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Ann Thorac Surg 2010;89:497-503. doi:10.1016/j.athoracsur.2009.09.071
© 2010 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

The Effect of Various Fenoldopam Doses on Renal Perfusion in Patients Undergoing Cardiac Surgery

Massimo Meco, MD*, Silvia Cirri, MD

Cardiac Surgery and Anesthesia and Intensive Care Department, Sant'Ambrogio Hospital, Milan, and Centro Malan, IRCCS San Donato Hospital, San Donato Milanese, Italy

Accepted for publication September 29, 2009.

Abbreviations and Acronyms AVA = aortic valve area; BMI = body mass index; CI = cardiac index; CPB = cardiopulmonary bypass; CSA = cross-sectional area; CVP = central venous pressure; DAP = diastolic arterial pressure; EDA = end diastolic area; EDID = end diastolic internal dimension; EDV = end diastolic velocity; EF = ejection fraction; ESID = end systolic internal dimension; ESMWS = end systolic meridional wall stress; ESPWT = end systolic posterior wall thickness; FDS = fractional diameter shortening; HR = heart rate; LAP = left atrial pressure; LVEDV = left ventricle end diastolic volume; LVSWT = left ventricle systolic wall tension; MAP = mean arterial pressure; MV = mean velocity; PI = pulsatility index; PSV = peak systolic velocity; RBF = renal blood flow; RF = renal failure; RI = resistive index; RRBFI = right renal artery blood flow index; SAP = systolic arterial pressure; SV = stroke volume; SVR = systemic vascular resistances; TDI = tissue Doppler imaging; TVI = time velocity integral

* Address correspondence to Dr Meco, Cardiac Surgery and Anesthesia and Intensive Care Department, Istituto Clinico Sant'Ambrogio, Via Faravelli 16, Milano, 20171, Italy (Email: massimo.meco{at}virgilio.it).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 References
 
Background: The hypothesis that fenoldopam mesylate, by increasing renal flow, could reduce renal damage in patients undergoing cardiac surgery with cardiopulmonary bypass has gained great interest. The aim of the current study was to quantify the relationship of the increase of the renal blood flow as a function of the fenoldopam dose in these patients and to evaluate renal flow distribution within the renal parenchyma using Doppler.

Methods: Twenty-five patients admitted to cardiac surgery have been enrolled. We used the Doppler technique to measure renal blood flow at the level of the renal, segmental, interlobar, and interlobular arteries. We calculated both the resistive and pulsatility indexes in all the renal segments. Moreover, we calculated echographically all the variables of preload, afterload, and cardiac index. Measurements were performed at baseline and after the infusion of fenoldopam mesylate at the doses of 0.05, 0.1, 0.2, and 0.3 µg · kg–1 · min–1.

Results: Fenoldopam infusion at doses more than 0.1 µg · kg–1 · min–1 significantly increases blood flow in all renal compartments, thus improving the resistive and pulsatility indexes starting at a dose of 0.1 µg · kg–1 · min–1. The highest renal flow increase is observed with 0.3 µg · kg–1 · min–1. Fenoldopam seems to increase the renal flow directed to the most external kidney areas. Systemic hemodynamically significant changes are observed only in patients receiving doses more than 0.1 µg · kg–1 · min–1.

Conclusions: In hemodynamically stable patients undergoing cardiac surgery with preserved renal function, fenoldopam shows a pharmacodynamic dose-dependent profile: it significantly increases renal flow and reduces the resistances of the renal circulation starting at a dose of 0.1 µg · kg–1 · min–1.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 References
 
Fenoldopam mesylate is a benzazepine derivative that is a potent short-acting dopamine A1 receptor agonist that decreases systemic vascular resistance (SVR) while, at the same time, increases renal blood flow (RBF) [1, 2]. The hypothesis that fenoldopam mesylate could reduce the renal damage in several clinical conditions has recently gained high interest, for example, for patients undergoing cardiac surgery in cardiopulmonary bypass conditions (CPB) [3], for the protection against radiocontrast-induced nephropathy, and for several conditions of intensive care medicine.

The studies conducted so far have been performed with fenoldopam mesylate at various doses, although the most commonly used is 0.1 µg · kg–1 · min–1. Currently, there is no study highlighting the dose-relationship effect of fenoldopam mesylate on RBF in patients undergoing cardiosurgery with CPB.

