Objective: It has been suggested that hypoalbuminemia in dialysis patients leads to a hypercoagulable state, however, the relationship between serum albumin and fibrinogen or fibrinolytic activity has not been well-documented. The aim of this study was to investigate the changes of fibrinogen, tissue plasminogen activator (tPA), plasminogen activator inhibitor type-1 (PAI-1), and lipid levels in continuous ambulatory peritoneal dialysis (CAPD) patients with atherosclerosis, and the relationship between those factors and serum albumin.
Design: A cross-sectional study.
Setting: A university hospital.
Patients: Twenty CAPD patients with atherosclerosis, 49 CAPD patients without atherosclerosis, and 33 normal controls were included. Presence of atherosclerosis was determined by positive results in a stress thallium single-photon emission computed tomography or an ankle brachial index less than 0.9. Coronary angiography and/or Doppler ultrasound of extremities were followed for the patients with positive results to confirm atherosclerotic cardiovascular disease.
Main outcome measures: tPA and PAI-1 levels were determined with ELISA method, and fibrinogen with thrombin time method. Serum albumin and lipids were also measured.
Results: Serum albumin and HDL-cholesterol levels were significantly lower, and the ratio of total cholesterol/HDL was significantly higher, in CAPD patients than in normal controls. CAPD patients with atherosclerosis had significantly higher fibrinogen, tPA, and PAI-1 levels than other groups: tPA was an independent predictor of atherosclerotic vascular disease in CAPD patients in stepwise logistic regression analysis. Serum albumin level was inversely correlated with fibrinogen (r = -0.28; p < 0.05) in CAPD patients, but not with tPA or PAI-1 levels. PAI-1 level was correlated with tPA (r = 0.37; p < 0.01) and triglycerides (r = 0.32; p < 0.05).
Conclusions: Association of high levels of fibrinogen and PAI-1 with lipid disorders may be of importance in the development of atherosclerosis in CAPD patients. Hypoalbuminemia may contribute to atherosclerosis via increased synthesis of fibrinogen.