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Biomedical subjects

Jolanta Małyszko

Publications and source records attributed to Jolanta Małyszko.

At least 19 recordsLinked to original sources
PubMed2006

Apelin and cardiac function in hemodialyzed patients: possible relations?

BACKGROUND: Apelin, a newly discovered adipocytokine, is produced by white adipose tissue and is also expressed in the kidney and heart. Increasing evidence suggests a role for apelin in the pathology of the cardiovascular system. Cardiovascular disease is a major contributor to the mortality and morbidity in patients with chronic renal failure. The aim of this study was to assess associations between apelin, coronary artery disease (CAD) and echocardiographic parameters in hemodialyzed patients. PATIENTS AND METHODS: We investigated plasma apelin levels (using commercially available kits) in 81 nondiabetic, clinically stable hemodialyzed patients (38 females, 43 males) with and without CAD. RESULTS: Patients with CAD were significantly older, with significantly increased left ventricular internal end-diastolic dimension (LVIDd), left ventricular internal end-systolic dimension (LVISd), right ventricle (RV), left atrium (LA), interventricular septum in diastole, left ventricle posterior wall in diastole (LVPW), aorta, pulmonary artery, significantly lower ejection fraction and apelin than patients without CAD. We observed statistically significant correlations between apelin and echocardiographic parameters: LVIDd, LVISd, RV, LA, right atrium, LVPW, aorta, and serum lipids: cholesterol, LDL, triglycerides. In multiple logistic regression analysis, the only associate of apelin was LVIDd. CONCLUSIONS: Apelin level was significantly lower in dialyzed patients with CAD and it was associated with cardiac function. Apelin might be involved in the pathophysiology of cardiovascular disease in chronic renal failure. Since apelin is an inotrope in normal and failing hearts, this finding may have clinical implications for future use of apelin as a novel inotropic agent also for patients with uremic cardiomyopathy.

Aged↗
PubMed2005

Is hepcidin a link between anemia, inflammation and liver function in hemodialyzed patients?

BACKGROUND: Hepcidin synthesis in hepatocytes is modulated in response to anemia, hypoxia or inflammation. A cross-sectional study was performed to assess hepcidin correlations with markers of iron status, erythropoietin therapy and markers of inflammation in hemodialyzed patients and in the healthy volunteers. METHODS: Iron status, complete blood count, creatinine, albumin, lipids were assessed using standard laboratory methods. Hepcidin and high-sensitivity CRP were measured using commercially available kits. RESULTS: Serum iron, TIBC, TSAT, erythrocyte count, Hb, Ht, platelet count, albumin, and cholesterol were lower, whereas ferritin and hepcidin were higher in hemodialyzed patients over controls. Hepcidin correlated positively with triglycerides, albumin, aspartate aminotransferase, lymphocyte count, ferritin and erythropoietin dose and negatively with erythrocyte count, Hb, and Ht in hemodialyzed patients. In multiple regression analysis, triglycerides (beta value was 0.28, p = 0.02) and albumin (beta value was -0.31, p = 0.006) were correlates of hepcidin in hemodialyzed patients. CONCLUSIONS: Elevated hepcidin levels in hemodialyzed patients may be due to functional iron deficiency and anemia. Liver plays an important role in the synthesis of hepcidin. Low-grade inflammation, frequently found in hemodialyzed patients, might also contribute to elevated hepcidin concentration. Hypothesis that hepcidin might link anemia, inflammation and liver function in kidney disease should be further evaluated.

Adult↗
PubMed2005

Markers of endothelial cell activation/injury: CD146 and thrombomodulin are related to adiponectin in kidney allograft recipients.

BACKGROUND: Adiponectin may be used for assessing the risk of coronary artery disease (CAD) and may be related to the development of acute coronary syndrome. Decreased adiponectin has been associated with some risk factors for cardiovascular diseases such as male sex, obesity and diabetes mellitus. Adiponectin has antiatherogenic properties and attenuates endothelial inflammatory responses. CD146, a novel cell adhesion molecule, is localized at the endothelial junction. In kidney allograft recipients, endothelial dysfunction and atherosclerosis are almost universal. The aim of this cross-sectional study was to evaluate possible relations between adiponectin, CD146, and other markers of endothelial cell injury in 82 stable kidney transplant recipients (mean age 45 years, mean time after transplantation 47 months) with and without CAD. METHODS: Adiponectin and markers of endothelial injury: CD146, von Willebrand factor, thrombomodulin, ICAM, CD40L, P-selectin and other hemostatic markers were assessed using commercially available kits. RESULTS: Patients with CAD had evidence of more pronounced endothelial dysfunction, procoagulant state and lower adiponectin than patients without CAD. Adiponectin correlated significantly, in univariate analysis, with CD146 (r = 0.29, p = 0.009), thrombomodulin (r = 0.37, p = 0.001), protein Z (r = -0.25, p = 0.03), BMI (r = -0.26, p = 0.047), serum creatinine (r = 0.26, p = 0.02) and urea (r = 0.38, p = 0.001). CD146 correlated significantly with von Willebrand factor (r = 0.33, p = 0.002), thrombomodulin (r = 0.25, p = 0.025), age (r = 0.34, p = 0.001), platelets (r = -0.33, p = 0.002), serum urea (r = 0.24, p = 0.039), cholesterol (r = 0.24, p = 0.046), ICAM (r = 0.23, p = 0.036), protein C activity (r = -0.26, p = 0.019) and tended to correlate with serum creatinine and time after transplantation. In multivariate linear regression, independent predictors of adiponectin were CD146, thrombomodulin and urea, and of CD146 was mainly age of patients. CONCLUSIONS: Endothelial dysfunction and procoagulant state are more pronounced in kidney transplant recipients with CAD, particularly in those with lower GFR. In kidney transplant recipients, markers of endothelial cell injury are significantly increased relative to healthy volunteers. Elevation of adiponectin may be a defense mechanism against endothelial damage, reflected by elevated CD146 and thrombomodulin.