The aim of the current study was to evaluate the effects of various increasing doses (0.05, 0.1, 0.2 and 0.3 µg · kg–1 · min–1) of fenoldopam mesylate infusion on RBF and on ventricular afterload. The effects on systemic hemodynamic were also evaluated.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 References
 
Patient Population
The study protocol was approved by the Ethics Committee of our institution, and all enrolled patients provided their written informed consent to participate. The study was conducted in accordance with the ethical standards of human investigation and with the Declaration of Helsinki (1975, revised in 1983).

Patients undergoing myocardial revascularization were asked to participate in the current study. All patients had preserved presurgical cardiac function, normal creatinine values, and age less than 75 years without concomitant major diseases. On arrival at the intensive care unit, after volemia normalization, patients considered hemodynamically stable, with no need of inotropic substances or mechanical supports, were included. All patients were sedated with propofol (0.5 mg · kg–1 · h–1) and mechanically ventilated (FiO2 0.5, tidal volume 7 mL/kg, positive end-expiratory pressure 5 cm/H2O, 10 breaths per minute).

Echocardiographic Evaluation
After hemodynamic stabilization, mivacurium (0.1 mg/kg) was administered and a probe for transesophageal echocardiography was inserted (Omniplane II, Hewlett-Packard 5-MHz probe; Hewlett-Packard, Andover, MA).

We recorded the following transesophageal views: mid-esophageal four chamber, mid-esophageal long axis, mid-transgastric short axis, and deep transgastric. The tissue Doppler imaging was measured on the lateral wall of the mitral annulus in the four-chamber projection. All the measurements were done by a single operator (MM). The spectral Doppler signal settings were adjusted at the lowest wall filter and at the minimum optional gain. The measurements were carried out during expiration, using the mean of three consecutive cardiac cycles.

The preload was evaluated by left ventricle end-diastolic volume (LVEDV), end-diastolic area (EDA), and central venous pressure (CVP). Left atrial pressure (LAP) was calculated according to Nagueh and colleagues [4], using the formula: LAP = 2 + 1.3 (E/E'). The afterload was evaluated by end-systolic meridional wall stress (ESMWS) = 0.33*SAP*(ESID/ESPWT)*(1 + ESPWT/ESID), where SAP is systolic arterial pressure, ESID is end-systolic internal dimension, and ESPWT is end-systolic posterior wall stress; left ventricle systolic wall tension (LVSWT) = 1.33*SAP*(ESID/2); and systemic vascular resistance (SVR) indexed (SVRI) = MAP – CVP/CI*80, where MAP is mean arterial pressure and CI is cardiac index. Cardiac index was calculated as SV*HR/BMI, where SV is stroke volume, HR is heart rate, and BMI is body mass index; and SV was calculated as SV = TVI*AVA, where TVI (cm/s) is the time velocity integral of the flow across the aortic valve obtained with a continuous-wave Doppler in a deep transgastric view, and AVA (cm2) is the mean effective aortic valve area throughout the ejection phase. The cross-sectional area was calculated as {pi}*r2, where r represents half of the annular diameter measured immediately proximal to the point of insertion of the aortic leaflet at the time of maximal separation. Cardiac contractility was calculated by measuring ejection fraction and fractional diameter shortening (FDS) = EDID – ESID/EDID*100, where EDID is end-diastolic internal dimension.

Renal Perfusion
Renal blood flow in the renal artery was evaluated by the technique described by Garwood and colleagues [5]. From the transgastric position with a depth regulated at 12 cm, the probe was deflexed in a neutral position and turned 180 degrees clockwise. If the kidneys were not visible in the bottom left-hand sector of the screen in this position, the probe was moved 5 to 10 cm, turning the probe by 30 to 45 degrees to the patient's right to picture the kidney. By using the color Doppler in this position, the operator could identify the main renal, segmental, interlobar, and interlobular arteries.

It was not possible to apply this technique to all patients. Because the renal artery was not clearly identifiable with the use of transesophageal Doppler in 12 of the patients, the transabdominal approach—the so-called flank approach—was used [6]. The flow velocity in the renal artery was measured at 1 cm from its entrance to the kidney and the flow velocity in the segmental artery, at 0.5 cm from its origin, as well as the flow velocities in the interlobar and interlobular arteries. Peak systolic velocity (PSV), end-diastolic velocity (EDV), and mean velocity (MV) were recorded.

