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THERAPEUTIC REVIEW |
From the Department of Medicine Division of Nephrology, University of Miami School of Medicine, Miami, Florida.
Address for reprints: Murray Epstein, MD, Professor of Medicine, University of Miami School of Medicine, 1600 NW 10th Avenue (R 7168), Miami, FL 33136.
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ABSTRACT |
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 TOP ABSTRACT RENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Key Words: Fenoldopam • radiocontrast-induced nephropathy • dopamine-1 receptor agonist
Fenoldopam preferentially increases renal medullary blood flow through selective stimulation of dopamine-1 receptors (DA-1)8-12 and provides the basis for protection against radiocontrast-induced acute renal failure. However, conflicting data exist regarding the effectiveness of fenoldopam to protect against RIN.13-19 The current report reviews the renal effects of fenoldopam and provides a critical analysis of recently published studies in an attempt to clarify fenoldopam's role against radiocontrast-induced acute renal failure.
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RENAL EFFECTS OF FENOLDOPAM |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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In contrast to dopamine, which produces vasodilation in the renal cortex and creates a medullary steal phenomenon, fenoldopam is advantageous as it induces vasodilation both in the renal cortex and medulla, consequently minimizing the possibility of medullary hypoxia (ie, "medullary steal").8,9,12 Even at high doses, it is devoid of DA-2 and alpha- or beta-adrenergic stimulation and is thus free of the unwanted effects of concomitant stimulation of these receptors.8 DA-1 stimulation produces vasodilation by inducing vascular smooth muscle relaxation.22 The postulated mechanisms of vasodilation include a reduction in cytosolic calcium and an increase in cyclic adenine monophosphate levels.23 Several investigators have characterized the renal effects of fenoldopam, which include a decrease in RVR and increases in renal blood flow (RBF), GFR, renal sodium, and water excretion. Furthermore, these effects are observed in normotensive subjects as well as hypertensive and critically ill patients.8-12,24-31
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RENAL EFFECTS OF FENOLDOPAM IN HEALTHY NORMOTENSIVE SUBJECTS |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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These findings have been confirmed by a recent study by Mathur et al.25 This randomized, double-blind, placebo-controlled crossover study (n = 14) was undertaken to determine a dose of fenoldopam that would increase RBF without inducing hypotension in healthy male volunteers. RPF and GFR were measured using para-aminohippurate and inulin clearance, respectively, during 3 fixed escalating doses of fenoldopam (0.03, 0.1, and 0.3 µg/kg/min) on both a high- and a low-sodium diet. At 0.1- and 0.3-µg/kg/min infusion rates, the mean plasma concentration of fenoldopam increased proportionally from approximately 1 ng/mL for 0.03 µg/kg/min to 8.5 ng/mL for 0.3 µg/kg/min, suggesting linear pharmacokinetics over the dose range studied (0.03-0.3 µg/kg/min). RPF increased in a dose-dependent manner as compared to placebo: 670 ± 148 versus 576 ± 85 mL/min at 0.03 µg/kg/min (P < .05), 777 ± 172 versus 579 ± 80 mL/min at 0.1 µg/kg/min (P < .05), and 784 ± 170 versus 592 ± 165 mL/min at 0.3 µg/kg/min (P < 0.05). Systolic blood pressure did not change at any of the 3 infusion rates, whereas diastolic pressure decreased minimally (fenoldopam, 62.5 ± 6.4 mmHg vs. placebo, 63.6 ± 2.6 mmHg; P < .05). However, even in this scenario, RPF increased significantly.
