| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
* From the Departments of Anesthesiology and Critical Care Medicine; Thoracic and
Cardiac Surgery, Klinikum Ludwigshafen, Ludwigshafen, Germany.
Address correspondence to: Dr. Swen N. Piper, Department of Anesthesiology and Critical Care Medicine, Klinikum Ludwigshafen, Bremserstraße 79, D-67063 Ludwigshafen, Germany. Phone: 0049 621-503-3000; Fax: 0049-621-503-3024; E-mail: swen.n.piper{at}t-online.de
 |
Abstract |
|---|
 TOP Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
-GST), alpha-1-microglobulin (1-MG) and N-acetyl-ß-glucosaminidase (ß-NAG) after extracorporeal circulation.
Methods: In a randomized, placebo-controlled, double-blind trial we evaluated the efficacy of dopamine (2.5 µg•kg-1•min-1), diltiazem (2 µg•kg-1•min-1) or placebo administered over 48 hr postoperatively to maintain renal tubular integrity in 60 elective cardiac surgery patients. -GST, 1-MG, ß-NAG, and creatinine clearance were measured from urine collected during surgery (T0), the first four hours (T1), 24 hr (T2) and 48 hr (T3) postoperatively.
Results: Cumulative urine output in the diltiazem group (9.0 ± 2.8 L) increased significantly compared with placebo (7.0 ± 1.6 L), but not compared with dopamine (7.8 ± 1.8 L). Creatinine clearance showed no significant intergroup differences. In all groups 1-MG increased from T0 to T3, but we found no significant intergroup differences. -GST increased significantly from T0 to T3 in the placebo (2.1 ± 1.8 to 11.4 ± 8.6 µg•L-1) and in the dopamine groups (2.7 ± 1.8 to 13.6 ± 14.9 µg•L-1), but not in the diltiazem group (1.8 ± 1.4 to 3.2 ± 3.2 µg•L-1). Forty-eight hours postoperatively -GST was significantly lower in the diltiazem group than in both other groups.
Conclusions: Diltiazem stimulates urine output, reduces excretion of -GST and ß-NAG and may be useful to maintain tubular integrity after cardiac surgery.
|
Introduction |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Aside from creatinine and its clearance, new sensitive markers of renal dysfunction have become available. Alpha-glutathion s-transferase (-GST) is abundant in the cytosol of proximal renal tubular cells as well as in hepatocytes and small intestinal mucosa.14 The detection of this enzyme in the urine is specific to the proximal tubule.15 It has a molecular weight (mw) of 51 KD.16 -GST has been detected in the urine after proximal tubular damage, while glomerular disorders do not result in an increase of -GST.16 Alpha-1-microglobulin (1-MG) is a low molecular weight glycoprotein (mw 25–33 KD) that is filtered through the glomeruli and reabsorbed in the renal tubules.17 It can be used for diagnosing tubular damage and it is a sensitive marker for the early phase of renal failure.18 N-acetyl-ß-glucosaminidase (ß-NAG) is widely used for the assessment of renal disease and the detection of nephrotoxicity.19 It is a lysosomal enzyme found mainly in proximal tubular cells.20 Elevation of ß-NAG activity in the urine provides an early marker of renal tubular damage.19 Using these markers of renal function and integrity, we studied the influence of dopamine and diltiazem in patients undergoing cardiac surgery. The study drugs differed from other studies9,10,12 and were started after arrival in the intensive care unit (ICU), not during surgery, as we wanted to avoid interference with the surgical procedure.
