Haemorrhagic complications, though uncommon in SLE, may be life-threatening in individual patients, and they require treatment along appropriate lines. Thrombotic problems are more commonly encountered, and are a significant cause of morbidity and mortality. Not only is clinical thrombosis important in SLE, but there is increasing evidence that low-grade coagulopathy contributes substantially to many of the pathological features seen in lupus. The mechanisms involved in the pathogenesis of thrombosis have been discussed and their possible interrelationship is summarized in Figure 4, though it remains speculation that low-grade coagulopathy predisposes to clinical thrombosis. Several of these mechanisms may be operating during periods of disease activity; this was suggested in a recent study of clinical and histological features in SLE (Kant et al, 1981). The study was designed to look at the prevalence of glomerular thrombosis in SLE, and its significance as a histological feature. A striking association was observed between the presence of a circulating anticoagulant and the appearance of glomerular thrombosis on renal biopsy. Also, factor VIII levels were significantly increased and circulating platelets decreased in association with "active' histological features. On later re-biopsy glomerulosclerosis was a much more common finding if the first biopsy showed thrombosis, suggesting that thrombosis is a marker of more severe disease activity and inflammation. A greater understanding of the mechanisms promoting thrombosis will undoubtedly provide insight into the pathogenesis of SLE, as well as suggesting new therapeutic possibilities.