The pulsatility index (PI) was calculated using the formula PI = PSV – EDV/MV; and the resistive index (RI) was calculated using the formula RI = PSV – EDV/PSV [7]. Time velocity integral (TVI) was measured as the area under the outermost portion of the spectral velocity envelope. The right renal artery blood flow index (RRBFI [mL/min]) was calculated as the product of the right renal artery cross-sectional area (CSA) and the TVI, according to the following formula: flow = HR*TVI*CSA/BSA, where BSA is body surface area.

All measurements were performed at baseline and 30 minutes after fenoldopam mesylate infusion at the doses of 0.05, 0.1, 0.2, and 0.3 µg · kg–1 · min–1.

Statistical Analysis
All study variables are expressed as mean ± SD. To analyze the effect of fenoldopam mesylate infusion on all studied variables, we applied the analysis of variance test for repeated measures. The comparison among doses was analyzed by the two-tailed Student t test. The categorical variables were analyzed by either the {chi}2 test or the exact Fisher test, when possible. The normality of sample distribution was verified by applying the Kolmogorov-Smirnov test; because both RI and PI do not have a normal distribution, a logarithmic transformation was applied before analyzing them. A p value of less than 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 References
 
Patient Population
Between November 2008 and February 2009, 25 patients were enrolled. Table 1 shows the general characteristics of the patients. No severe or serious complications occurred during the study, and no patients died.


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  		Table 1 Characteristics of the Patients
 
Echocardiographic Evaluation
Table 2 shows the hemodynamic indexes at baseline and during fenoldopam mesylate infusion at various doses. The variables that we used to evaluate the preload do not show significant changes with fenoldopam mesylate at the doses of 0.05 and 0.1 µg · kg–1 · min–1. They start changing at the dose of 0.2 µg · kg–1 · min–1 and continue showing a statistically significant reduction with the dose of 0.3 µg · kg–1 · min–1. Also, the afterload indexes change significantly with doses greater than 0.1 µg · kg–1 · min–1: with the dose of 0.3 µg · kg–1 · min–1, there is the highest decrease of the afterload indexes.


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  		Table 2 Hemodynamic Indexes at Baseline and During Fenoldopam Mesylate Infusion at Various Doses
 
Systolic arterial pressure and mean pressure change statistically with the dose of 0.2 µg · kg–1 · min–1, whereas the diastolic arterial pressure does not show any change. Cardiac index statistically increases if compared with baseline starting with the dose of 0.2 µg · kg–1 · min–1. The increase of heart rate observed with the dose of 0.3 µg · kg–1 · min–1 does not reach statistical significance.

Renal Perfusion
0.05 µg · kg–1 · min–1
The flow velocity in the renal, segmental, interlobar, and interlobular arteries shows a not statistically significant increase (Table 3, Fig 1). The RI and PI show a not statistically significant decrease (Table 4, Fig 1). Also, the RRBFI shows a not statistically significant increase but the dimension of the renal artery statistically significantly increases (Table 5, Fig 2).


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  		Table 3 Systolic, Diastolic, and Mean Flow Velocities of Various Arterial Districts at Baseline and During Fenoldopam Mesylate Infusion at Various Doses
 

Figure 1
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  		Fig 1. (A) Right artery mean flow velocity (RAMFV) at different doses of fenoldopam mesylate. (B) Renal artery resistive index at different doses of fenoldopam mesylate.

 

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  		Table 4 Resistive and Pulsatility Indexes of Various Arterial Districts at Baseline and During Fenoldopam Mesylate Infusion at Various Doses
 

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  		Table 5 Variations of Renal Blood Flow Variables During Fenoldopam Mesylate Infusion at Various Doses
 

Figure 2
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  		Fig 2. (A) Indexed renal flow of the right renal artery at different doses of fenoldopam mesylate. (B) Percentage cardiac index (C.I.) directed to the right renal artery at different doses of fenoldopam mesylate.*Versus baseline; #Versus previous dose; §Versus 0.1 µg · kg–1 · min–1 dose.

 
0.1 µg · kg–1 · min–1
The flow velocity in the renal artery shows a statistically significant increase relative to baseline and 0.05 µg · kg–1 · min–1 dose. Similar results were recorded for the other arteries if compared with baseline (Table 3, Fig 1). The RI and PI of the renal artery showed a statistically significant decrease compared with baseline values (Table 4, Fig 1). However, at the level of the segmental and interlobar arteries, the decrease of these indexes is not significant. The RI of the interlobular artery showed a significant decreases versus baseline (Table 4, Fig 1). With the dose of 0.1 µg · kg–1 · min–1 fenoldopam mesylate, the diameter of the renal artery, the RBF, and the percentage cardiac index directed to the renal circulation are significantly higher if compared with baseline and with the 0.05 µg · kg–1 · min–1 dose (Table 5, Fig 2).