The primary endpoint of our study was the value of -GST 48 hr postoperatively. The secondary endpoints were the measurements of creatinine clearance, ß-NAG, 1-MG, fluid balance, diuresis, furosemide consumption and hemodynamics. The incidence of ARF requiring hemofiltration was also recorded. Assessment of requirement for hemofiltration was according to clinical criteria by our nephrologists who were blinded to group assessment.
|
Methods |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Ex ante exclusion criteria (screened the day before surgery) were severe left ventricular dysfunction (ejection fraction < 25%), renal insufficiency (creatinine > 177 µmol•L-1), liver dysfunction (aspartate aminotransferase > 40 U•L-1 or alanine aminotransferase > 40 U•L-1), repeat cardiac surgery, known allergy to dopamine or diltiazem, anemia (hemoglobin < 9.0 g•dL-1), insulin-dependent diabetes mellitus and use of diuretics or calcium antagonists. Ex post exclusion criteria were perioperative myocardial infarction, death, and low output syndrome requiring intra-aortic balloon counter pulsation (IABP) and the use of aminoglycosides during the study period or an intolerance to the study drug. Randomization was performed by the use of closed envelopes after inclusion in the study and prior to anesthesia. The groups were, however, closed after enrollment of 20 patients in each group with allocation of additional patients to adjust for ex post excluded patients (balanced randomization). The anesthesiologists in the cardiac operating suite and the physicians in the ICU were blinded to grouping. All study medications were prepared as clear colourless fluids in standard syringe pump systems.
Patients management
All patients received premedication with flunitrazepam (0.02 mg-1•kg-1) 45-60 min before surgery. After the patients arrived in the induction room, a peripheral vein and the left radial artery were cannulated. Induction of anesthesia was performed with midazolam (0.1 mg•kg-1), sufentanil (1 µg•kg-1), and pancuronium (0.1 mg•kg-1). Anesthesia was maintained by continuous infusion of sufentanil and intermittent boli of midazolam and pancuronium. A standard "high-dose" (6 million kallikrein inhibiting units) aprotinin regimen was used in all patients. The CPB circuit was primed with 2000 mL of Ringer’s solution, 500 mL of 3.5% gelatine, 10000 IU heparin, and mannitol 15% (3 mL•kg-1). During CPB the mean arterial pressure (MAP) was kept between 50–70 mmHg using norepinephrine or nitroglycerine. Moderate hypothermia (32°C) was used during CPB. If necessary, Ringer’s solution was given to maintain filling volume. When the hemoglobin was < 7 g•dL-1, packed red blood cells (PRBC) were transfused. During weaning from bypass, the pulmonary capillary wedge pressure (PCWP) was kept between 11–14 mmHg. After termination of CPB, the residual blood remaining in the extracorporeal circuit was concentrated using a cell saving device and retransfused.
All patients were transferred to the ICU and controlled mechanical ventilation was continued during the following four hours at least. Prior to extubation, sedation was maintained using a continuous infusion of propofol and, if necessary, boli of piritramide. At arrival in the ICU patients received either dopamine (2.5 µg•kg-1•min-1) or diltiazem (2 µg•kg-1•min-1) or 0.9% saline as placebo in a double-blind fashion. Ringer’s solution 100 mL•hr-1 was infused. When the urine output was less than 80 mL•hr-1 patients received a diuretic therapy with furosemide (10 mg). Heart rate (HR) MAP, PCWP, systemic vascular resistance (SVR), cardiac output (thermodilution technique), and cardiac index (CI) were measured or calculated from standard formulae. Dobutamine was given when MAP was < 60 mmHg (8 k Pa) and CI was 2.5 L•min-1•m2 in spite of a PCWP ranging from 11 to 14 mmHg. The target for CI was 2.5 to 3.0 L•min-1•m2. Norepinephrine was administered when SVR was < 650 dyn•sec-1•cm5 and MAP was < 60 mmHg. The target for SVR was 650–1000 dyn•sec-1•cm5. If the MAP was above 100 mmHg nitroglycerine was given. PRBC were administrated when the hemoglobin was < 9 g•dL-1 and fresh-frozen plasma (FFP) was used to normalize coagulation if fibrinogen was < 150 mg•dL-1, activated thromboplastin time > 60 sec, antithrombin < 50%.
