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*
Department of Cardiothoracic and Vascular Anesthesia and Intensive Care,
Division of Nephrology, University Clinic of Vienna, Austria.
Department of Internal Medicine I, Division of Nephrology, University
Clinic of Vienna, Austria.
Department of Internal Medicine III, Division of Nephrology, University
Clinic of Vienna, Austria.
Correspondence to Dr. Michael Hiesmayr, University Clinic of Anesthesia (HTG), Währinger Gürtel 18-20, A-1090 Vienna, Austria. Phone: +43 1 40400 4109; Fax: +43 1 40400 6404; E-mail: michael.hiesmayr{at}akh-wien.ac.at
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Creamax) were determined. The
increase in plasma creatinine was twice as high in group F as in groups D and
P (P < 0.01). Acute renal injury (defined as
Creamax >0.5 mg/dl) occurred more frequently in group F
(six of 41 patients) than in group D (one of 42) and group P (zero of 40)
(P < 0.01). (The difference between group D and group P was not
significant.) Creatinine clearance was lower in group F (P <
0.05). Two patients in group F required renal replacement therapy. The mean
volume of infused fluids, blood urea nitrogen, serum sodium, serum potassium,
and osmolar- and free-water clearance was similar in all groups. It was shown
that continuous infusion of dopamine for renal protection was ineffective and
was not superior to placebo in preventing postoperative dysfunction after
cardiac surgery. In contrast, continuous infusion of furosemide was associated
with the highest rate of renal impairment. Thus, renal-dose dopamine is
ineffective and furosemide is even detrimental in the protection of renal
dysfunction after cardiac surgery. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The pathophysiology of ARF in cardiac surgery patients includes a broad pattern of mechanisms, such as hemodynamic factors, especially intraoperative hypoperfusion of the kidney, effects of nephrotoxic drugs, the sequels of the systemic inflammatory reaction induced by cardiopulmonary bypass, and the interactions of blood components and artificial membranes (1,7,8). During cardiopulmonary bypass, the release of vasoconstrictor compounds, including catecholamines, vasopressin, and thromboxane, is enhanced, the renin-angiotensin system is activated, and renal perfusion is compromised (9). Moreover, cardiopulmonary bypass also induces tubular damage, as suggested by the persistence of microalbuminuria and of elevated urinary N-acetyl-ß-D-glucosaminidase up to 6 d after cardiac surgery (10).
Although the concept of low-dose dopamine in the prevention of ARF remains controversial (11), "renal-dose" dopamine is still one of the most frequently used prophylactic measures to prevent renal dysfunction in postoperative patients. Clearly, the effects of dopamine on renal function are well documented, both in healthy subjects and in patients with various diseases. Potentially advantageous effects include an increase in renal blood flow via activation of dopaminergic receptors in the renal vasculature (12,13), an increase in GFR, and an increase in sodium and water excretion. Dopamine inhibits sodium reabsorption in the proximal tubule, in the medullary thick ascending limp of the loop of Henle, and in the cortical collecting duct, thus reducing renal oxygen consumption (14,15,16,17). In addition, dopamine increases the formation and the release of prostaglandin E2, which dilates medullary vessels and also inhibits oxygen consumption in tubular cells (17). Whether a benefit can be derived from these effects on renal function in the prevention of postoperative ARF in the clinical situation has not been convincingly demonstrated.
An alternative approach to renal protection is the use of loop diuretics such as furosemide. Loop diuretics are clearly ineffective in established ARF (18,19) but, at least in the experimental situation, can exert a protective effect if given before a potential renal insult (20,21,22). Furosemide inhibits sodium reabsorption in the thick ascending limp of the loop of Henle, thus inducing a reduction in tubular oxygen consumption and improving renal tolerance to hypoxia (21). An increased excretion of renal vasodilatory prostaglandin E has been reported after intravenous administration of furosemide (23). By increasing tubular flow, dopamine and loop diuretics can both decrease the concentration of toxins such as myoglobin or hemoglobin in the tubular fluid and prevent the development of tubular obstruction (2). On the other hand, a renoprotective effect was not confirmed in other clinical situations, and renal vasodilation induced by furosemide might cause a maldistribution of blood flow within the kidney (24,25).
Despite this ongoing debate about the protective effects of low-dose dopamine and loop diuretics in the prevention of ARF, both substances continue to be broadly used in many institutions throughout the world. In a recent survey of the members of the European Workgroup of Cardiothoracic Intensivists, nine of 38 centers used low-dose dopamine perioperatively, 11 of 38 used furosemide continuously for renoprotection, and 34 of 38 used furosemide bolus injections when diuresis decreased to <0.5 ml/kg per h (39,000 cases of cardiac surgery per year).
