To the Editor:
In the August 2004 issue of CHEST, Albanese and colleagues (1) evaluated the effect of norepinephrine (NE) in 26 patients, especially 12 patients with head trauma without infection. The glomerular filtration rate (GFR) was assessed using the formula (urinary creatinine x urinary flow rate)/serum creatinine in the head trauma group, and the Cockroft and Gault formula, published in 1976, (2) in the septic shock group. We were surprised, despite missing data, that mean the GFR was above the normal value in the head trauma patients, approximately 165 mL/min/ 1.73 [m.sup.2]. This remains significant after NE infusion, with a mean value of approximately 150 mL/min/1.73 [m.sup.2]. A similar observation was previously published by Benmalek et al (3) in 1999. Using the same formula to evaluate GFR in 20 young head trauma patients, also treated with NE, they found values of 132 [+ or -] 22 mL/min/1.73 [m.sup.2]. No more explanation was provided. Renal failure is a common complication observation observed after acute brain injury. (4) Indeed, in our knowledge, no other data concerning the increase of GFR in head trauma patients have been published. To confirm this fact, we retrospectively reviewed the charts of brain-dead patients undergoing renal sharing for transplantation. Data were provided by the Etablissement Francais des Greffes when one of our patients was selected to undergo transplantation. During the last 6 months, 58 renal grafts were proposed, obtained in 58 heart-beating donors. In 20 cases, data concerning the donor were insufficient to evaluate GFR before brain death. We also excluded four patients dead after cardiocirculatory arrest and two who died from meningitis. We studied the 32 remaining patients classified as head trauma or stroke (ischemic or hemorrhagic). With one exception, they were treated with NE to obtain a mean arterial pressure > 75 mm Hg. Data were obtained before brain death. The GFR was calculated using the Cockroft and Gault formula, or the recently proposed Modified Diet in Renal Disease formula. (5) We confirmed the existence of hyperfiltration in patients with head trauma (Table 1). No known factors may explain this fact. There was no difference in age, incidence of diabetes mellitus (one in both groups), body mass index, or use of medications as cimetidine or trimethoprime available to diminish the tubular secretion of creatinine. No woman was pregnant. Two questions arise from this. First is the physiologic comprehension: difference in sympathetic tone, neurotransmitters, use of renal functional reserve, difference in nutritional support? Second is the value to study the "renal" effect of NE in patients with such "supranormal" renal function. Other studies are needed to get answers.
Francois Vincent, MD
Noujoud El-Khoury, MD
Guillaume Bonnard, MD
Eric Rondeau, MD, PhD
Tenon University Hospital
Paris, France
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/misc/reprints.shtml).
Correspondence to: Francois Vincent, MD, Department of Renal Intensive Care Unit, Hopital Tenon, 4, Rue De La Chine, 75020 Paris, France; e-mail: frncsvncnt@aol.com
REFERENCES
(1) Albanese J, Leone M, Garnier F, et al. Renal effects of norepinephrine in septic and nonseptic patients. Chest 2004; 126:534-539
(2) Cockroft DW, Gault MH, Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16:31-37
(3) Benmalek F, Behforouz N, Benoist JF, et al. Renal effects of low-dose dopamine during vasopressor therapy for posttraumatic intracranial hypertension. Intensive Care Med 1999; 25:399-405
(4) Davenport A. Renal replacement therapy in the patient with acute brain injury. Am J Kidney Dis 2001; 37:457-466
(5) Levey AS, Bosch JP, Lewis JB, et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Ann Intern Med 1999; 130:461-470
COPYRIGHT 2005 American College of Chest Physicians
COPYRIGHT 2005 Gale Group
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