Renal support in critically ill patients: Low-dose dopamine or low-dose dobutamine?

Duke, Graeme; Briedis, Juris; Weaver, Rupert A.

doi:10.1097/00003246-199422120-00006

Cited by 133 publications

(33 citation statements)

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“…6 -10 Dopamine has been reported both in experimental animals and in a variety of patient populations to enhance RBF by multiple mechanisms, including an increase in CO and local vasodilation due to stimulation of dopamine receptors in renal blood vessels. 11 For many years, a small dose of dopamine often has been used by clinicians to enhance RBF in critically ill patients 12,13 ; however, this selective effect of dopamine on the renal circulation may be eliminated or markedly attenuated by other vasoconstrictive mechanisms known to be activated in patients with HF. 14 In addition, the magnitude of its renal vasodilatory effects and site of action in patients with HF have not been clearly defined.…”

Section: Clinical Perspective P 205mentioning

confidence: 99%

Renal Vasodilatory Action of Dopamine in Patients With Heart Failure

et al. 2008

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Background— A “renal dose” of dopamine is often used to increase renal blood flow; however, data on the magnitude of effect and site of action in patients with heart failure are scarce. Methods and Results— Renal effects of intravenous dopamine (1, 2, 3, 5, and 10 μg · kg −1 · min −1 ) were evaluated in 13 patients with chronic heart failure. Renal blood flow was calculated from renal artery cross-sectional area measured with intravascular ultrasound and renal blood flow velocity-time integral measured by the intravascular Doppler technique. Cross-sectional area increased and was significantly higher than baseline (0.30±0.04 cm 2 ) at 5 μg · kg −1 · min −1 (0.36±0.05 cm 2 ) and 10 μg · kg −1 · min −1 (0.38±0.06 cm 2 ). The velocity-time integral was significantly higher than baseline (22±3 cm) at doses of 3 and 5 μg · kg −1 · min −1 (both 31±4 cm). Renal blood flow increased, whereas renal vascular resistance decreased, reaching statistical significance at 2 μg · kg −1 · min −1 through 10 μg · kg −1 · min −1 . Cardiac output gradually increased, reaching statistical significance at doses of 5 and 10 μg · kg −1 · min −1 (5.5±0.5 and 6.1±0.7 versus 4.5±5.2 L/min at baseline), but the increase in renal blood flow appeared proportionately larger than corresponding increases in cardiac output. Conclusions— Dopamine is associated with an increase in renal blood flow in patients with heart failure. This effect is due to dilation of both the large conductance and small resistance renal blood vessels. Further evaluation of the efficacy and safety of dopamine for improvement of renal function in hospitalized patients with heart failure is warranted.

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Section: Clinical Perspective P 205mentioning

confidence: 99%

Renal Vasodilatory Action of Dopamine in Patients With Heart Failure

et al. 2008

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“…In a study of 18 critically ill patients, short-term infusions of lowdose dopamine, low-dose dobutamine, and placebo were compared in a randomized, double-blind, crossover fashion. Dobutamine improved creatinine clearance without affecting diuresis, while dopamine induced diuresis without changing creatinine clearance (20). In a larger study, primarily investigating the value of atrial natriuretic peptide, patients not treated with dopamine were compared with those treated with either low-dose (3 g/kg per min) or high-dose (Ͼ3 g/kg per min) dopamine.…”

Section: Low-dose Dopaminementioning

confidence: 99%

Prevention and Treatment of Acute Renal Failure in Sepsis

Vriese

2003

Journal of the American Society of Nephrology

111

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“…Renal dysfunction is an important complication of cardiac surgery with an incidence from 0.1% to 39% [1][2][3][4]. Patients at high-risk of postoperative renal dysfunction include those with pre-existing renal dysfunction [5,6], diabetes [7], impaired left ventricular (LV) function [7], and those undergoing non-elective and/or complicated procedures involving prolonged cardiopulmonary bypass (CPB) or circulatory arrest [6].…”