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RENAL EFFECTS OF FENOLDOPAM IN HYPERTENSIVE PATIENTS |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Studies in hypertensive patients have confirmed a decrease in RVR and an increase in RBF, GFR, urinary sodium, and water excretion with fenoldopam administration.28-30 Since the initial demonstration of efficacy and safety of fenoldopam administration in hypertensive patients with decreased renal function by Reisin et al,27 several studies have documented a decline in systemic blood pressure without deteriorating renal function. In a study of severely hypertensive patients (diastolic blood pressure > 120 mmHg) with and without impaired renal function, Shusterman et al29 compared the effects of fenoldopam with those of sodium nitroprusside on blood pressure and renal function. In patients with impaired renal function (n = 19), both agents reduced blood pressure (fenoldopam: 214 ± 8/139 ± 6 mmHg to 176 ± 8/107 ± 3 mmHg, P < .001; nitroprusside: 226 ± 4/145 ± 5 mmHg to 171 ± 6/108 ± 2 mmHg, P < .001). However, only the fenoldopam group demonstrated a significant increase in creatinine clearance (from 39 ± 7 mL/min to 75 ± 16 mL/min, P < .05), urine flow (from 119 ± 37 mL/h to 276 ± 84 mL/h, P < .01), and sodium excretion (from 75 ± 22 microEq/min to 227 ± 60 microEq/min, P < .01). In those patients with normal renal function (n = 22), a significant blood pressure reduction was observed with both agents. Again, a significant increase in creatinine clearance, urine flow, and sodium excretion was only seen in the fenoldopam group. The mean doses of fenoldopam were similar for patients with renal impairment (0.34 ± 0.06 µg/kg/min) and those with normal renal function (0.28 ± 0.03 µg/kg/min). It is not uncommon for renal function to deteriorate when blood pressure is reduced in severely hypertensive patients. However, the authors clearly showed that despite a substantive reduction in blood pressure, fenoldopam improved renal function. In addition, the improvement was seen at all levels of baseline renal function. As detailed in Table II, other investigators have also found similar results.
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FENOLDOPAM IN HYPOTENSIVE AND CRITICALLY ILL PATIENTS |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Taken together, the above-cited studies demonstrate that fenoldopam can effectively increase RBF, sodium excretion, and urine volume in a dose-dependent manner. These findings have suggested fenoldopam as a potential protective agent against RIN. The changes in renal function occur despite a decrease in systemic arterial pressure. Clinical trials using this agent must select a dose that is anticipated to achieve the desired renal benefits while avoiding a profound decrease in mean arterial pressure. At minimal doses, the benefits of fenoldopam may not be achieved, whereas administration to higher doses may accomplish the desired renal effects.
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FENOLDOPAM AND RADIOCONTRAST-INDUCED NEPHROPATHY |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Bakris et al13 were the first to evaluate the effect of fenoldopam on renal hemodynamics following radiocontrast administration. They examined the effects of fenoldopam and a DA-1 antagonist (Schering 23390) in an animal model of radiocontrast-induced intrarenal vasoconstriction and reduction of GFR. The objective of the study was to test the hypothesis that DA-1 stimulation blunted the decline in RBF and GFR. Six anesthetized volume-depleted adult mongrel dogs (baseline GFR 35 mL/min) were evaluated. Fenoldopam was infused at 0.01 µg/kg/min in the renal artery. This study demonstrated that fenoldopam prevented reductions in GFR (-17 ± 2 mL/min, control vs 2 ± 1 mL/min, fenoldopam; P < .001). In contrast, GFR was further reduced in the presence of the DA-1 antagonist (-15 ± 2 mL/min, control vs -23 ± 1 mL/min, Schering 23390; P < .05). Similarly, the maximal reduction in RBF was blunted with fenoldopam (-17 ± 12 mL/min, control vs -3 ± 2 mL/min, fenoldopam; P < .01), whereas Schering 23390 magnified the radiocontrast-induced reduction in RBF (-85 ± 11 mL/min, control vs -119 ± 14 mL/min, Schering 23390; P < .05). The authors concluded that DA-1 stimulation with fenoldopam protected against the adverse effect of radiocontrast on renal hemodynamics in this animal model.
These observations have recently been extended to humans (Table III). Several investigators have demonstrated a protective role of fenoldopam against RIN.11-15 Hunter et al14 evaluated the renal effects of fenoldopam in 29 patients with decreased renal function (mean serum creatinine = 2.3 mg/dL) who underwent radiocontrast study. Of the patients, 59% were diabetics. Fenoldopam infusion was begun 2 hours prior to radiocontrast administration at a rate of 0.1 µg/kg/min. The dose was increased in increments of 0.1 µg/kg/min every 20 minutes until a rate of 0.5 µg/kg/min was achieved or the systolic blood pressure fell by more than 40 mmHg or below 110 mmHg. The use of a dose ranging from 0.1 to 0.5 µg/kg/min was based on the previous documentation that fenoldopam produces a dose-related increase in RPF in healthy volunteers of up to 75% at a dose of 0.5 µg/kg/min.24,25 After radiocontrast administration, the fenoldopam infusion was continued for up to 4 hours at the highest achieved dose. Twenty-four to 48 hours following contrast infusion, the mean serum creatinine was 12% lower than baseline. At 24 hours, 16 of the 29 patients demonstrated a decrease in serum creatinine ranging from 0.2 to 1.4 mg/dL, whereas 3 patients showed an increase in serum creatinine ranging from 0.2 to 0.9 mg/dL. The authors did not observe a decrease in systemic blood pressure. Although these data suggest that administration of fenoldopam protects against RIN, several limitations of the study do not allow definite conclusion because of the small sample size, the absence of a control group, and the failure to control other factors, such as the state of hydration. Nevertheless, the lack of a significant reduction in blood pressure using 0.1- to 0.5-µg/kg/min fenoldopam infusion was evident in this study.
