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Ann Thorac Surg 1998;65:1588-1593
© 1998 The Society of Thoracic Surgeons

Original articles: cardiovascular

Hyperglycemia During Normothermic Cardiopulmonary Bypass: The Role of the Kidney

Hal Braden, MDa, Surinder Cheema-Dhadli, PhDb, C. David Mazer, MDa, David J. McKnight, MDa, William Singer, MDb, Mitchell L. Halperin, MDb

a Department of Anesthesia, St. Michael’s Hospital, University of Toronto, Toronto, Ontario, Canada
b Department of Medicine, St. Michael’s Hospital, University of Toronto, Toronto, Ontario, Canada

Accepted for publication January 9, 1998.

Address reprint requests to Dr Mazer, Department of Anesthesia, St. Michael’s Hospital, 30 Bond St, Toronto, Ont M5B 1W8 Canada
e-mail: (mazerd{at}smh.toronto.on.ca)


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Hyperglycemia commonly occurs during cardiopulmonary bypass. We studied the quantitative impact of glucose input and its renal excretion on hyperglycemia during cardiopulmonary bypass.

Methods. The quantity of glucose infused and metabolite and hormone concentrations in plasma, as well as oxygen consumption, carbon dioxide production, and renal glucose excretion, were determined before, during, and after cardiopulmonary bypass in 8 patients.

Results. Hyperglycemia (14 to 29 mmol/L) was accompanied by an increase in plasma insulin levels. The degree of hyperglycemia was directly related to the amount of glucose infused. The rate of oxygen consumption did not decrease and the rate of urea appearance (gluconeogenesis) did not rise. Despite a very high filtered load of glucose, there was very little glucosuria, indicating a markedly enhanced renal absorption of glucose.

Conclusions. Hormonal and metabolic factors permit the development of hyperglycemia during cardiopulmonary bypass but its severity depends on the quantity of glucose infused and, what appears to be a new finding, a markedly enhanced renal reabsorption of filtered glucose. Thus the kidney plays an important role in the development of severe hyperglycemia during cardiopulmonary bypass.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Hyperglycemia is frequently observed during cardiopulmonary bypass (CPB) [1]. This hyperglycemia could be detrimental to organs such as the brain, which may be rendered ischemic and then reperfused [1]. Indeed, hyperglycemia has been shown to be associated with a poorer neurologic outcome after global or focal cerebral ischemia [2, 3]. As with other substrates in the body, the concentration of glucose in plasma depends on the interaction of its input into the body, shifts into and out of storage compartments, oxidation, and excretion into the urine.

Previous authors have speculated that hyperglycemia during CPB is caused by exogenous administration of glucose either in intravenous or in cardioplegia fluids [4, 5]. Others have suggested that the shifts of glucose are deranged during CPB because of altered hormone levels (reviewed in reference [6]), and that this leads to the observed hyperglycemia. The rate of consumption of glucose as a fuel during CPB is known to be less than during normal conditions [5, 7, 8]. There is little information on the role of the kidney in this setting with respect to influencing the degree of hyperglycemia once hormonal derangements are present to permit a higher blood sugar level.