Unfortunately, only a few placebo-controlled studies have been performed to resolve this ongoing controversy. Thus, in a placebo-controlled double-blind trial, we investigated whether continuous infusion of dopamine or furosemide can exert a renoprotective effect in the early postoperative period in patients after cardiac surgery.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Intervention
The study medications and placebo were provided in uniformly appearing
50-ml syringes blinded to attending physicians and nurses involved in intra-
and postoperative care. The syringes, labeled "renal protection,"
contained one of the following:
The infusion rate was 1.5 to 3 ml/h, depending on body weight, to yield 2 µg/kg per min dopamine or 0.5 µg/kg per min furosemide. After induction of anesthesia, infusion of the study drug was started via a central venous line using a motor-driven syringe (Perfusor Secura FT; Braun Medical, Germany). The study medication was continued until discharge of the patient from the intensive care unit (ICU) or 48 h after surgery, whichever came first. Study drug infusion was discontinued when urine output was >2000 ml in 4 h.
Data Acquisition
The primary end point was the change in serum creatinine values over time
(2). Secondary end points were
the occurrence of acute renal injury (ARI), changes in creatinine clearance
over time, urine output per hour, volume intake per hour, serum sodium, serum
potassium, other parameters of renal function (see below), necessity for
hemodialysis or hemofiltration, and hospital mortality rate. ARI was defined
as an increase in serum creatinine values of >0.5 mg/dl between baseline
value and the maximum value within 48 h (Creamax)
(24).
Perioperative Management
Patients were premedicated with midazolam. All patients received standard
general anesthesia with midazolam, etomidate, fentanyl, and pancuronium. In
all patients a central venous catheter, and in two-thirds of the patients a
Swan-Ganz catheter, was inserted for monitoring of hydration state. Ringer's
aspartate (Fresenius Pharma) was infused during induction of anesthesia, and
Ringer's lactate or 6% hydroxy-ethyl-starch (Fresenius Pharma) was infused if
required thereafter. Patients were ventilated with oxygen in air; ventilation
was set to a tidal volume of 8 ml/kg, a respiratory rate of 12/min, and a
positive end-expiratory pressure of 5 mmHg.
The cardiopulmonary bypass circuit consisted of a hollow-fiber oxygenator (Bard HF 5701; C. R. Bard, Inc., Havorhill, MA) primed with Ringer's lactate (2000 ml), mannitol (20 g), heparin (8000 IU) (Immuno, Vienna, Austria), and aprotinin (1,000,000 KIU) (Trasylol; Bayer Pharma, Leverkusen, Germany). Flow during cardiopulmonary bypass was maintained at 2.5 L/min per m2, and mild hypothermia (30 to 32°C) was employed. Myocardial protection consisted of cold, intermittent blood cardioplegia administered via a combination anterograde and retrograde technique. Hematocrit was kept at >20%, with donor blood if necessary. BP was maintained at >50 mmHg by intermittent administration of phenylephrine. After weaning from cardiopulmonary bypass, mean arterial pressure was maintained above 60 mmHg with fluid loading and appropriate vasoactive drugs (epinephrine). Treatment in the ICU was defined by institutional standards.
Blood and Urine Samples
The flow chart of the study protocol is shown in
Figure 1. After preoperative
urine collection (period P0) and urine volume measurement, 10 ml of urine was
collected for analysis. Urine sodium, urine potassium, urine creatinine, urine
urea nitrogen, and urine osmolarity were determined. After inclusion of the
patient in the study, blood was sampled simultaneously with the preoperative
urine (time points T1 and T2) to determine blood urea nitrogen, serum
creatinine, serum sodium, serum potassium, and serum osmolarity. After
surgery, blood samples were collected in the ICU at five time points (T3 to
T7), and urine was collected during four periods (PII to PV). At 5 to 7 d
after surgery (T8), only blood urea nitrogen, serum creatinine, serum sodium,
and serum potassium levels were determined. Creatinine clearance, osmolar
clearance, free-water clearance, and fractional excretion of sodium
(FENa) were calculated by standard formulas:
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Statistical Analyses
Data are expressed as mean ± SD. Statistical analysis was performed
based on intention to treat, with the use of a commercial package (SAS 6.12,
1996, Cary, NC). Continuous demographic data were analyzed using one-way ANOVA
with the Newman-Keuls test for multiple comparisons. Categorical data were
analyzed using 
2 analysis. 
