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Capillary Damage (capillary + damage)
Selected AbstractsPeritubular Capillary Damage in Acute Humoral Rejection: An Ultrastructural Study on Human Renal AllograftsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2005P. Lipták The ultrastructural features of peritubular capillary (PC) damage was studied in 12 kidney allografts with acute humoral rejection (AHR). AHR manifested in diffuse linear PC staining for C4d, and histology consistent with Banff grade III in 7 recipients and Banff grade II in 5. Allografts with acute tubular necrosis served as controls. First biopsies (post-transplantation day 16.2 ± 2.2): The intra-capillary exudate comprised monocytes (59%), polymorphonuclears (14%), lymphocytes (12%) and not otherwise specified mononuclears (15%). Three patterns of focal PC endothelial injury were observed: lysis, an increased rate of apoptosis and fragmentation. No correlation was found between the respective damage types and the inflammatory cell types or the Banff grades. Controls revealed endothelial swelling, detachment from basement membrane and fragmentation. Follow-up biopsies: Monocytes transformed into macrophages intra-luminally. The reparative changes comprised endothelial cytoplasmic protrusions, binucleated endothelial cells and capillary sprouts. Early transplant capillaropathy and transplant glomerulopathy were noted in 2 recipients. Literature data indicate that lysis is mediated by anti-HLA alloantibodies; apoptosis, demonstrated first in the present study, may be induced by non-HLA-type anti-endothelial antibodies. Fragmentation is caused by ischemia. Ongoing endothelial injury leads to transplant capillaropathy and transplant glomerulopathy, the characteristic lesions of chronic rejection. [source] Vascular pathology in dermatomyositis and anatomic relations to myopathologyMUSCLE AND NERVE, Issue 1 2010Alan Pestronk MD Abstract The causes of perifascicular myofiber atrophy and capillary pathology in dermatomyositis are incompletely understood. We studied 11 dermatomyositis muscles by histochemistry, immunohistochemistry, and ultrastructure. We found that endomysial capillaries within regions of perifascicular atrophy are not entirely lost, but they have reduced size, endothelial loss, C5b9 complement deposits, and relatively preserved connective tissue molecules and pericytes. In all muscles, the perimysium varies regionally. Some areas contain intermediate-sized vessels. Others are avascular. In dermatomyositis, vascular perimysium contains abnormal vessel fragments, perivascular inflammation, and increased PECAM-1. Perifascicular myofiber atrophy and capillary pathology are concentrated near the avascular perimysium. We conclude that both perimysial intermediate-sized vessels and endomysial capillaries within regions of perifascicular myofiber atrophy are abnormal in dermatomyositis. Capillary damage and myofiber atrophy are concentrated in regions distant from intermediate-sized perimysial vessels. Chronic immune vascular damage and insufficiency in dermatomyositis may cause ischemia, myofiber atrophy, and capillary damage in "watershed" regions of muscle near the avascular perimysium. Muscle Nerve, 2010 [source] Fatal Renal Hemorrhage After Extracorporeal Shock Wave LithotripsyJOURNAL OF FORENSIC SCIENCES, Issue 5 2008Klára Tör, Ph.D. Abstract:, Renal hematoma is one of the most severe complications of extracorporeal shock wave lithotripsy (ESWL). ESWL is used in the noninvasive treatment of urinary calculosis. The shock waves can lead to capillary damage, renal parenchymal or subcapsular hemorrhage. We present a case with fatal complication and the result of the medico-legal evaluation. A 71-year-old woman was treated by ESWL, renal hematoma was detected during the clinical observation, and the patient died. The death occurred despite close clinical observation as a consequence of a rare complication of ESWL. The mechanism of death was hemorrhagic hypovolemic shock due to renal hemorrhage complications due to ESWL for treatment of renal calculi. This therapeutic complication is a known complication of appropriate treatment. [source] Vascular pathology in dermatomyositis and anatomic relations to myopathologyMUSCLE AND NERVE, Issue 1 2010Alan Pestronk MD Abstract The causes of perifascicular myofiber atrophy and capillary pathology in dermatomyositis are incompletely understood. We studied 11 dermatomyositis muscles by histochemistry, immunohistochemistry, and ultrastructure. We found that endomysial capillaries within regions of perifascicular atrophy are not entirely lost, but they have reduced size, endothelial loss, C5b9 complement deposits, and relatively preserved connective tissue molecules and pericytes. In all muscles, the perimysium varies regionally. Some areas contain intermediate-sized vessels. Others are avascular. In dermatomyositis, vascular perimysium contains abnormal vessel fragments, perivascular inflammation, and increased PECAM-1. Perifascicular myofiber atrophy and capillary pathology are concentrated near the avascular perimysium. We conclude that both perimysial intermediate-sized vessels and endomysial capillaries within regions of perifascicular myofiber atrophy are abnormal in dermatomyositis. Capillary damage and myofiber atrophy are concentrated in regions distant from intermediate-sized perimysial vessels. Chronic immune vascular damage and insufficiency in dermatomyositis may cause ischemia, myofiber atrophy, and capillary damage in "watershed" regions of muscle near the avascular perimysium. Muscle Nerve, 2010 [source] | ||||||||||