Normally, the kidney filters and then reabsorbs glucose from the filtrate to a maximum of close to 10 mmol/L of glomerular filtrate. This level is called the tubular threshold for glucosuria [9]. If a renal threshold for glucose exists, serum glucose levels in excess of this threshold should cause the appearance of appreciable amounts of glucose in the urine. At the nephron level, some nephrons behave as if they have a smaller capacity to reabsorb filtered glucose—thus, there is a small degree of glucosuria before the overall tubular maximum for its reabsorption is reached (splay in the glucose filtration curve [9]). Conditions with hyperglycemia, a well-maintained glomerular filtration rate (GFR), and little glucosuria are rare in clinical medicine. Overall, either a reduction in GFR or an increase in the renal threshold (ie, enhanced reabsorption of glucose) could give rise to a more severe degree of hyperglycemia, if combined with a large enough intravenous glucose load. Although GFR is generally thought to be well maintained during CPB [10], we were interested in the role of enhanced tubular reabsorption of glucose as a possible cause of the marked hyperglycemia often seen during CPB. This prospective study was designed to quantify and evaluate the contribution of glucose input and its renal excretion to the elevated serum glucose levels noted during CPB.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
After Ethics Committee approval and informed consent were obtained, 8 patients who were free of renal disease and diabetes mellitus and who were undergoing CPB for elective coronary artery bypass grafting or valve operations were studied. Administration of all concurrent cardiac medications was continued up until the time of operation. Patients were premedicated with benzodiazepines or morphine and perphenazine as indicated. Anesthesia was induced with fentanyl, 50 µg/kg, midazolam, 40 µg/kg, and pancuronium, 0.1 mg/kg, followed by further increments of fentanyl, midazolam, and enflurane as appropriate. Radial artery and pulmonary artery catheters were placed in all patients for pressure monitoring and for blood sampling. After sternotomy and placement of single-stage atrial and aortic cannulas, CPB was initiated using a nonpulsatile pump and membrane oxygenator primed with 2 L of Ringer’s lactate solution. During CPB, systemic flows were maintained at greater than 2.5 L · m-2 · min-1, and body temperature was kept between 33° and 38°C. Mean arterial pressure was maintained between 50 and 90 mm Hg with the use of phenylephrine or isoflurane as appropriate. Blood cardioplegia consisting of 4 parts blood and 1 part Freme’s solution (KCl, 100 or 30 mmol/L; THAM, 12 mmol/L; MgSO4, 9 mmol/L; and CPD with adenine, 20 mL in 5% dextrose) was used to induce and maintain cardiac arrest during the surgical procedure. After an induction dose of approximately 1 L, cardioplegia was delivered continuously, or intermittently after each distal anastomosis at the discretion of the attending surgeon. The only intraoperative fluid administered that contained glucose was the cardioplegic solution. Thus, the exogenous glucose load was determined from the amount of cardioplegic solution given to each patient plus the lactate in the Ringer’s lactate solution.

Protocol
Samples of urine and arterial and mixed venous blood were obtained at the following intervals: before CPB (and before the administration of heparin), 15 minutes after initiation of CPB, 30 minutes after initiation of CPB, at the termination of CPB, on arrival in the intensive care unit, and approximately 2 hours after arrival in the intensive care unit. The samples were analyzed for blood gases, electrolytes, glucose, L-lactate, free fatty acids, urea, creatinine, albumin, and hormone levels (see next section). At each of these measurement intervals, cardiac output was measured either by using thermodilution techniques or by measurement of CPB flow rate.

Analytical methods
At each time point, the blood samples for analysis of L-lactate and glucose were mixed immediately with a measured volume of ice-cold 10% perchloric acid and centrifuged. The concentrations of glucose and L-lactate in the protein-free supernatant were determined by enzymatic methods as previously described [11]. Urine electrolytes, creatinine, and urea were also measured as previously described [11]. Oxygen tension, carbon dioxide tension, and pH were measured immediately at 37°C using a medical blood gas analyzer (Radiometer, Copenhagen, Denmark). Insulin, cortisol, and growth hormone were measured using radioimmunoassay techniques, and urinary catecholamines were determined by high-pressure liquid chromatography [12].

Calculations
Arterial and mixed venous oxygen content were determined as previously described [11]. Glomerular filtration rate was estimated from the creatinine clearance. The quantity of glucose reabsorbed was calculated as its filtered load minus that excreted. The expected amount of glucose in the urine was determined as (serum glucose - 10) x GFR x time. The fractional excretion of sodium, chloride, and urea were calculated as previously described.

Statistical analyses
Data were analyzed using repeated measures analysis of variance and Dunnett’s t test where appropriate, with p less than 0.05 being considered statistically significant. Data are reported as mean ± standard error of the mean.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
The clinical characteristics of the study patients are listed in Table 1. The quantity of glucose administered ranged from 16 to 65 g. The average amount of cardioplegia given was 234 ± 46 mL of high-potassium solution and 594 ± 108 mL of low-potassium solution. Hyperglycemia developed in all patients with peak values occurring at 30 minutes after initiation of CPB (Table 2). The range of peak values for blood sugar was 14 to 29 mmol/L (250 to 410 mg/dL). The measured maximum serum glucose during CPB correlated directly with its anticipated level if all the glucose administered was retained in its volume of distribution (Fig 1). This rise in blood glucose was associated with a large, parallel, and significant rise in plasma insulin (Table 2). Although the levels of norepinephrine, epinephrine, and cortisol tended to rise in most patients, these changes were not statistically significant (Table 2). The level of growth hormone rose markedly at the end of CPB. The fatty acid level in plasma was very high after induction of anesthesia (1.7 mmol/L) at a time when the blood sugar level was in the normal range (6 ± 1 mmol/L). The amount of phenylephrine administered during CPB (0 to 8 mg total) did not correlate with the measured maximum serum glucose level. There were two other changes that were striking during CPB—the fall in plasma albumin (Table 2) and hematocrit (Table 3), reflecting dilution with the solution in the CPB reservoir.