0.2 µg · kg–1 · min–1
The flow velocity of all the arteries shows a statistically significant increase versus baseline (Table 3, Fig 1). At the level of the renal artery, this increase is significant also versus the dose of 0.1 µg · kg–1 · min–1. The RI and PI of the renal artery show a statistically significant decrease versus both baseline and 0.05 and 0.1 µg · kg–1 · min–1 doses (Table 4, Fig 1). With the dose of 0.2 µg · kg–1 · min–1, the diameter of the renal artery, the RRBFI, and the percentage of CI directed to the renal circulation are significantly higher versus baseline and the 0.1 µg · kg–1 · min–1 dose (Table 5, Fig 2).

0.3 µg · kg–1 · min–1
The flow velocity of all the arteries shows a statistically significant increase versus baseline and both 0.05 and 0.1 µg · kg–1 · min–1 doses, and, for the renal artery, also for the dose of 0.2 µg · kg–1 · min–1 (Table 3, Fig 1). The RI and PI of both the renal and the interlobular arteries show a statistically significant decrease both versus baseline and versus all the lower doses. The same finding was observed for the interlobular artery (Table 4, Fig 1). With the dose of 0.3 µg · kg–1 · min–1 fenoldopam mesylate, the diameter of the renal artery, the RRBFI, and the percentage of CI directed to the renal circulation are significantly higher versus baseline and all the lower doses (Table 5, Fig 2).


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
References
 
The current study shows that, by increasing the dose of fenoldopam infusion, there is a parallel increase of renal perfusion and a parallel decrease of both RI and PI. In addition, our study shows that, in normovolemic patients, there is a decrease of both the preload and the afterload with doses greater than 0.1 µg · kg–1 · min–1 with a subsequent CI increase. Heart rate never changes significantly with any dose.

There are two major considerations: (1) a clinically significant effect of fenoldopam mesylate on renal perfusion is obtained with a dose of at least 0.1 µg · kg–1 · min–1; and (2) a statistically significant decrease of the afterload is detected with doses greater than 0.1 µg · kg–1 · min–1.

Our results are quite in keeping with those obtained by Mathur and coworkers [2]. Those authors used various doses of fenoldopam mesylate in healthy volunteers, and they measured inuline and creatinine clearances. They found that fenoldopam significantly and dose-dependently increases RBF starting with the lowest doses, with a dose-dependent increase up to 0.3 µg · kg–1 · min–1. From a hemodynamic point of view, the above-mentioned study shows that systolic arterial pressure is not affected by any dose whereas diastolic arterial pressure significantly decreases with doses greater than 0.05 µg · kg–1 · min–1. This is in contrast with our findings: we showed that systolic arterial pressure significantly decreases with doses greater than 0.1 µg · kg–1 · min–1, as well as systemic vascular resistance and wall stress. This difference can be attributed to the different types of populations (healthy volunteers versus cardiac patients) enrolled in the two studies.

A very interesting issue elicited by our data is that, by analyzing the RI of the kidney vessels, although there is a reduction of both RI and PI in all renal circulation, the highest RI and PI decrease occurs in the interlobular arteries, namely, the arteries directed to the more external layers of the kidney. This finding is in keeping with the results obtained by Aravindan and associates [8]: by studying a rat model of acute ischemic nephropathy to test the hypothesis that fenoldopam improves corticomedullary tissue oxygen tension, they showed that fenoldopam increases the RBF in the external areas of the kidney.

The pathophysiology of renal damage is multifactorial and related to perioperative renal hypoperfusion [9]. A decrease in RBF is of critical importance in initiating and extending the pathophysiology of the ischemic renal failure. Under physiologic conditions, the oxygen tension of the kidney decreases as one moves from the outer cortex to the inner medulla [10]. Mechanisms involved in the alteration of renal perfusion after ischemic injury are somewhat understood. An imbalance between mediators of renal vasoconstriction and vasodilatation has been proposed to play a role in animal models of ischemic acute renal failure [11]. In addition to the increase of RRBFI, the possible therapeutic role of fenoldopam in these conditions is the redistribution of the flow toward both the corticomedullar junction and the external regions of the kidney.

