In the August 2004 issue of CHEST, Albanése and colleagues1evaluated 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 × urinary flow rate)/serum creatinine in the head trauma group, and the Cockroft and Gault formula, published in 1976,2in 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 m2. This remains significant after NE infusion, with a mean value of approximately 150 mL/min/1.73 m2. A similar observation was previously published by Benmalek et al3 in 1999. Using the same formula to evaluate GFR in 20 young head trauma patients, also treated with NE, they found values of 132 ± 22 mL/min/1.73 m2. 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 Français 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.