title: Impaired fibrinolytic activity in type II diabetes: correlation with urinary albumin excretion and progression of renal disease.
abstract: Progression of renal disease and cardiovascular complications in type II diabetes mellitus have been shown to correlate with control of blood glucose, lipids, blood pressure, and smoking. These factors, however, do not appear to totally explain these diabetic complications. Renal disease and cardiovascular complications in type II diabetes are associated with vascular abnormalities and fibrosis, both of which may occur with impaired fibrinolysis. A cross-sectional study was therefore performed in 107 type II diabetic patients recruited from the Denver Metropolitan Area to examine the effect of impaired fibrinolysis, as assessed by the ratio of plasminogen activator inhibitor (PAI-1) to tissue-type plasminogen activator (t-PA). With urinary albumin excretion (UAE) as a risk factor for both renal disease progression and cardiovascular complications, the patients were analyzed with respect to UAE less than and greater than 1 gm/day. The age, blood glucose, hemoglobin A1C, duration of diabetes, lipids, body mass index, and smoking were no different between the groups. As expected, the group with greater UAE had worse renal function, the serum creatinine (1.98 +/- 0.24 vs 1.21 +/- 0.05 mg/dl, P < 0.001) and creatinine clearance (55.5 +/- 6.0 vs 76.8 +/- 2.7 ml/min, P < 0.001) were significantly different. The type II diabetic patients with greater UAE exhibited significantly higher PAI-1/t-PA (2.43 +/- 0.26 vs 1.85 +/- 0.07, P < 0.03). The past history of cardiac complications was also higher (87.5 vs 72.3%, P < 0.07) in the diabetic patients with more impaired fibrinolysis and greater UAE. Thus a prospective, randomized clinical trial in type II diabetes with PAI-1 inhibitors is needed.
authors.affiliation: Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Health Sciences Center, Denver, 80262, USA.
authors.forename: M
authors.initials: M
authors.lastname: Kamgar
authors.forename: N
authors.initials: N
authors.lastname: Nobakhthaghighi
authors.forename: A A
authors.initials: AA
authors.lastname: Shamshirsaz
authors.forename: R O
authors.initials: RO
authors.lastname: Estacio
authors.forename: K K
authors.initials: KK
authors.lastname: McFann
authors.forename: R W
authors.initials: RW
authors.lastname: Schrier
mesh_terms: D000368:Aged; D000419:Albuminuria / Q000503:physiopathology*; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001262:Atenolol / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000150:complications; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D018450:Disease Progression; D004656:Enalapril / Q000627:therapeutic use; D005342:Fibrinolysis; D005500:Follow-Up Studies; D006801:Humans; D006852:Hydrochlorothiazide / Q000627:therapeutic use; D006973:Hypertension / Q000150:complications / Q000188:drug therapy; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D012307:Risk Factors; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D000959:Antihypertensive Agents; D017395:Plasminogen Activator Inhibitor 1; D006852:Hydrochlorothiazide; D001262:Atenolol; D004656:Enalapril; D003404:Creatinine; D010959:Tissue Plasminogen Activator