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In a retrospective analysis, Madyoon et al15 evaluated 46 consecutive radiocontrast procedures in both diabetic and nondiabetic patients with an entry serum creatinine concentration of greater than 1.5 and 1.7 mg/dL, respectively. These investigators used the same dose range that was used by Hunter et al14 to infuse fenoldopam. RIN was defined as an increase in serum creatinine greater than 25% over baseline at 48 hours after administration of the contrast media. The results were compared with a historical control group, that is, those from a representative benchmark study with similarly at-risk patients (n = 50).34 The baseline serum creatinine averaged 2.3 ± 1.5 mg/dL in this study and 2.5 ± 0.1 mg/dL for the historical group. The incidence of RIN was 13% (6/46) in the fenoldopam group as compared to 38% (19/50) in the comparator group. The incidence of RIN in the diabetic cohort was only 14% as opposed to 67% for the comparator group. Compared with the control group, study patients had an average increase in serum creatinine of 16% versus 118% for the control group. In the fenoldopam-treated patients, there was a decrease of 26 mmHg in systolic and 12 mmHg in diastolic blood pressure. Temporary discontinuation of fenoldopam infusion was required in 7 patients (15%) because blood pressure fell below the specified protocol (systolic pressure 
100 mmHg; diastolic pressure to remain within 20 mmHg of baseline). Nonetheless, RIN did not develop in these patients. Madyoon et al15 concluded that fenoldopam offered protection against RIN. Although the results of the study were encouraging, the lack of randomization and the use of a historical comparator group make it difficult to conclude that routine use of fenoldopam for this purpose is warranted. The study, however, confirmed the successful application of a dose range of 0.1 to 0.5 µg/kg/min fenoldopam, as used in a previous study by Hunter et al.14
Kini and Sharma17 investigated protective effects of fenoldopam against RIN in the setting of patients undergoing percutaneous coronary interventions. Inclusion criteria were baseline serum creatinine exceeding 1.5 mg/dL and inclusion of at least 1 of the following risk factors: diabetes, compensated heart failure, age older than 70 years, or hypertension. Low-osmolar nonionic contrast agent iohexol was administered to all patients. Fenoldopam (0.1 µg/kg/min) was infused 15 to 20 minutes prior to administration of contrast medium and continued for 6 hours after the procedure. In addition, hydration was attained with half-normal saline given intravenously for 10 to 12 hours prior to and 10 to 12 hours after the procedure. Patients with matching baseline demographics (n = 177) were used as historical controls for the prospectively studied group (n = 110). RIN was defined as an increase in serum creatinine greater than 25% from baseline within 48 to 72 hours after the procedure or an absolute increase in serum creatinine greater than 0.5 mg/dL. Compared with historical controls, fenoldopam-treated patients had a significantly lower incidence of RIN (4.5% vs 18.8%, P = .009). These investigators used a dose of fenoldopam that was significantly lower than that used by Hunter et al14 and Madyoon et al.15 Nonetheless, the authors reported a significant drop in blood pressure (systolic pressure below 90 mmHg) following fenoldopam infusion in 4 patients (3.8%). The blood pressure rapidly returned to baseline after decreasing the dose of fenoldopam, and no serious adverse effect was attributed to hypotension. Interestingly, the incidence of hypotension was not significantly different than in the historic control group (fenoldopam = 3.8% vs control = 1.7%, P = ns). Coronary interventions in this study included stent, Rotablator, Rota + stent, and AngioJet + stent, all of which are well known in carrying the risk of bradycardia and hypotension.35-41 This study clearly documented the prophylactic effect of fenoldopam against radiocontrast-induced nephropathy in patients with kidney disease both with and without diabetes. Regretfully, the lack of randomization precludes definitive conclusion of fenoldopam's protective role against RIN.
