Injuries of the pancreas, gallbladder, and bile ducts due to blunt trauma are relatively uncommon and difficult to detect but are associated with high morbidity and mortality, especially if diagnosis is delayed. Accurate and early diagnosis is imperative, and imaging plays a key role in detection. Knowledge of the mechanisms of injury, the types of injuries, and the roles of various imaging modalities is essential for prompt and accurate diagnosis. Early recognition of disruption of the main pancreatic duct is important because such disruption is the principal cause of delayed complications. Computed tomography (CT) can demonstrate pancreatic parenchymal injuries and complications such as abscess, fistula, pancreatitis, and pseudocyst. CT findings can also suggest disruption of the pancreatic duct; however, the ability of CT to indicate this finding depends on the degree of parenchymal injury. Magnetic resonance (MR) cholangiopancreatography allows direct imaging of the pancreatic duct and sites of disruption. Gallbladder injuries can be detected with CT, ultrasonography, hepatobiliary scintigraphy, or MR cholangiopancreatography. CT findings include a collapsed gallbladder, wall thickening, inhomogeneous mural enhancement, and pericholecystic fluid. Bile duct injuries can be suggested with CT, which may show ascites and associated liver injuries, and can be confirmed with hepatobiliary scintigraphy.

Attachment of podocytes to the glomerular basement membrane is thought to be mediated primarily by alpha 3/beta 1-integrins and by cytoskeletal proteins including actin, talin, vinculin, and alpha-actinin. We analyzed the expression of those molecules in rat glomeruli at several time points during induction of podocyte foot process effacement and nephrotic syndrome with puromycin aminonucleoside (PAN). PAN injection resulted in marked induction of glomerular alpha-actinin (40% increase vs. paired controls, P < 0.01), which clearly preceded development of podocyte foot process effacement and proteinuria and localized almost exclusively to podocytes. Delayed induction of glomerular alpha 3-integrin (44% increase vs. paired controls, P < 0.01) following foot process effacement was also observed but was not restricted to podocytes. No significant changes in glomerular vinculin, talin, beta 1-integrin, or total actin expression occurred at any time point during disease development. We conclude that foot process effacement is preceded by induction of alpha-actinin in podocytes in experimental nephrotic syndrome. Altered expression of this actin cross-linking protein in podocytes may have a pathogenic role in foot process effacement in nephrotic syndrome.

Although nephrotic syndrome is a very common kidney disease, little is known about the molecular changes occurring within glomerular capillary loops during development of disease. The characteristic histologic change is retraction (effacement) of the distal "foot" processes of glomerular epithelial cells (GEC) which surround the capillary loops. The GEC foot processes are an essential part of the kidney's filtration barrier, and their structure is regulated primarily by actin microfilaments, cytoskeletal proteins present in high concentrations in foot processes. Actin polymerization has been reported to be regulated via phosphorylation of the low molecular weight heat shock protein, hsp27. We localized hsp27 within normal rat GECs using immunofluorescence and immunoelectron microscopy. Induction of nephrotic syndrome and GEC foot process effacement using the puromycin aminonucleoside rat model resulted in significant increases in: ( a ) renal cortical hsp27 mRNA expression