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  		Table 1. Demographic Data

 

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  		Table 2. Metabolites and Hormonesa

 


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  		Fig 1. Relationship between the predicted plasma glucose level based on the quantity of glucose infused and the maximum plasma glucose concentration during cardiopulmonary bypass. The solid line is the regression line, p < 0.05; the dashed line is the line of identity.

 

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  		Table 3. Oxygen Delivery and Consumptiona

 
The initiation of CPB led to only small changes in acid-base status, electrolytes, and blood gases (Table 4); the only significant change was the development of a modest degree of hyponatremia reflecting both the sodium concentration ([Na]) in the reservoir solution (130 mmol/L) and the hyperglycemia (see Tables 2, 4). The plasma creatinine level remained relatively constant and in the normal range in all subjects; of special importance, there was no rise in the plasma creatinine level during periods when hyperglycemia was present. Similarly, there was no rise in the plasma urea level throughout CPB (see Table 4).


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  		Table 4. Blood Gases and Plasma Electrolytesa

 
Urinary parameters are shown in Table 5. The rate of filtration and excretion of glucose was monitored as hyperglycemia developed. Comparison of the observed level of glucosuria and the level expected assuming a normal tubular threshold are shown in Figure 2. Despite plasma glucose levels as high as 28.7 mmol/L (410 mg/dL), there was surprisingly little glucosuria. During a glucose-induced osmotic diuresis, typical values for urinary glucose are 300 mmol/L [13]. Therefore, urine glucose concentrations that are less than 5% of this expected value imply either a very low filtered load of glucose (low GFR) or an enhanced renal reabsorption of glucose. Because the GFR, as reflected by the clearance of creatinine (see Table 5), did not fall when hyperglycemia was at peak value, the results suggest an enhanced renal reabsorption of glucose. To evaluate whether there was a more generalized enhanced proximal tubular reabsorption, the fractional excretion of Na, Cl, and urea were calculated. As shown in Table 5, there was a significant rise in the fractional excretions of Na and Cl, and no change in the fractional excretion of urea. Hence hypovolemia is not evident as a cause for enhanced renal reabsorption of glucose.


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  		Table 5. Urine Biochemistrya

 


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  		Fig 2. Relationship between expected and observed renal glucose excretion. The line of identity (dashed line) represents perfect matching of expected and observed renal glucose excretion assuming a tubular maximum for glucose reabsorption of 10 mmol/L for glucose.

 
Other metabolic pathways of glucose metabolism were also evaluated. As shown in Tables 4 and 5, the plasma level and the rate of excretion of urea did not rise appreciably, suggesting that there was not a large increment in the conversion of protein to glucose [14]. Oxygen delivery and consumption were relatively unchanged throughout the procedure, as was carbon dioxide production (see Table 3).


   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
The principal finding in this study is the markedly low rate of renal excretion of glucose in patients in whom a modestly severe degree of hyperglycemia developed during CPB. Normally, virtually all the filtered glucose is reabsorbed in the proximal convoluted tubule through a cotransport system driven by active reabsorption of Na [15]. When hyperglycemia is present, the filtered load of glucose rises and more glucose is filtered and reabsorbed. When the quantity of glucose filtered rises enough, glucosuria develops. Typical values for the maximum rate of reabsorption of glucose are close to 1,800 mmol/day (324 g/day) and glucosuria is seen when the plasma glucose exceeds 10 mmol/L (180 mg/dL, the tubular maximum for glucose reabsorption) [9]. Therefore, the finding of very little glucosuria in the patients of this study who show a marked degree of hyperglycemia (considerably greater than 10 mmol/L) suggests an important renal contribution in this setting.

