7 patients with atheroembolic renal disease were found to have hypocomplementaemia. Evidence obtained in an experimental model of atheroembolic disease shows that the hypocomplementaemia is the result of complement activation by the atheromatous material in vivo. In addition to hypocomplementaemia, 6 patients had thrombocytopenia and 5 had eosinophilia. These observations indicate that atheroembolic disease should now be included in the differential diagnosis of hypocomplementaemia. In addition, atheroembolic disease should be considered in patients presenting with a combination of multisystem disease, hypocomplementaemia, thrombocytopenia, and eosinophilia-a syndrome which previously would have been regarded as diagnostic of immune-complex-mediated vasculitis.
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