Another interesting aspect raised from the current study is the precise quantification of the effect of fenoldopam by varying its doses (a dose increase results in RBF increase). In our study, we clearly show a dose-dependent effect of fenoldopam; thus, the selection of fenoldopam's correct dose is crucial: it must be taken into account that the almost maximum RBF is reached with the dose of 0.2 µg · kg–1 · min–1, with an additional increase by increasing the dose up to 0.3 µg · kg–1 · min–1. This observation might explain why this drug failed to improve renal function in the only large randomized study examining the efficacy of fenoldopam in preventing contrast nephropathy in patients undergoing stent procedures: patients in that trial received 0.05 µg · kg–1 · min–1 [12]. Probably, the dose used in the study by Stone and colleagues [12] was too small for this type of patients, since other studies—by using higher doses (as high as 0.5 µg · kg–1 · min–1)—showed a protective activity of fenoldopam against radiocontrast-induced nephropathy [13–15].

The role of fenoldopam in cardiovascular surgery patients has been studied by different authors. The lack of quantitative data on the effect of fenoldopam on renal flow and renal hemodynamics encouraged clinical studies on the performance on the performance on the nephroprotective efficacy of fenoldopam using different dosages of the compound.

There are several studies in the literature evaluating the nephroprotective effects of fenoldopam mesylate in cardiac surgery patients. In the study by Bove and coworkers [16], a dose of 0.05 µg · kg–1 · min–1 fenoldopam mesylate was used to prevent renal failure in high-risk patients undergoing cardiac surgery. It was compared with dopamine infusion at the dose of 2.5 µg · kg–1 · min–1. In this study, the authors did not find any significant difference between the two compounds. Ranucci and associates [17] analyzed the effect of fenoldopam in high-risk cardiosurgery patients at the dose of 0.08 µg · kg–1 · min–1. The results of this study are contradictory as they showed an effect of fenoldopam in decreasing the incidence of postoperative renal failure, in counteracting the reduction of postoperative creatinine clearance, an effect that was not confirmed by the multivariate analysis. In this patient population, patients who benefitted the most were those with low postoperative cardiac output.

Roasio and associates [18] have studied the effects of a continuous infusion of 0.1 µg · kg–1 · min–1 fenoldopam on the prevention of postoperative renal failure in patients undergoing cardiosurgery. These authors have demonstrated that patients treated with fenoldopam showed a reduced need of substitutive renal therapy. Caimmi and colleagues [19] have studied the effects of fenoldopam on the prevention of renal damage in patients undergoing CPB. They used a dose of fenoldopam between 0.1 and 0.3 µg · kg–1 · min–1 selected as a function of the clinical condition of the patients. The study showed that fenoldopam does protect the kidney from the renal postoperative dysfunction.

In a recent meta-analysis, Landoni and associates [20] showed that fenoldopam mesylate reduced the need for renal substitutive therapy and hospital mortality among patients undergoing cardiac surgery. In this meta-analysis, these authors showed that the best results were obtained with a dose of 0.1 µg · kg–1 · min–1.

Although the aim of the current study was not the demonstration of the effects of CPB on renal flow, we showed that, after CPB, renal flow significantly decreases versus normal baseline renal perfusion determinants. This very interesting finding needs further investigation.

Limitations of the Study
All the measurements were performed by a single operator, thus rendering the obtained measures less objective. Another limitation of our study is that it has been performed with patients who had preserved cardiac and renal functions. We included this type of patients intentionally because the aim of our study was to investigate the effects of fenoldopam mesylate in normal kidneys after CPB; in addition, we did not want to use other drugs that could interfere with the activity of fenoldopam.