The two possible mechanisms for the relatively low amount of glucosuria are a marked reduction in GFR or increased tubular reabsorption of glucose. Because GFR did not appear to decrease significantly and a decrease in GFR would have had to be extremely large to explain the near absence of glucosuria, enhanced reabsorption of glucose by the proximal convoluted tubule is a more likely explanation for the unexpectedly low degree of glucosuria in the face of hyperglycemia in this setting. The mechanism for the increased tubular reabsorption of glucose seen during CPB is not known, but could be related to alterations in the glucose transport mechanism, nonpulsatile flow, or the decreased hematocrit and albumin levels that occur during CPB. The activity of the glucose transporter appears to undergo regulation. There is a membrane-associated protein that modifies activity of the Na-dependent renal glucose transporter [16]; whether CPB or hypothermia affect glucose transporter kinetics is unknown.

The effect of nonpulsatile flow on organ function is controversial. Some but not all studies have demonstrated greater L-lactate levels with nonpulsatile flow when compared with pulsatile [17, 18]. Some authors have noted better preservation of renal blood flow with pulsatile CPB [19]. It is interesting to note that hyperglycemia of similar magnitude has been observed despite the higher serum levels of insulin noted with pulsatile [17] versus nonpulsatile CPB, perhaps implying that these factors are less important than renal considerations.

Perhaps the very large and acute decrease in plasma albumin and hematocrit during CPB together with the alteration in blood flow characteristic of CPB are perceived by the kidney as a decrease in extracellular fluid volume, leading to a greater than expected glucose reabsorption. However, the higher fractional excretions of Na and Cl, and the absence of a fall in the fractional excretion of urea during periods of hyperglycemia are not consistent with a low effective circulating volume. A series of physiologic manipulations was undertaken in dogs by Schultze and colleagues in 1973 [20]; the extracellular fluid volume was expanded and this was followed by an acute hemorrhage. This did in fact lead to alterations in the tubular maximum for glucose reabsorption, although not to the extent seen in our patients.

Input of glucose occurs either from exogenous sources, glycogenolysis, or gluconeogenesis. True gluconeogenesis (amino acids to glucose) [21], cannot be implicated in the observed hyperglycemia because urea appearance rates are only high enough to raise the concentration of glucose by a maximum of 4 mmol/L (as protein is converted to glucose, 1.72 mmol of urea is liberated for each mmol of glucose generated [21]). Instead, the serum levels observed correspond closely to the exogenous loads administered. Glucose tends to distribute in the extracellular plus the intracellular fluid of organs such as the liver where insulin does not influence glucose transport (reviewed in [13]). This means that glucose distributes in about half of the body water, or 20 L for simplicity in the average 70-kg patient. Because the mean rise in glycemia was 10 mmol/L (see Table 2), an additional 200 mmol of glucose would be retained in the body of an average 70-kg patient during CPB. This number closely reflects the quantity of glucose infused (30 g glucose = 167 mmol). In this study, there was a correlation between the quantity of glucose infused and the rise in glycemia in each patient.

Insulin levels rose when hyperglycemia developed, suggesting that the hyperglycemia was not caused by a simple lack of this hormone. Although catecholamine levels rose in most patients during periods of hyperglycemia, the changes failed to reach statistically significant levels. Finally, a decrease in oxidation of glucose may not be an important cause of hyperglycemia during CPB because oxygen consumption and respiratory quotient remained relatively constant throughout the procedure (see Table 3).

There are some limitations to our study. Although creatinine clearance is not the best way to measure GFR, it does provide a reasonable reflection of this parameter when in the normal range [22]. In addition, we chose to study a currently used clinical temperature management strategy for CPB. Others have found a rise in serum glucose levels during normothermic CPB, even without glucose administration [5, 8]. Although we believe similar results may occur with other CPB techniques, further studies to confirm our findings are required.

