Abstract
Background: S100B protein is a well-established marker of brain damage. Its importance in urine assessment is the convenience of a collection and sampling procedure that can be repeated without risk for the newborn. Since S100B is mainly eliminated by the kidneys and perinatal asphyxia (PA) is often associated with kidney failure we investigated whether S100B release might be kidney-mediated, thereby modifying the protein's reliability as a brain-damage marker. Methods: We examined a cohort of healthy (n = 432) and asphyxiated newborns (n = 32) in whom kidney function parameters (blood urea and creatinine concentrations and urine gravity) and urine S100B concentrations were assessed in the first hours after birth. Data were analyzed by multiple logistic regression analysis with S100B as independent variable among a variety of clinical and laboratory monitoring parameters. Results: s100B urine concentrations were significantly higher (P0.05, for all) between total urine S100B levels and kidney function parameters such as creatinine (r = 0.03), urea (r = 0.04) and urine gravity (r = 0.06) were found. Multiple logistic regression analysis of a series of clinical and laboratory monitoring parameters (odds ratio at sampling: 9.47) with S100B as independent variable showed a positive significant correlation only between S100B levels (P
Original language | English |
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Pages (from-to) | 150-153 |
Journal | Clinica Chimica Acta |
Volume | 413 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 18 Jan 2012 |
Keywords
- Asphyxia
- Hypoxic-ischemic encephalopathy
- Kidney function
- Newborn
- S100B protein
- Brain