The Fractional S100B Excretion is Attenuated Following Neurotrauma Suggesting an Innate Conservation System for Neurotrophic Proteins

Background/Objectives: S100B is a well-established neuromarker for cerebral damage, with renal elimination playing a key role in interpreting its serum levels. The aim of this study was to assess whether the renal S100B elimination is different in neurotrauma and control patients. Methods. In a prospective single-center study, 129 patients were consecutively enrolled admitted to the intensive care unit either because of traumatic brain injury, subarachnoid hemorrhage, stroke (neurotrauma, n=54) or following elective extracranial surgery (control, n=75). Blood and urine samples were collected daily at 6AM. S100B levels were measured using the LIAISON® Sangtec®100 immunoanalyzer, and creatinine was determined enzymatically with the Advia 2400 Chemistry system. The fractional S100B excretion (FES100B) was calculated using the formula CS100B(urine)*Ccreatinine(serum) /CS100B(serum)*Ccreatinine(urine). Results. Neurotrauma patients were younger than controls (mean 66 vs. 69 years, p=.007) and suffered from less comorbidities (Charlson index 3 vs. 6, p=.009). S100B serum levels increased significantly after neurotrauma, peaking on day 3 and 4 (0.94±1.84µg/l, p=.028 and 0.86±1.67ug/l, p=.027) as compared to control patients. S100B urine levels were increased both in neurotrauma and control patients. The fractional S100B excretion was significantly attenuated on day 3 and 4 (0.18±0.27µg/l, p<.001 and 0.31±0.61ug/l, p=.045) following neurotrauma. Conclusions. The 21kDa dimeric protein S100B is not fully reabsorbed by the kidneys after increased serum release, making urinary measurements a potential alternative for detecting elevated S100B levels. However, the attenuated renal elimination respectively enhanced reabsorption of S100B following neurotrauma may indicate a physiological mechanism to conserve neurotrophic proteins.