In summary, we have found that the kidneys play an important and previously unrecognized role in the maintenance of marked hyperglycemia during CPB. Although hormonal and metabolic factors provide the basis to develop hyperglycemia, its severity depends on the quantity of glucose infused and the markedly enhanced renal reabsorption of filtered glucose. In a broader context, perhaps the more severe degrees of hyperglycemia seen in a number of other clinical settings, such as brittle diabetes mellitus, may in part also be the result of an increased capacity of the renal tubules to reabsorb glucose.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
Supported by a grant from the Medical Research Council of Canada.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Lanier W.L. Glucose management during cardiopulmonary bypass: cardiovascular and neurologic implications. Anesth Analg 1991;72:423-427.[Free Full Text]
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  3. Pulsinelli W.A., Levy D.E., Sigsbee B., Scherer P., Plum F. Increased damage after ischemic stroke in patients with hyperglycemia with or without established diabetes mellitus. Am J Med 1983;74:540-544.[Medline]
  4. Mescheryakov A.V., Kozlov I.A., Dementyeva I.I., Lakhter M.A., Ermolyn A.F., Galyibin A.A. Glucose metabolism and insulin activity during cardiac surgery. J Cardiothorac Anesth 1989;3:536-543.[Medline]
  5. Kuntschen F.R., Galetti P.M., Hahn C., Arnulf J.J., Isetta C., Dor V. Alterations of insulin and glucose metabolism during cardiopulmonary bypass under normothermia. J Thorac Cardiovasc Surg 1985;89:97-106.[Abstract]
  6. Taylor S.I., Accili D., Imai Y. Perspectives in diabetes: insulin resistance or insulin deficiency; which is the primary cause of NIDDM?. Diabetes 1994;43:735-740.[Medline]
  7. Yokota H., Kawashima Y., Takao T., Hasimoto S., Manabe H. Carbohydrate and lipid metabolism in open-heart surgery. J Thorac Cardiovasc Surg 1977;73:543-548.[Abstract]
  8. Kuntschen F.R., Galetti P.M., Hahn C. Glucose–insulin interactions during cardiopulmonary bypass. Hypothermia versus normothermia. J Thorac Cardiovasc Surg 1986;91:451-459.[Abstract]
  9. In: Deetjen P., Baeyer H.V., Drexel H., eds. Renal glucose transport, 2nd ed. New York: Raven Press, 1992:2873-2888.
  10. Weinstein G.S., Rao P.S., Vretakis G., Tyras D.H. Serial changes in renal function in cardiac surgical patients. Ann Thorac Surg 1989;48:72-76.[Abstract]
  11. Halperin M.L., Vinay P., Gougoux A., Pichette C., Jungas R.L. Regulation of the maximum rate of renal ammoniagenesis in the acidotic dog. Am J Physiol 1985;248:F607-F615.
  12. Ruder H.J., Guy R.L., Lipsett M.B. A radioimmunoassay for cortisol in plasma and urine. J Clin Endocrinol Metab 1972;35:219-224.[Abstract/Free Full Text]
  13. Halperin M.L., Goguen J.M., Scheich A.M., Kamel K.S. Clinical consequences of hyperglycemia and its correction. In: Seldin D.W., Giebisch G., eds. Clinical disturbances of water metabolism. New York: Raven Press, 1993:249-272.
  14. Jungas R.L., Halperin M.L., Brosnan J.T. Lessons learnt from a quantitative analysis of amino acid oxidation and related gluconeogenesis in man. Physiol Rev 1992;72:419-448.[Abstract/Free Full Text]
  15. Kanai Y., Lee W.-S., You G., Brown D., Hediger M.A. The human kidney low affinity Na+/glucose cotransporter SGLT2: delineation of the major renal reabsorptive mechanism for D-glucose. J Clin Invest 1994;93:397-404.
  16. Veyhl M., Spangenberg J., Puschel B., et al. Cloning of a membrane-associated protein which modifies activity and properties of the Na+-D-glucose cotransporter. J Biol Chem 1993;268:25041-25053.[Abstract/Free Full Text]
  17. Nagaoka H., Innami R., Watanabe M., Satoh M., Murayama F., Funakoshi N. Preservation of pancreatic beta cell function with pulsatile cardiopulmonary bypass. Ann Thorac Surg 1989;48:798-802.[Abstract]
  18. Louagie Y.A., Conzalez M., Collard E., et al. Does flow character of cardiopulmonary bypass make a difference?. J Thorac Cardiovasc Surg 1992;104:1628-1638.[Abstract]
  19. Nakamura K., Koga Y., Sekiya R., et al. The effects of pulsatile and nonpulsatile cardiopulmonary bypass on renal blood flow and function. Jpn J Surg 1989;19:334-335.[Medline]
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