Data collection
Intraoperative blood losses were recorded. Fluid balance was calculated from crystalloids, gelatine, PRBC and FFP administration, subtracting blood losses and losses from nasogastric drainage. Arterial blood gases and serum creatinine were measured at the end of surgery (T0), four hours (T1), 24 hr (T2) and 48 hr postoperatively (T3). Urine output was measured during surgery (T0), the first four hours in ICU (T1), 24 hr (T2) and 48 hr (T3) postoperatively. We measured urine -GST (Biotrin NEPHKITTM –Alpha; Biotrin International GmbH, Sinsheim-Reihen, Germany). Normal values for -GST in patients undergoing cardiac surgery are not available, but normal values for healthy volunteers are 0–11.1 µg•L-1 (cited from the manufacturer’s instructions). ß-NAG (Cobasmira; Hoffmann-La Roche, Basel, Switzerland; normal value < 0.56 U•mmol-1 creatinine), and 1-MG (Nephelometer; Behring Werke, Marburg, Germany; normal value < 14 mg•L-1) were measured. Creatinine clearance was calculated using standard formulae.
Statistical analysis
When the present study was planed (in 1996) no data on urinary -GST in patients after cardiac surgery were available, therefore no power analysis was possible. The study size of 20 patients in each group was an estimation based on similar studies by Amano et al.10 and Zanardo et al.12 who enrolled 23 in two groups (13 patients received diltiazem and ten patients placebo) and 35 patients in three groups (11 patients received 1 µg•kg-1•min-1 diltiazem, 12 patients 2 µg•kg-1•min-1 diltiazem and 12 patients placebo), respectively. All quantitative data are expressed as mean ± SD. Categorical variables were assessed by using a Chi-square test. Furosemide consumption was analyzed using the rank-sum-test of Raatz.21 Demographic data were analyzed by using a one-way analysis of variance for repeated measures. A SPPS/PC + software package (v 4.0.; SPPS, Inc., Chicago, IL, USA) was used for the statistical analyses (except Raatz-test, for which we used an in-house program). Additionally we compared hemodynamic and renal variables for different periods by using the Wilcoxon rank order test. Only a Bonferroni corrected P-value of 0.05/2 (P < 0.025) was considered as significant.
|
Results |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-GST increased significantly from T0 to T3 in the placebo (2.1 ± 1.8 to 11.4 ± 8.6 µg•L-1) and in the dopamine group (2.7 ± 1.8 to 13.6 ± 14.9 µg•L-1), whereas patients treated with diltiazem (1.8 ± 1.4 to 3.2 ± 3.2 µg•L-1) showed no significant increase (Figure 1
). At T3 the -GST levels were significantly lower in the diltiazem group compared to placebo (P < 0.001) as well as compared to dopamine (P < 0.01; Figure 1). At T3 eight patients in the placebo group showed pathological values compared to seven patients in the dopamine group and one patient receiving diltiazem. An ad hoc Fisher’s exact test showed that the incidence in pathologic values of -GST was significantly different between diltiazem and placebo (P < 0.02) but not between diltiazem and dopamine (P < 0.04).
|
). The three groups did not differ with regard to demographic variables, perioperative data (Table I) and fluid administration, including crystalloids, gelatine, PRBC and FFP. Fluid balance in the diltiazem group was significantly lower compared to placebo on the first postoperative day (Figure 2). In patients treated with dopamine diuresis (mL•hr-1) was significantly higher at T2 and in patients treated with diltiazem at T1 and T2 in comparison with patients of the placebo group (Figure 2). The cumulative urine output in the diltiazem group (8997 ± 2785 mL) was significantly higher compared with placebo (7074 ± 1580 mL), but there were no significant differences between placebo and dopamine (7816 ± 1800 mL) or between diltiazem and dopamine. MAP, HR, and CI were not different between groups (Table II). At T1 PCWP was significantly lower (P < 0.01) in the diltiazem group (7.1 ± 4.0 mmHg) than in the dopamine (12.0 ± 6.4 mmHg) or in the control group (12.0 ± 5.2 mmHg; Table 0II).
