Fibrinolysis Defect in Long-Term Hemodialysis Patients with Type 2 Diabetes mellitus and Its Relation to Metabolic Disorders
| Autor: | Karel Opatrný, Jaromír Eiselt, Shaul G. Massry, Pavlína Zemanová, Martina Tomsů, Ladislav Vít, Sylvia Opatrná, Jan Mares, Frantisek Sefrna, Václav Hejda |
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| Rok vydání: | 2002 |
| Předmět: |
Male
endocrine system medicine.medical_specialty medicine.medical_treatment Gastroenterology Renal Dialysis Diabetes mellitus Internal medicine Plasminogen Activator Inhibitor 1 Fibrinolysis medicine Humans Deamino Arginine Vasopressin Diabetic Nephropathies Homocysteine Aged Apolipoprotein A-I T-plasminogen activator business.industry Metabolic disorder Type 2 Diabetes Mellitus Middle Aged medicine.disease Endocrinology Diabetes Mellitus Type 2 Nephrology Tissue Plasminogen Activator Kidney Failure Chronic Female Hemodialysis Complication business hormones hormone substitutes and hormone antagonists Kidney disease |
| Zdroj: | American Journal of Nephrology. 22:429-436 |
| ISSN: | 1421-9670 0250-8095 |
| DOI: | 10.1159/000065270 |
| Popis: | Background/Aims: Patients with chronic renal failure (CRF) secondary to diabetes mellitus show a high incidence of atherosclerosis with its thrombotic complications. Both CRF and type 2 diabetes mellitus (DM2) results in fibrinolysis defects causally related to atherogenesis and thrombogenesis. It is not well known whether or not and, if so, how fibrinolysis is altered in patients with both CRF and DM2. Our study was designed (1) to identify the fibrinolysis defect present in patients with DM2-mediated CRF and treated by long-term hemodialysis (DM2HD), and (2) to establish whether the fibrinolysis defect is related to the metabolic abnormalities observed in CRF or DM2. Methods: Sixteen DM2HD patients and 23 healthy individuals (HI) had their euglobulin clot lysis time (ECLT), and tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) activities (act) and concentrations (ag) assessed before and after standard fibrinolytic stimulus (i.v. administration of 0.4 µg/kg BW 1-deamino-8-D-arginine vasopressin, DDAVP) along with metabolic status markers. Results: DDAVP caused a significant shortening of ECLT, rises in tPA act and ag, and a significant decrease in PAI-1 act. PAI-1 ag declined significantly in HI, but not in DM2HD. A comparison of responses to DDAVP revealed the groups differed significantly in the change in PAI-1 ag. Whereas, in HI, PAI-1 ag decreased by 11.8 ng/ml, no decrease was seen in DM2HD (0.0 ng/ml) (p < 0.0001; medians given; unpaired Wilcoxon’s test). Stepwise regression analysis showed the change in PAI-1 ag was highly group-specific (DM2HD vs. HI, regression coefficient 21.22; partial correlation 0.58; p < 0.0001) and, also dependent on the serum concentrations of apolipoprotein A-I (–32.41; –0.46; p < 0.01) and homocysteine (0.35; 0.36; p < 0.05). Conclusions: Patients with type 2 DM and CRF on long-term hemodialysis have a fibrinolysis defect manifesting itself after standard fibrinolytic stimulus by an insufficient decrease in PAI-1 concentrations. The defect is related to decreased serum levels of apolipoprotein A-I and increased serum levels of homocysteine. The defect might be a factor contributing to accelerated atherosclerosis and thrombotic complications in these patients. |
| Databáze: | OpenAIRE |
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