Creamax was
analyzed by ANOVA with one grouping factor, the three randomized treatments;
covariates were creatinine value during the baseline period, duration of
extracorporeal circulation time and aortic cross-clamping time, furosemide
bolus injection, left ventricular function, diabetes, hypertension, the need
for inotropic support, and age over 70 yr. We used a backward elimination
technique, and only covariates with an F > 2 remained in the final
model. The study power was 80% with a P value <0.05 to detect a
difference of 0.14 mg/dl in Creamax between treatment
groups. Comparisons between the three treatments were performed only when the
treatment factor was significant in the ANOVA (SAS 6.12, GLM, Type III SS).
Changes of study variables over time were analyzed by a similar technique. A
P value <0.05 was considered statistically significant.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The study drug was discontinued in two patients in group D and in three patients in group F because urinary output exceeded 2000 ml within the first 4 h. Furosemide bolus injections (20 mg) within 48 h were considered clinically necessary (decrease in urine output to <0.5 ml/kg per h) in 16 of 42 patients in group D, eight of 41 in group F, and 20 of 40 in group P (P < 0.02) (Table 2). In group F, two patients died of myocardial infarction, and two patients died of a mesenteric artery thrombosis. In group P, one patient died from severe sepsis. There were no deaths in group D.
The time course of changes in serum creatinine
(Table 3) showed a significant
increase in group F that started in PII and was significant during PIII and
PIV. Creamax was more pronounced in group F than in both of
the other groups (P < 0.001)
(Figure 2), and creatinine
clearance was lower in group F than in both of the other groups during PII to
PIV (P < 0.05 for PIV). The frequency of ARI was significantly
higher in group F (six of 41) than in group D (one of 42) and group P (zero of
40) (P < 0.01). Renal replacement therapy became necessary in two
patients, both in group F.
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The rise in serum creatinine in group F was preceded by an increase in FENa and an increase in urine output during PII and PIII (Table 3). During PV, an increase in serum creatinine occurred in all groups. Urinary output was compensated by intravenous fluids during all periods.
In a regression analysis to identify factors contributing to the change of serum creatinine, the duration of cardiopulmonary bypass was significant during PII, and the use of additional furosemide bolus injections became significant in PV.
Creamax was increased in patients who received additional
furosemide injections, regardless of the treatment group (P <
0.01). Creamax was directly correlated with duration of
cardiopulmonary bypass (coefficient ± SEM; 0.22 ± 0.04 mg
· dl-1 · h-1) (P < 0.001), but
was negatively correlated with duration of aortic cross-clamp time (-0.19
± 0.07 mg · dl-1 · h-1) (P
< 0.01). For the average of our study population, the effect of
cardiopulmonary bypass and aortic cross-clamp time on
Creamax was about 0.02 mg/dl.
To assess any potential effect of cardiopulmonary bypass time on these
findings, we separately analyzed all patients with a cardiopulmonary bypass
time greater than 2 h. The distribution was comparable between groups: group
D, 14 of 42; group F, 14 of 41; and group P, 10 of 40. Restricting the
analysis to the patients with prolonged cardiopulmonary bypass, results were
similar to those for the whole study population, significant factors being the
study drug (P < 0.01), duration of cardiopulmonary bypass
(P < 0.001), and furosemide bolus injection (P <
0.01). However, Creamax was not dependent on the use of
catecholamines, left ventricular function, history of hypertension, diabetes
mellitus, or age.
The only additional measured parameters that showed a significant difference between groups were FENa and urinary output (Table 3). During all periods, there were no differences between the groups with regard to volume intake per hour, serum sodium, serum potassium, blood urea nitrogen, or osmolar- and free-water clearance (Table 3).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The controversy surrounding the effectiveness of dopamine and/or furosemide in the prevention of postoperative ARF is not new (18,24,26,27,28,29,30). Nevertheless, both substances continue to be widely used in the prevention of perioperative renal injury (12,13,21,26,31). The main effects of furosemide include inhibition of sodium reabsorption and promotion of diuresis, but also vasodilation of cortical vessels. Inhibition of sodium reabsorption mitigates tubular oxygen consumption and thus might enhance renal tolerance to hypoperfusion (21). Augmentation of tubular flow is also considered to be advantageous in several types of ARF by decreasing the tubular concentration of toxins and preventing tubular obstruction (2).
