTIVE To evaluate the influence of the alpha2-adrenergic receptor agonist clonidine on creatinine clearance as a measure of renal function . DESIGN Prospect i ve , double-blind , r and omized , placebo-controlled clinical trial . SETTING University hospital . PATIENTS Patients undergoing coronary artery bypass graft surgery ( n = 48 ) with normal risk . INTERVENTIONS Administration of clonidine ( 4 micrograms/kg iv ) ) or placebo 1 hr before induction of anesthesia . MEASUREMENTS AND MAIN RESULTS Induction and maintenance of anesthesia ( etomi date , midazolam , and fentanyl ) and cardiopulmonary bypass technique ( nonpulsatile , normothermic , intermittent cold blood cardioplegia ) were st and ardized in all patients . The night before surgery and the first and third night after surgery , creatinine clearance was calculated from a 12-hr urine collection period . Venous blood sample s for determination of plasma antidiuretic hormone ( ADH ) concentrations were taken the evening before surgery , immediately before induction of anesthesia and the evening after surgery ( n = 16 ) . Arterial catecholamine plasma concentrations were determined ( high-performance liquid chromatography ) before induction , 15 mins after induction of anesthesia , immediately after sternotomy , before initiation of cardiopulmonary bypass , as well as 5 , 15 , and 30 mins after initiation of cardiopulmonary bypass ( n = 16 ) . The total amount of anesthetics , infusions , transfusions , diuresis , and blood loss was not different between the groups . Creatinine clearance decreased over the first postoperative night from 98 + /- 18 ( preoperatively ) to 68 + /- 19 mL/min ( p < .05 ) in placebo-treated patients . Creatinine clearance remained unchanged in clonidine-treated patients ( 90 + /- 19 [ preoperatively ] to 92 + /- 17 mL/min ) . There was a significant difference in creatinine clearance between the groups during the first postoperative night ( p < .05 ; Mann-Whitney U test ) . In the third postoperative night , mean creatinine clearance of both groups was not different ( 75 + /- 31 vs. 86 + /- 28 mL/min ) . ADH concentrations were not different between the groups at any time , while plasma catecholamine concentrations were always significantly lower in clonidine-treated patients . CONCLUSIONS Preoperative treatment with clonidine ( 4 microgram/kilogram ) prevents the deterioration of renal function after cardiac surgery . This effect might be due to clonidine-induced reduction in the sympathetic nervous system response to coronary artery bypass graft surgery BACKGROUND In cardiac surgery with cardiopulmonary bypass ( CPB ) , corticosteroids are administered to attenuate the physiological changes caused by the systemic inflammatory response . The effects of corticosteroids on CPB-associated renal damage have not been documented . The purpose of this study was to evaluate the effects of dexamethasone on perioperative renal dysfunction in patients undergoing cardiac surgery with CPB . METHODS Renal damage was prospect ively studied in 20 patients without concomitant morbidity undergoing coronary artery surgery with CPB . Patients were r and omized in a double-blind fashion to receive dexamethasone or placebo .  Markers of glomerular function ( creatinine clearance ) and damage ( microalbuminuria ) , and markers of tubular function ( fractional excretion of sodium and free water clearance ) and damage ( N-acetyl-beta-D glucosaminidase ( NAG ) ) were evaluated in addition to plasma and urinary glucose levels . Plasma and urinary specimens were obtained at the following time periods : ( 1 ) baseline , during the 12 h before surgery ; ( 2 ) skin incision before heparinization ; ( 3 ) from heparinization until the end of CPB ; ( 4 ) during the 2 h following weaning from CPB ; ( 5 ) in the intensive care unit from 2 to 6 h after weaning of CBP ; ( 6 ) and from 36 to 60 h after weaning of CPB . RESULTS CPB was associated with an increase in markers in the placebo group , which returned to baseline during the second postoperative day , demonstrating a transient impairment of glomerular and tubular renal function . Similar patterns were observed in patients treated with dexamethasone . While postoperative glycosuria was significantly higher in the dexamethasone-treated group , no other differences between groups were observed . CONCLUSION Dexamethasone administration before CPB has no protective effect on perioperative renal dysfunction in low-risk cardiac surgical patients OBJECTIVE The purpose of this study was to evaluate the renoprotective effects of fenoldopam in patients at high risk of postoperative acute kidney injury undergoing elective cardiac surgery requiring cardiopulmonary bypass . DESIGN A double-blind r and omized clinical trial . SETTING Hospital . PARTICIPANTS One hundred ninety-three patients . INTERVENTIONS Patients undergoing cardiac surgery were r and omly assigned to receive a continuous infusion of fenoldopam , 0.1 microg/kg/min ( 95 patients ) , or placebo ( 98 patients ) for 24 hours . Patients were included if at least 1 of the following risk factors was present : preoperative serum creatinine > or = 1.5 mg/dL , age > 70 years , diabetes mellitus , or prior cardiac surgery .  Serum creatinine and urinary output were measured at baseline ( T1 ) , 24 hours ( T2 ) , and 48 hours after surgery ( T3 ) . Acute kidney injury was defined as a postoperative serum creatinine level of > or = 2 mg/dL with an increase in serum creatinine level of 0.7 mg/dL or greater from preoperative to maximum postoperative values . MEASUREMENTS AND MAIN RESULTS Acute kidney injury developed in 12 of 95 ( 12.6 % ) patients receiving fenoldopam and in 27 of 98 ( 27.6 % ) patients receiving placebo ( p = 0.02 ) , whereas renal replacement therapy was started in 0 of 95 and 8 of 98 ( 8.2 % ) patients , respectively ( p = 0.004 ) . Serum creatinine was similar at baseline ( 1.8 + /- 0.4 mg/dL v 1.9 + /- 0.3 mg/dL ) in the fenoldopam and placebo groups but differed significantly ( p < 0. 
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Conclusion : Cette analyse n’a pas démontré que le traitement avec la NAC a été associé à une protection rénale clinique pendant la chirurgie cardiaque , ni d’amélioration dans les autres devenirs cliniques