|
|
|
). At all time points, there were no differences in ß-NAG-concentrations between all groups (Figure 3). At T3, four patients in the placebo group, two patients in the dopamine group and two patients receiving diltiazem showed pathological values (P < 0.66).
|
|
1-MG levels increased significantly from T0 to T3, showing no significant differences between the groups throughout the study period (Figure 3
). At T3 18 patients in the placebo group showed pathological values compared to 18 patients in the dopamine group and 16 patients receiving diltiazem (P < 0.66). There were no adverse reactions that could be ascribed to the study drugs, especially no allergic reactions and no proven or suspected cardiovascular reactions necessitating discontinuation of the study drugs. No patient developed ARF requiring hemofiltration.
|
Discussion |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
-GST, a parameter of proximal tubule integrity, increased significantly in patients receiving either placebo or dopamine, but not diltiazem 48 hr after cardiac surgery. ß-NAG and 1-MG, both parameters of proximal tubule function, showed no significant intergroup differences.
An important limitation of our study was that it was performed in patients at a comparatively low risk of postoperative renal dysfunction, as patients with a preoperative creatinine higher than 2 mg•dL-1 were excluded. Consequently this is not an outcome study, as the incidence of hemodialysis was zero, as expected. Another limitation was that this was a pilot study for which no ex ante power analysis concerning the main variable (urinary -GST) was possible. Also, we did not perform a formal correction for multiple comparisons. However, as the main result of this study (urinary -GST) was significant at the P < 0.001 level (diltiazem compared to placebo), we can be reasonably sure that the effect is real and not the result of multiple comparisons. -GST may also be released by the gut and the liver. We did not measure -GST in the serum and cannot exclude that the urinary -GST we measured was secondary to extrarenal damage. However, no patient of the present study suffered hepatic failure or a bowel infarction. A further limitation in our study design was that fluid administration was not strictly controlled by the protocol. However, in our study there were no significant differences between the groups concerning fluid administration.
In patients undergoing cardiac surgery a mild degree of renal ischemia occurs secondary to CPB, which may predispose to ARF.12 The mechanism by which CPB causes damage to the kidney is not completely understood. Authors have hypothesized that the excessive release of stress mediators during CPB may be a reason for loss of renal integrity.2,22 Several therapeutic approaches to prevent ARF are used in this situation. Schrier et al. showed that an elevated intracellular calcium is an important factor in developing ARF.23 The normal cell membrane is relatively impermeable to calcium but, secondary to ischemia, a disturbance in permeability arises and calcium flows into the cytoplasm. Consequently the intracellular calcium concentration increases and cell damage may develop.24 Calcium channel blockers appear to possess specific protective effects on the renal tubule.25 Wagner et al. reported on kidney transplant patients who received diltiazem immediately after graft placement. They found that graft function was improved and the incidence of postoperative ARF was less in diltiazem-treated patients.26,27
In our study we observed an increased diuresis in the diltiazem group at four hours and 24 hr and in the dopamine group 24 hr postoperatively compared with placebo. This is in accordance with findings of other authors. Amano et al.10 and Zarnado et al.12 described an improvement of urine output after diltiazem administration in patients undergoing cardiac surgery. The controversy regarding the effect of dopamine on diuresis during cardiac surgery continues. Some authors have reported an increase of urine output after dopamine administration8,28 while others described no effect.29–31 In our study, cumulative urine output was not increased by dopamine, contrary to diltiazem. More specific markers of renal integrity are necessary to completely assess the worth of different renal protective strategies.
