The atrial natriuretic peptide does not serve osmoregulation but predicts outcome following brain injury.

Atrial natriuretic peptide (ANP) plays an important role in body fluid homeostasis. ANP has been established as a marker of cardiac dysfunction and may play a role in brain edema development after traumatic brain injury (TBI). In order to identify its specific assignment following TBI, we related clinical data and treatment variables in 63 patients to longitudinal midregional (MR) proatrail natriuretic peptide (ANP) measurements. ANP correlated significantly to age (p < 0.0001) and vasopressin release (p < 0.001). Following TBI, ANP was increased initially and on day 3 (cut-off 100 pg/L) in 22% of the patients, in 31% on day 7, and was normalized at follow-up examination. The group comparison revealed that ANP levels did not significantly differ with regard to injury severity, but that high ANP levels predicted a worse Glasgow Outcome Score at 6 months (p < 0.05). While the initially intact osmoregulation - a correlation of urine volume and high serum sodium (r = 0.536, p = 0.003) or low urine osmolality (r = -0.556, p = 0.009) - got lost post-injury, the ANP release was triggered by volume load (p < 0.005). High ANP levels correlated with the neuroendocrine stress response, i.e., high cortisol (p = 0.05) and prolactin (p < 0.001) levels. We conclude that MR-proANP measurements reveal a significant predictive function for the prognosis of TBI.