Background: In the study carrying out in the cooperation of the Department of Diabetology and Kxperimental Therapy and Specialized Research Laboratories of the Institute for Clinical and Experi- mental Medicine Prague, authors have sought to determine the relation between alteratians of the hemostatic system and deveiopment of diabetic com- plications and have tried to solved the question: Whether disturbances of hemostatic system lead to the development of diabetic nephropathy (and renal insufficiency), or whether these complications are the cause of hemocoaguletion disorders. 5fethods: 44 diabetics, 23 males, 21 females, aged 17-63years (mean 35+-10) were examined. Mean duration of diabetes 16+-10 years, are divided into subgroups by the presense or absence of prolifer- ative (non-proliferative respectively) retinopathy (20 and 24 patients), and further were divided according to presence of proteinuria and its levels. Control group consisted of 14 healty age matched volunteers (10 males, 4 females). Followed parameters of con- trol of diabetes (glycaemia, BbA1C), plasminogen a A and a,M. Used eligible statistical analysis tests. Results: Comparison af 44 type-I diabetics and 11 healthy volunteers revealed higher levels of fi- brinogen and a, macroglobulin (a, M) in the diabetics and a correlation between a,M leve) and duration of diabetes as well as accurence of proliferative retinopathy. Hyperfibrinogenemia and increased level of a,M were present in diabetics without ne- phropathy and with or without proliferative retinopathy and aM level depended on diabetes compensation but no on its duration. The highest levels of fibrinogen and a,M were found in patients with diabetic nephropathy irrespective of duration of diabetes. In all diabetic and, especially, in those with diabetic nephropathy a, antiplasmin (a,A) activity inversely correlated with a,M level. Conclusion. It is suggested that, besides its genetic origin, diabetic angiopathy is the result of poor ci>rnpensation (control of diabetes) and hyper- coagulation state of the diabetics with diabetic nephropathy causing further enhancement of fibrinogen and a,M levels.