Becker and co-workers reported that the nephrotoxicity of tacrolismus following ischemia and reperfusion in rats induced a significant increase of ß-NAG. The additional administration of diltiazem reduced ß-NAG excretion and histological damage without affecting creatinine clearance.32 We calculated creatinine clearance during surgery and in the first four hours in ICU and found no differences between the groups. This differs from Amano et al.10 and Zanardo et al.12 who showed a beneficial influence of diltiazem on glomerular filtration rate. Zanardo and colleagues found an increase of ß-NAG activity in all patients undergoing cardiac surgery. Diltiazem resulted in a smaller (but not significant) increase compared to the control group.12 Similarly, in our study, ß-NAG concentrations were not lower in diltiazem treated patients compared with dopamine and placebo treated patients. Yet, we found no significant differences regarding creatinine clearance. Thus, the protective effect of diltiazem seems to be, at least partially, focused on preventing tubular damage. An investigation by Wagner et al.33 on postischemic ARF in conscious dogs corroborates this inference. They found that when diltiazem was given solely postischemically there was an improvement in renal blood flow, but no influence on glomerular filtration rate. The authors concluded that mainly tubular factors are involved in the protective effect of diltiazem.33 Inhibition of pathological calcium influx into the cells during ischemia or drug-induced nephrotoxicity may be the reason for the protective effect of diltiazem.
In all three groups we found a significant increase of 1-MG, but the rise of 1-MG was not different between groups. A pathological excretion of urinary proteins (e.g., ß-NAG, 1-MG) is a main symptom of kidney dysfunction.34 In contrast to this, an increase of -GST (formerly known as ligandin) is not always associated with renal dysfunction because tubular cells release their cytosolic contents into the urinary space secondary to injury.35 Therefore the value of urinary -GST may reflect the number of tubular cells damaged.36 In fresh kidney biopsies -GST is found exclusively in the proximal tubules.15 Tubular injury is the only phenomenon known to cause an increase in urinary -GST.35
We conclude that both dopamine (24 hr postoperatively) and diltiazem increase diuresis. Tubular function, was not influenced beneficially by any study medication. Only diltiazem decreased the urinary excretion of -GST, an indicator of tubular integrity. Consequently, we assumed that the slight damage to tubular cells after cardiac surgery may be prevented by diltiazem. Renal function was only marginally influenced after cardiac surgery in our patients without prior renal dysfunction. Therefore, at present, we cannot recommend the use of diltiazem on a routine basis in such patients. Whether or not diltiazem may protect high-risk patients for development of ARF needs to be elucidated in further clinical trials.
|
Footnotes |
|---|
Revision received November 29, 2002. Accepted for publication June 3, 2002.
|
References |
|---|
|
TOPAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
2 Kulka PJ, Tryba M, Zenz M. Preoperative 2-adrenergic receptor agonists prevent the deterioration of renal function after cardiac surgery: results of a randomized, controlled trial. Crit Care Med 1996; 24: 947–52.[Medline]
3 Suen WS, Mok CK, Chiu SW, et al. Risk factors for development of acute renal failure (ARF) requiring dialysis in patients undergoing cardiac surgery. Angiology 1998; 49: 789–800.
4 Lema G, Meneses G, Urzua J, et al. Effects of extracorporeal circulation on renal function in coronary surgical patients. Anesth Analg 1995; 81: 446–51.[Abstract]
5 Gamoso MG, Phillips-Bute B, Landolfo KP, Newman MF, Stafford-Smith M. Off-pump versus on-pump coronary artery bypass surgery and postoperative renal dysfunction. Anesth Analg 2000; 91: 1080–4.
6 Lema G, Canessa R, Urzua J. Renal preservation in cardiac surgery. Curr Opin Anesthesiol 1998; 11: 9–13.
7 Bailey JM. Dopamine. One size does not fit all (Editorial). Anesthesiology 2000; 92: 303–5.[Medline]
8 Georghi S. Cardiopulmonary bypass and the kidney. Curr Opin Crit Care 1998; 4: 347–53.
9 Bertolissi M, Antonucci F, De Monte A, Padovani R, Giordano F. Effects on renal function of a continuous infusion of nifedipine during cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1996; 10: 238–42.[Medline]
10 Amano J, Suzuki A, Sunamori M, Tofukuji M. Effect of calcium antagonist diltiazem on renal function in open heart surgery. Chest 1995; 107: 1260–5.