Section: Introductionmentioning

confidence: 99%

Does furosemide prevent renal dysfunction in high-risk cardiac surgical patients? Results of a double-blinded prospective randomised trial☆☆☆

Mahesh¹,

Yim²,

Robson³

et al. 2008

European Journal of Cardio-Thoracic Surgery

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Objective: Renal dysfunction following cardiac surgery is more apparent in high-risk patients with pre-existing renal dysfunction, diabetes and impaired left-ventricular function, and following complicated procedures involving prolonged cardiopulmonary bypass (CPB). The aim of this prospectively randomised double-blinded placebo-controlled study was to evaluate reno-protective effect of low-dose furosemide infusion in this high-risk group. Methods: Patients with preoperative serum creatinine >130 mmol/l (1.4 mg/dl), left-ventricular ejection fraction <50%, congestive heart failure, diabetes, or procedures involving prolonged CPB were randomised to receive either saline at 2 ml/h (n = 21), or furosemide at 4 mg/h (n = 21). Infusion was commenced after induction of anaesthesia and continued for 12 h postoperatively. Renal dysfunction was defined as >50% increase in serum creatinine postoperatively, or >130 mmol/l (1.4 mg/dl), or requirement for haemodialysis, or all of these. In patients with preoperative serum creatinine >130 mmol/l, >50% increase over preoperative levels was used to define postoperative renal dysfunction. Results: Following cardiac surgery, patients receiving furosemide had a higher urine output (3.4 AE 1.2 ml/kg/h in furosemide group and 1.2 AE 0.5 ml/kg/h in placebo group; p < 0.001), higher postoperative fluid requirement (4631 AE 1359 ml in furosemide group and 3714 AE 807 ml in placebo group, p = 0.011), and lower urinary-creatinine (2 AE 1.3 mmol/l in furosemide group and 5.9 AE 2.5 mmol/l in placebo group p < 0.001). Both groups had significant increase in retinol binding protein/creatinine ratio (7.2 AE 6 to 3152 AE 1411 in furosemide group; 4.9 AE 2.1 to 2809 AE 1125 in placebo group; p < 0.001) and peak serum creatinine (98 AE 33 to 177 AE 123 mmol/l in furosemide group; 96 AE 20 to 143 AE 87 mmol/l in placebo group; p < 0.001), and a significant decrease in peak creatinine-clearance (64.3 AE 29.4 to 39.1 AE 16.6 ml/min in furosemide group; 65.5 AE 38.6 to 41.8 AE 17.8 ml/min in placebo group; p < 0.001) following cardiac surgery, implying significant renal injury following cardiac surgery. Peak creatinine levels (177 AE 123 mmol/l in furosemide group and 143 AE 87 mmol/l in placebo group; p = 0.35) and peak creatinine-clearance (39.1 AE 16.6 ml/min in furosemide group and 41.8 AE 17.8 ml/min in placebo group; p = 0.61) were similar in the two groups. Importantly, there was no difference in incidence of renal dysfunction between the furosemide group (9/21) and the control group (8/21) (relative risk 1.1, 95% confidence interval 0.6-2.2; p = 0.99). Conclusions: Our randomised trial did not demonstrate any benefit of furosemideinfusion postoperatively in high-risk cardiac surgical patients. Although urinary output increased with furosemide, there was no decrease in renal injury, and no decrease in incidence of renal dysfunction. #

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Renal support in critically ill patients: Low-dose dopamine or low-dose dobutamine?

Cited by 133 publications

References 0 publications

Renal Vasodilatory Action of Dopamine in Patients With Heart Failure

Renal Vasodilatory Action of Dopamine in Patients With Heart Failure

Prevention and Treatment of Acute Renal Failure in Sepsis

Does furosemide prevent renal dysfunction in high-risk cardiac surgical patients? Results of a double-blinded prospective randomised trial☆☆☆

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