Recently, Tumlin et al18 reported the results of a multicenter, randomized, double-blind trial to evaluate the use of fenoldopam for the prevention of RIN. The patient population consisted of 45 patients with a baseline serum creatinine between 2 and 5 mg/dL who were undergoing angiography with or without coronary angioplasty. There were no significant differences between the groups with respect to the presence of diabetes, volume of contrast, demographics, and baseline serum creatinine. Patients were randomized to receive either half-normal saline or half-normal saline plus fenoldopam 0.1 µg/kg/min, starting at 60 to 90 minutes prior to radiocontrast injection and for 4 hours thereafter. Renal vasoconstriction at 1 hour postcontrast was predictive of the development of RIN. Fenoldopam fully attenuated early vasoconstriction, as evidenced by an increase in RPF in the fenoldopam group of 15.8% above the baseline at 1 hour versus a decrease in RPF in the half-normal saline group of -33.2% (P < .05). RPF in both groups was significantly lower (half-normal saline group = -41%, -49.6%; fenoldopam group = -47.8%, -64%) than baseline values at 3 and 4 hours, respectively, indicating that fenoldopam did not prevent a late decline in RPF. At 72 hours, peak serum creatinine increased significantly in the half-normal saline group (3.6 ± 1.0 mg/dL) versus the fenoldopam group (2.8 ± 0.35 mg/dL, P < .05). The incidence of RIN, prospectively defined as an increase in serum creatinine of 0.5 mg/dL at 48 hours following radiocontrast injection, was reduced by 50% in the fenoldopam arm (21% vs 41%). However, this trend did not attain statistical significance.
The study demonstrated that, when administered at a dose of 0.1 µg/kg/min, fenoldopam increased renal plasma flow by only 15%. Previous studies have documented that fenoldopam increases RPF in a dose-dependent manner,24,25 and it is conceivable that a higher dose of fenoldopam might have mitigated the decline in RPF encountered at 3 to 4 hours. Hence, a higher dose may be needed to achieve an optimal prophylactic action against RIN. By documenting a significant reduction in RPF even at 4 hours after contrast administration, this study provided the first direct evidence for the intense and prolonged nature of radiocontrast-induced vasoconstriction. This suggests that in addition to an increment in the dose, a longer infusion period may also be needed. Increasing the dose, however, increases the risk of hypotension, with resultant intrarenal vasoconstriction. In the study by Tumlin et al,18 3 patients in the fenoldopam group and 1 in the half-normal saline group became hypotensive, of whom 2 developed hypotension soon after radiocontrast administration. The hypotension was reversed promptly (within 5 minutes) by withholding the drug and infusing saline.
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In contrast to the above-mentioned studies, a recent multicenter, double-blind, randomized trial was interpreted as failing to demonstrate a beneficial effect of fenoldopam against RIN.19 A total of 315 patients (50% diabetics) with baseline creatinine clearance less than 60 mL/min undergoing percutaneous coronary interventions were hydrated with half-normal saline and randomized 1:1 to intravenous fenoldopam (0.05 µg/kg/min titrated up to 0.1 µg/kg/min) or placebo, starting 1 hour before coronary intervention and continuing for 12 hours thereafter. The authors concluded that fenoldopam did not protect against RIN. However, several problems with the experimental design confound this interpretation. Fenoldopam has dose-dependent pharmacodynamics up to 0.3 µg/kg/min, with smaller additional effects up to a dose of 0.5 µg/kg/min.24,25 The CONTRAST study used an initial dose of 0.05 µg/kg/min that was increased to a maximal dose of only 0.1 µg/kg/min. Consequently, because the cohort receiving fenoldopam was restricted to a maximum dose of only 0.1 µg/kg/min, this may have confounded the results of this study. Conversely, it is conceivable that a slow uptitration of fenoldopam to higher doses would have attenuated or prevented radiocontrast-induced nephropathy. Patients with renal insufficiency probably have a dose-response curve that is higher (right shifted) versus healthy volunteers, and they likely need higher doses to attain the same increment in RBF that normal volunteers attain at a lower dose. This is supported by the fact that Tumlin et al,18 in a study with patients with chronic renal insufficiency (mean creatinine = 2.6 mg/dL), demonstrated only a 16% increase in para-aminohippuric acid clearance at a dose of 0.1 µg/kg/min, whereas the same dose increased para-aminohippuric acid clearance by 30% in normal volunteers.24,25 Previous studies demonstrated a protective effect of fenoldopam against RIN in patients pretreated with fenoldopam for a longer duration (1.5-2 hours) than did Stone et al19 (1 hour). Perhaps a longer pre-treatment period would have better prepared the kidney to counter the adverse effects of radiocontrast medium and, consequently, might have produced more favorable clinical results. In addition, mean volume infused in this trial was higher than that administered in other studies. Saline per se has pharmacologic properties against radiocontrast-induced nephropathy. It is plausible that administration of increased volume per se may have been renoprotective, thereby rendering fenoldopam's effect more difficult to detect.