11 Bergman ASF, Odar-Cederlöf I, Westman L. Renal and hemodynamic effects of diltiazem after elective major vascular surgery – a potential renoprotective agent? Renal Failure 1995; 17: 155–63.[Medline]
12 Zanardo G, Michielon P, Rosi P, et al. Effects of a continuous diltiazem infusion on renal function during cardiac surgery. J Cardiothorac Vasc Anesth 1993; 7: 711–6.[Medline]
13 Young EW, Diab A, Kirsh MM. Intravenous diltiazem and acute renal failure after cardiac operations. Ann Thorac Surg 1998; 65: 1316–9.
14 Feinfeld DA, Fuh VL. Urinary glutathione-s-transferase in cisplatin nephrotoxicity in the rat. J Clin Chem Clin Biochem 1986; 24: 529–32.[Medline]
15 Sundberg A, Appelkvist EL, Dallner G, Nilsson R. Glutathione transferases in the urine: sensitive methods for detection of kidney damage induced by nephrotoxic agents in humans. Environ Health Perspect 1994; 102(Suppl 3): 293–6.
16 Backman, L, Appelkvist EL, Ringden O, Dallner G. Urinary levels of basic glutathione transferase as an indicator of proximal tubular damage in renal transplant recipients. Transplant Proc 1989; 21: 1514–6.[Medline]
17 Weber MH, Scholz P, Stibbe W, Scheler F. Alpha 1-microglobulin in the urine and serum in proteinuria and kidney insufficiency (German). Klin Wochenschr 1985; 63: 711–7.[Medline]
18 Yu H, Yanagisawa Y, Forbes MA, Cooper EH, Crockson RA, MacLeennan ICM. Alpha-1-microglobulin: an indicator protein for renal tubular function. J Clin Pathol 1983; 36: 253–9.
19 Price RG. Measurement of N-acetyl-ß-glucosaminidase and its isoenzymes in urine methods and clinical applications. Eur J Clin Chem Clin Biochem 1992; 30: 693–705.[Medline]
20 Kumle B, Boldt J, Piper S, Schmidt C, Suttner S, Salopek S. The influence of different intravascular volume replacement regimens on renal function in the elderly. Anesth Analg 1999; 89: 1124–30.
21 Raatz U. A modification of the White tests for large random samples (German). Biom Z 1966; 8: 42–54.[Medline]
22 Lehot JJ, Villard J, Piriz H, et al. Hemodynamic and hormonal responses to hypothermic and normothermic cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1992; 6: 132–9.[Medline]
23 Schrier RW, Arnold PE, Van Putten VJ, Burke TJ. Cellular calcium in ischemic acute renal failure: role of calcium entry blockers. Kidney Int 1987; 32: 313–21.[Medline]
24 Pomer S, Drexler U, Wiesel M, Kälble T, Staehler G, Möhring K. Calcium channel blockers in acute renal failure after kidney transplantation – a comparison of diltiazem and nifedipine (German). Nieren Hochdruck 1994; 23: 493–502.
25 Rodicio JL, Morales JM, Alcazar JM, Ruilope LM. Calcium antagonists and renal protection. J Hypertens 1993; 11(Suppl. 1): S49–S53.
26 Wagner K, Albrecht S, Neumayer HH. Prevention of posttransplant acute tubular necrosis by the calcium antagonist diltiazem: a prospective randomized study. Am J Nephrol 1987; 7: 287–91.[Medline]
27 Wagner K, Albrecht S, Neumayer HH. Prevention of delayed graft function in cadaveric kidney transplantation by a calcium antagonist. Preliminary results of two prospective randomized trials. Transplant Proc 1986; 18: 510–5.
