Abstract
Cholesterol emboli (CE) are an increasingly recognised cause of renal impairment in the elderly population, especially following diagnostic vascular procedures and aortic surgery. They can present as part of a multisystem disease which can mimic many conditions, depending on the site of the emboli. As a pathological entity, it was described by Florey in 1945. Relatively few cases have been reported in the literature. At this stage there is no accepted treatment protocol for CE induced renal failure. Little is known about the precise nature of the cells involved in the proliferating tissue surrounding CE in the kidney. To date, all studies on CE have involved routine Haematoxylin and Eosin (H & E) stains. By studying the cellular interactions, hopefully this will contribute further to our understanding of CE in the kidney. Nine (n = 9) out of 1150 consecutive renal biopsies over a six year period were analysed. Standard three- and four-layered peroxidase-antiperoxidase techniques were employed. A panel of antibodies to specific cells were used. The particular cells analysed were the myofibroblast, smooth muscle, endothelium, macrophage, neutrophil, T cell and B cell. All vessels in the biopsy specimen containing CE were analysed. T cell, B cell, macrophage and neutrophil infiltrates were counted and expressed as cells/mm 2 using a 0.022 mm 2 graticule under 400 (10 2 40) magnification. The vessel and perivascular space were analysed. The myofibroblast, smooth muscle and endothelial cell proliferation were graded semiquantitatively. Vessels without evidence of CE were used as controls. The data were subjected to statistical analysis using the unpaired non-parametric Mann-Whitney Two Sample test. P values < 0.05 were accepted as significant. Histological sections demonstrated the host response in the vessel to CE involve a significant response including the myofibroblast, endothelium, T cell and macrophage. The B cell response was absent and the smooth muscle cell response was not significantly different. The perivascular responses were not different for the cells studied. This study has characterised the host response to CE in the human kidney by demonstrating the presence of the myofibroblast, macrophage T cell and endothelial cell response. The myofibroblast is a cell which is increasingly being recognised in the host response of both granulation tissue and pathological tissue. The population at risk for CE is growing and the disease is increasingly iatrogenic in origin. Currently our only treatment is prevention.