Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study.

摘要: This report describes light and transmission electron microscopy (LM EM, respectively) studies of kidneys from five cases hepatorenal syndrome. The were removed fixed for LM EM between 30 120 min after death. All patients had progressive renal failure admission to the hospital. jaundiced, ascites, exhibited features hepatic encephalopathy. study revealed severe acute tubular lesions (ATL) or, more conventionally, necrosis (ATN). demonstrated proximal tubules characterized by swelling, disorganization cristae appearance dark bodies in mitochondria, coalescence, fragmentation or displacement microvilli, loss plasma membranes, rupture basement separation cells membranes. Rupture membranes (tubulorrhexis) mitochondrial suggest an ATN due ischemia induced vasoconstrictor substance(s). Glomerular infrequent (one five) therefore, do not seem have contributed failure. terminally extremely low urinary sodium (11 mEq/liter), high potassium (50 a remarkably sodium/potassium ratio (0.26, normal = 4.27), osmolality (less than 400 mOsm/kg). From this we conclude that variable severity may be associated with Since developed without preceding shock, sepsis, hypotension it is possible like ischemic reduced blood flow intense cortical vasoconstriction which has been reported Finally, our data imply consistent pathologic lesion clinical setting.