As expected, furosemide significantly augmented diuresis during the perioperative period. Although the overall incidence of renal dysfunction observed in our study was similar to that in other series (1,3,5), plasma creatinine was higher, creatinine clearance was lower, and ARI occurred predominantly in the group receiving furosemide. The simultaneous increase in FENa suggests that sodium reabsorption was effectively inhibited. The negative effects of furosemide on renal function are illustrated by the fact that in subjects in whom additional injections of furosemide were necessary, a significant increase in serum creatinine became apparent in all patient groups.
Thus, in contrast to findings from several animal experiments in which furosemide prevented the development of tubular lesions in isolated rat kidneys during a pulsatile flow perfusion (21), we not only failed to demonstrate a renoprotective effect of furosemide, but even observed the contrary, an impairment of renal function by this loop diuretic. Similar conclusions were drawn in a study in patients undergoing cardiac angiography who received furosemide or mannitol, compared with placebo, to prevent radiocontrast-induced renal damage (24). In that study, as in ours, an increase in serum creatinine values was most pronounced in the group receiving furosemide, and it was concluded that adequate hydration is more effective than pharmacologic interventions in preventing ARF. Moreover, in the case of established ARF, it is well documented that furosemide does not exert any beneficial effects (19).
The negative effect of furosemide on renal function cannot be explained by induction of hypovolemia and a concomitant decrease in renal perfusion as a consequence of high urinary volume. All of our patients were well hydrated and had continuously monitored volume status and filling pressures. Alternatively, neurohumoral activation has been reported with furosemide, and transient rises in BP have been shown to result from activation of the sympathetic and renin-angiotensin systems (32). This can increase peripheral vascular resistance, left ventricular afterload, and cardiac work and can mediate a fall in cardiac output, thus at least potentially aggravating myocardial ischemia (33,34,35). Moreover, induction of maldistribution of renal blood flow with diversion of medullary perfusion by a decrease in cortical vascular resistance might promote tubular dysfunction (24).
Dopamine exerts well characterized effects on renal functions mediated by both vascular and tubular mechanisms (36,37,38), resulting in an increase in renal plasma flow and creatinine clearance and a stimulation of natriuresis and urinary flow. These at least potentially advantageous actions have been documented both in healthy subjects and in patients with various disease processes such as cardiac failure, septicemia, or liver disease (36,37,39). In several controlled trials with dopamine, improvement of several parameters of renal function (although not improved survival) has been reported (40,41,42,43). Even recently, dopamine administration was recommended for surgery patients (44).
Nevertheless, at least for the perioperative period, few data supporting the use of dopamine are available. Low-dose dopamine has been shown to reverse periods of oliguria after cardiopulmonary bypass in an uncontrolled study (36) and to induce diuresis and natriuresis in well hydrated patients compared with a group in whom fluids were restricted (16). However, in patients with normal renal function undergoing coronary revascularization, low-dose dopamine had no beneficial effect on urine flow, creatinine clearance, or incidence of transient renal impairment (45). After major vascular surgery, dopamine (3 µg/kg per min) was administered to 15 patients with a postoperative urinary output of <0.5 ml/kg per h (44). Three of these patients did not increase urinary output after dopamine infusion, and two of the three were treated with additional furosemide bolus injections and developed renal insufficiency.
In our study, the increase in urine output and FENa after cardiopulmonary bypass was nearly identical in group D and group P, as were the changes in renal function; thus, we could not identify a protective effect of dopamine on renal function. Our results are in accordance with several recent reports arguing against the routine use of dopamine for renal protection (2,11,46).
At least potentially, the beneficial effects of dopamine might be masked by untoward actions, such as the blockade of the tubuloglomerular feedback mechanism or maldistribution of intrarenal blood flow (26). Moreover, in the absence of clinically advantageous actions, undesired side effects such as induction of tachyarrhythmia (47), increase in myocardial oxygen consumption (48), inhibitory effects on minute ventilation and oxygen saturation (49,50), and suppression of circulating pituitary-dependent hormones should be taken into consideration (51).
In conclusion, this prospective randomized placebo-controlled trial evaluating the renal protective effect of dopamine or furosemide in cardiac surgery patients did not demonstrate any benefit in favor of these widely used drugs. Our results rather suggest an increased risk for renal impairment in patients receiving furosemide. Neither of these pharmacologic agents should be used in the prevention of development of perioperative ARF in cardiac surgery patients. These results again underscore the importance of maintaining adequate hydration for the prevention of ARF (24).
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