In conclusion, the selection of the correct dose of fenoldopam mesylate in patients undergoing cardiosurgery in CPB is crucial. We showed that fenoldopam significantly increases the RBF and reduces the resistance of the renal circulation starting at a dose of 0.1 µg · kg–1 · min–1. The maximum RBF increase is observed with the dose of 0.3 µg · kg–1 · min–1, but the differences between the doses of 0.2 and 0.3 µg · kg–1 · min–1, although present, are not statistically significant. Fenoldopam seems to increase RBF directed to the most external kidney areas. Systemic hemodynamically significant changes are observed only in patients receiving doses greater than 0.1 µg · kg–1 · min–1.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 References
 

  1. Kien ND, Moore PG, Jaffe RS. Cardiovascular function during induced hypotension by fenoldopam or sodium nitroprusside in anesthetized dogs Anesth Analg 1992;74:72-78.[Abstract/Free Full Text]
  2. Mathur VS, Swan SK, Lambrecht LJ, et al. The effects of fenoldopam, a selective dopamine receptor agonist on systemic and renal hemodynamics in normotensive subjects Crit Care Med 1999;27:1832-1837.[Medline]
  3. Cogliati AA, Vellutini R, Nardini A, et al. Fenoldopam infusion for renal protection in high-risk cardiac surgery patients: a randomized clinical study J Cardiothorac Vasc Anesth 2007;21:847-850.[Medline]
  4. Nagueh SF, Middeton KS, Kopelen HA, et al. Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures J Am Coll Cardiol 1997;30:1527-1533.[Medline]
  5. Garwood S, Davis E, Harris SN. Intraoperative transoesophageal ultrasonography can measure renal blood flow J Cardiothorac Vasc Anesth 2001;15:65-71.[Medline]
  6. Yura T, Yuasa S, Fukunaga M, et al. Role for Doppler ultrasound in the assessment of renal circulation: effects of dopamine and dobutamine on renal hemodynamics in humans Nephron 1995;71:168-175.[Medline]
  7. Loriga G, Vidili G, Ruggenti P, et al. Renal hemodynamics and renoprotection Nephron Clin Pract 2008;110:213-219.
  8. Aravindan N, Samuels J, Riedel B, et al. Fenoldopam improves corticomedullary oxygen delivery and attenuates angiogenesis gene expression in acute ischemic renal injury Kidney Blood Press Res 2006;29:165-174.[Medline]
  9. Yasir AO, Chandana R. Cardiopulmonary bypass and renal injury Perfusion 2006;21:209-213.[Abstract/Free Full Text]
  10. Brezis M, Rosen S. Hypoxia of the renal medulla. Its implications for disease. N Engl J Med 1995;332:647-655.[Medline]
  11. Manson J, Torhorst J, Welsch J. Role of the medullary perfusion defect in the pathogenesis of ischemic renal failure Kidney Int 1984;26:283-293.[Medline]
  12. Stone GW, McCullough PA, Tumlin J, et al. Fenoldopam mesylate for the prevention of contrast-induced nephropathy: a randomized controlled trial JAMA 2003;290:2284-2291.[Medline]
  13. Bakris GL, Lass NA, Glock D. Renal hemodynamics in radiocontrast medium-induced renal dysfunction: a role for dopamine-1 receptors Kidney Int 1999;56:206-210.[Medline]
  14. Madyoon H, Croushore L, Weaver D, et al. Use of fenoldopam to prevent radiocontrast nephropathy in high-risk patients Catheter Cardiovasc Interv 2001;53:341-345.[Medline]
  15. Asif A, Epstein DL, Epstei M. Dopamine-1 receptor agonist: renal effects and its potential role in the management of radiocontrast-induced nephropathy J Clin Pharmacol 2004;44:1342-1351.[Abstract/Free Full Text]
  16. Bove T, Landoni G, Calabrò MG, et al. Renoprotective action of fenoldopam in high-risk patients undergoing cardiac surgery. A prospective, double blind, randomized clinical trial. Circulation 2005;111:3230-3235.[Abstract/Free Full Text]
  17. Ranucci M, Soro G, Barzaghi N, et al. Fenoldopam prophylaxis of postoperative acute renal failure in high-risk cardiac surgery patients Ann Thorac Surg 2004;78:1332-1337.[Abstract/Free Full Text]
  18. Roasio A, Lobreglio R, Santin A, et al. Fenoldopam reduces the incidence of renal replacement therapy after cardiac surgery J Cardiothorac Vasc Anesth 2008;22:23-26.[Medline]
  19. Caimmi PP, Pagani L, Micalizzi E, et al. Fenoldopam for renal protection in patients undergoing cardiopulmonary bypass J Cardiothorac Vasc Anesth 2003;17:491-494.[Medline]
  20. Landoni G, Biondi-Zoccai GG, Tumlin JA, et al. Beneficial impact of fenoldopam in critically ill patients with or at risk for acute renal failure: a meta-analysis of randomized clinical trials Am J Kidney Dis 2007;49:56-68.[Medline]

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