28 Carcoana OV, Hines RL. Is renal dose dopamine protective or therapeutic? Yes. Crit Care Clin 1996; 12: 677–85.[Medline]
29 Myles PS, Buckland MR, Schenk NJ, et al. Effect of "renal-dose" dopamine on renal function following cardiac surgery. Anaesth Intensive Care 1993; 21: 56–61.[Medline]
30 Perdue PW, Balser JR, Lipsett PA, Breslow MJ. "Renal dose" dopamine in surgical patients. Dogma or science? Ann Surg 1998; 227: 470–3.[Medline]
31 Tang ATM, El-Gamel A, Keevil B, Yonan N, Deiraniya AK. The effect of "renal-dose" dopamine on renal tubular function following cardiac surgery: assessed by measuring retinol binding protein (RBP). Eur J Cardiothorac Surg 1999; 15: 717–22.
32 Becker G, Witzke O, Baltes A, Hamar P, Philipp T, Heemann U. Diltiazem minimizes tubular damage due to FK506-mediated nephrotoxicity following ischemia and reperfusion in rats. Transpl Immunol 1996; 4: 68–71.[Medline]
33 Wagner K, Schulze G, Molzahn M, Neumayer HH. The influence of long-term infusion of the calcium antagonist diltiazem on postischemic acute renal failure in conscious dogs. Klin Wochenschr 1986; 64: 135–40.
34 Dati F, Lammers M. Immunochemical methods for determination of urinary proteins (albumin and 1 microglobulin) in kidney disease. JIFCC 1989; 1: 68–77.
35 Sherman RA, Feinfeld DA, Ohmi N, Arias IM, Levine SD. A prospective study of urinary ligandin in patients at risk of renal tubular injury. Uremia Invest 1985; 8: 111–5.
36 Daemen JWHC, Oomen APA, Janssen MA, et al. Glutathione s-transferase as predictor of functional outcome in transplantation of machine-preserved non-heart-beating donor kidneys. Transplantation 1997; 63: 89–93.[Medline]
This article has been cited by other articles:
 |
|
 |
|
  M. H. Rosner, D. Portilla, and M. D. Okusa Analytic Reviews: Cardiac Surgery as a Cause of Acute Kidney Injury: Pathogenesis and Potential Therapies J Intensive Care Med, January 1, 2008; 23(1): 3 - 18. [Abstract] [PDF]
|
|
|
|
 |
|
 D. N. Wijeysundera, W. S. Beattie, V. Rao, J. T. Granton, and C. T. Chan N-acetylcysteine for preventing acute kidney injury in cardiac surgery patients with pre-existing moderate renal insufficiency: [Recours a la N-acetylcysteine pour prevenir une atteinte renale aigue chez les patients de chirurgie cardiaque souffrant d'une insuffisance renale moderee preexistante] Can J Anesth, November 1, 2007; 54(11): 872 - 881. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. H. Rosner and M. D. Okusa Acute Kidney Injury Associated with Cardiac Surgery Clin. J. Am. Soc. Nephrol., January 1, 2006; 1(1): 19 - 32. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. W. Sear Kidney dysfunction in the postoperative period Br. J. Anaesth., July 1, 2005; 95(1): 20 - 32. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. O. Friedrich, N. Adhikari, M. S. Herridge, and J. Beyene Meta-Analysis: Low-Dose Dopamine Increases Urine Output but Does Not Prevent Renal Dysfunction or Death Ann Intern Med, April 5, 2005; 142(7): 510 - 524. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Manabe, H. Tanaka, T. Yoshizaki, N. Tabuchi, H. Arai, and M. Sunamori Effects of the Postoperative Administration of Diltiazem on Renal Function After Coronary Artery Bypass Grafting Ann. Thorac. Surg., March 1, 2005; 79(3): 831 - 835. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
