ELEVATED PLASMINOGEN-ACTIVATOR INHIBITOR LEVELS IN CYCLOSPORINE-TREATED RENAL-ALLOGRAFT RECIPIENTS

Atherosclerosis and thrombosis, two major causes of morbidity and mort ality in renal transplant recipients, share the same clinical risk fac tors including decreased fibrinolysis and lipid disturbances. In a cro ss-sectional study we have determined parameters of fibrinolysis in co ntrol subjects (n = 23) and stable renal allograft recipients without cyclosporin (CsA) (n = 10) and with CsA (n = 87) in their immunosuppre ssive treatment. In CsA-treated patients, tissue-type plasminogen acti vator was moderately increased compared to patients without CsA (8.4+/ -3.3 vs 5.5+/-2.8 ng/ml). The plasminogen activator inhibitor (PAI) ac tivity in plasma was clearly increased in CsA-treated patients: 14.5+/ -8.8 vs 7.2+/-3.2 in normal controls and 8.5+/-2.4 AU/ml in patients w ithout CsA. Total cholesterol and LDL cholesterol levels were higher i n CsA-treated patients (256+/-62 and 169+/- 60 mg/dl) than in patients without CsA (209+/-45 and 136+/-44 mg/dl). The two groups did not dif fer in HDL cholesterol, triglycerides, and lipoprotein(a). Hypercholes terolaemia, obesity, and steroid-induced diabetes could be identified as risk factors for elevated plasma PAI activity in CsA-treated patien ts. Hypofibrinolysis induced by elevated PAI levels and increased LDL cholesterol may contribute to the increased thrombogenicity and accele rated atherosclerosis observed in cyclosporin-treated patients.