Traumatic hematuria in children can be evaluated as in adults.

PURPOSE: Controversy exists regarding whether children who present with blunt abdominal trauma and microhematuria should undergo renal imaging. Adult blunt trauma victims who present without gross hematuria, shock, or significant deceleration or other major associated injuries do not require renal imaging. This study was designed to evaluate whether the criteria for imaging the renal parenchyma in adult blunt trauma victims apply to the pediatric population. MATERIALS AND METHODS: We retrospectively reviewed 720 consecutive pediatric patients with suspected renal trauma to determine mechanism of injury, evaluation and treatment of subsequent injuries. RESULTS: Of the 720 trauma patients with hematuria (mean age 8 years) 334 underwent imaging, and 59 renal injuries were identified (grade I 32, grade II 6, grade III 8, grade IV 12, grade V 1). A total of 11 patients underwent exploration, resulting in 3 nephrectomies (grade IV 2, grade V 1). Renorrhaphy was not necessary and all other cases were managed conservatively. All patients with significant renal injuries experienced either gross hematuria, shock (systolic blood pressure less than 90 mm Hg) or a significant deceleration injury. CONCLUSIONS: The decision to image pediatric trauma cases based on the adult criteria of gross hematuria, shock and significant deceleration injury is appropriate. Among 720 pediatric cases of potential renal injury all would have been identified.

Maspin expression inhibits osteolysis, tumor growth, and angiogenesis in a model of prostate cancer bone metastasis.

Emerging evidence indicates that tumor-associated proteolytic remodeling of bone matrix may underlie the capacity of tumor cells to colonize and survive in the bone microenvironment. Of particular importance, urokinase-type plasminogen activator (uPA) has been shown to correlate with human prostate cancer (PC) metastasis. The importance of this protease may be related to its ability to initiate a proteolytic cascade, leading to the activation of multiple proteases and growth factors. Previously, we showed that maspin, a serine protease inhibitor, specifically inhibits PC-associated uPA and PC cell invasion and motility in vitro. In this article, we showed that maspin-expressing transfectant cells derived from PC cell line DU145 were inhibited in in vitro extracellular matrix and collagen degradation assays. To test the effect of tumor-associated maspin on PC-induced bone matrix remodeling and tumor growth, we injected the maspin-transfected DU145 cells into human fetal bone fragments, which were previously implanted in immunodeficient mice. These studies showed that maspin expression decreased tumor growth, reduced osteolysis, and decreased angiogenesis. Furthermore, the maspin-expressing tumors contained significant fibrosis and collagen staining, and exhibited a more glandular organization. These data represent evidence that maspin inhibits PC-induced bone matrix remodeling and induces PC glandular redifferentiation. These results support our current working hypothesis that maspin exerts its tumor suppressive role, at least in part, by blocking the pericellular uPA system and suggest that maspin may offer an opportunity to improve therapeutic intervention of bone metastasis.