Fenoldopam administration is clearly capable of inducing hypotension during radiocontrast studies. However, a variety of factors in addition to this agent have been documented to cause hypotension in this population, potentially confounding interpretation of many of the studies to date. The following section briefly discusses hypotension during radiocontrast studies.
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RADIOCONTRAST STUDIES AND HYPOTENSION |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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Furthermore, medications often administered during coronary intervention may also contribute to the hypotension. Midazolam, diazepam, diphenhydramine, fentanyl, and nitroglycerine (intracoronary, sublingual) all can produce hypotension.50
Finally, the administration of radiocontrast medium itself can cause a number of well-described acute hemodynamic and vascular effects, including vascular spasm, hypotension, and arrhythmias, both in animals and humans.43-49 It has been suggested that radiocontrast-induced hypotension is mediated predominantly by the cardiac-depressor reflex, which originates from chemosensitive endings in the ventricles.45 In addition, a direct depressor effect on the sinoatrial node resulting in mild sinus slowing plays a contributory role.51
A recent randomized study (n = 1034) by Lembo et al42 evaluating the effect of radiocontrast administration on blood pressure found an 18% incidence of hypotension in patients undergoing coronary interventions. There were no significant (P = ns) differences between hypotension caused by high-osmolarity (9.5% [n = 551]) versus low-osmolarity (8.5% [n = 507]) contrast agents. Indeed, both high- and low-osmolarity contrast agents were capable of producing hypotension.
A previous benchmark study by Wang et al52 also reported a 10% incidence of hypotension in patients undergoing radiocontrast administration during coronary interventions. In this study, the group that received mixed endothelin receptor A and B antagonist (SB 209670) demonstrated an 18% incidence of this adverse event.
The incidence of hypotension reported in the studies by Tumlin et al18 (6.6%), Kini and Sharma17 (3.6%), and Stone et al19 (13%), even with fenoldopam administration, clearly was within the range highlighted by the above-cited studies.
In summary, to ascertain the etiology of the hypotension encountered in the context of radiocontrast administration, one must take into consideration whether the study was a simple computed tomography scan of the abdomen or a percutaneous coronary intervention. In the latter scenario, the blood pressure instability could be due to a variety of factors highlighted above.
Most hypotensive episodes encountered during radiocontrast administration with a coronary procedure are transient and do not require a specific therapy. In patients in whom a significant decline in blood pressure is observed, the dose of fenoldopam should be reduced and the likely etiology of hypotension quickly assessed. In the event of hypotension immediately following radiocontrast administration or coronary interventions (Rotablator application, stent deployment, reperfusion arrhythmia and hypotension, AngioJet operation), fenoldopam may be slowly up-titrated once the hypotensive episode has been resolved. In patients with stable blood pressure, however, a slow uptitration of fenoldopam to an optimal dose as tolerated by blood pressure must be performed to achieve the maximal renal hemodynamic benefit and to properly evaluate its protective role against RIN. As highlighted above, indeed, fenoldopam is unique in that a decrease in systemic blood pressure does not lead to intrarenal vasoconstriction.
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OTHER INTERVENTIONS TO PREVENT RADIOCONTRAST-INDUCED NEPHROPATHY |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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CONCLUSION |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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ACKNOWLEDGEMENTS |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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FOOTNOTES |
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Submitted for publication May 26, 2004; Revised version accepted August 4, 2004.
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REFERENCES |
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TOPABSTRACTRENAL EFFECTS OF FENOLDOPAMRENAL EFFECTS OF FENOLDOPAM...RENAL EFFECTS OF FENOLDOPAM...FENOLDOPAM IN HYPOTENSIVE AND...FENOLDOPAM AND RADIOCONTRAST...RADIOCONTRAST STUDIES AND...OTHER INTERVENTIONS TO PREVENT...CONCLUSIONACKNOWLEDGEMENTSREFERENCES |
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