Cholesterol emboli to the kidney: An immunoperoxidase study

Cholesterol emboli (CE) are an increasingly recognised cause of renal impai rment in the elderly population, especially following diagnostic vascular p rocedures and aortic surgery. They can present as part of a multisystem dis ease which can mimic many conditions, depending on the site of the emboli. As a pathological entity, it was described by Florey in 1945. Relatively fe w cases have been reported in the literature. At this stage there is no acc epted treatment protocol for CE induced renal failure. Little is known about the precise nature of the cells involved in the proli ferating tissue surrounding CE in the kidney. To date, all studies on CE ha ve involved routine Haematoxylin and Eosin (H&E) stains. By studying the ce llular interactions, hopefully this will contribute further to our understa nding 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 t echniques were employed. A panel of antibodies to specific cells were used. The particular cells analysed were the myofibroblast, smooth muscle, endot helium, macrophage, neutrophil, T cell and B cell. All vessels in the biops y specimen containing CE were analysed. T cell, B cell, macrophage and neut rophil infiltrates were counted and expressed as cells/mm(2) using a 0.022 mm(2) graticule under 400 (10x40) magnification. The vessel and perivascula r space were analysed. The myofibroblast, smooth muscle and endothelial cel l 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 in volve a significant response including the myofibroblast, endothelium, T ce ll and macrophage. The B cell response was absent and the smooth muscle cel l 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 end othelial cell response. The myofibroblast is a cell which is increasingly b eing recognised in the host response of both granulation tissue and patholo gical tissue. The population at risk for CE is growing and the disease is i ncreasingly iatrogenic in origin. Currently our only treatment is preventio n.