Adiponectin↗
PubMed2005

Is there a link between CD146, a novel adhesion molecule and other markers of endothelial dysfunction in nephrotic syndrome and continuous ambulatory peritoneal dialysis?

BACKGROUND: CD146 is a novel cell adhesion molecule localized at the endothelial junction. Its increased plasma levels in chronic renal failure are linked to endothelial dysfunction. Endothelial dysfunction and hemostatic disturbances, a common feature of nephrotic syndrome (NS), mimics a state of protein loosing by peritoneal membrane in patients on chronic ambulatory peritoneal dialyses (CAPD). The aim of the study was to assess CD146 in relation to other markers of endothelial cell injury in patients with NS in comparison to patients on CAPD. MATERIALS AND METHODS: We studied 45 CAPD patients, 43 patients with nephrotic syndrome and 25 healthy volunteers. Markers of endothelial cell injury: TFPI total, full length, truncated, von Willebrand factor, trombomodulin, P-selectin, E-selectin, ICAM, VCAM and CD146 were assessed using commercially available kits. RESULTS: All these markers studied except selectins were significantly elevated in patients with NS and CAPD when compared to the healthy volunteers. In CAPD, VCAM, thrombomodulin and CD146 were significantly elevated over NS patients. CD146 correlated significantly with ICAM as well as total and truncated TFPI in CAPD patients. Moreover, total TFPI was positively related to VCAM. CD146 correlated with ICAM in NS, whereas in healthy volunteers CD146 correlated only with TFPI concentration. CONCLUSIONS: Our studies indicate that in nephrotic patients, as well as in CAPD, there is an evidence of endothelial cell injury. Correlations between CD146 and adhesion molecules and TFPI might further support its use as a endothelial cell function marker.

Adult↗
PubMed2005

[Treatment of hypertension in dialysis patients and renal transplant recipients].

Hypertension is often observed in dialysis patients and renal transplant recipients and is a very important risk factor for cardiovascular morbidity and mortality. Despite this high prevalence, the treatment of hypertension in these populations is poorly characterized. This article describes the current state of knowledge in treatment of hypertension in patients on renal replacement therapy. It is not appropriate, to limit the choice of drug to a single class of agents because people usually have other medical problems that affect this decision.

Cardiovascular Diseases↗
PubMed2004

Comparison of effects of different heparins on thrombin activatable fibrinolysis inhibitor in hemodialyzed patients.

BACKGROUND: Thrombin activatable fibrinolysis inhibitor (TAFI) is a regulator of endogenous fibrinolysis. Heparin is used routinely during dialysis sessions to prevent clot formation in the extracorporeal circuit; therefore the aim of the study was to assess whether unfractionated heparin or low-molecular-weight heparins affect TAFI concentration and activity in hemodialyzed patients. METHODS: Dalteparin (n = 16) or enoxaparin (n = 25) were administered before the second hemodialysis session in the week in a single dose, whereas unfractionated heparin (n = 18) was given first as a bolus, then in a pump. We also evaluated thrombin activity (thrombin-antithrombin complexes, prothrombin fragments 1 + 2), TAFI activator, thrombomodulin, a catalyzer of TAFI activation and a marker of endothelial cell injury, and the degree of plasmin generation (plasmin-antiplasmin complexes). RESULTS: TAFI concentration, activity and markers of ongoing coagulation, i.e. prothrombin fragments 1 + 2 and thrombin-antithrombin complexes, were significantly higher in patients anticoagulated with unfractionated heparin when compared to both enoxaparin and dalteparin groups. Thrombin-antithrombin complexes, plasmin-antiplasmin complexes, prothrombin fragments 1 + 2, and thrombomodulin did not differ between patients anticoagulated with dalteparin and enoxaparin. CONCLUSIONS: Our results suggest that low-molecular-weight heparins influence TAFI and other hemostatic parameters in hemodialyzed patients to a lesser degree than unfractionated heparin. Increased TAFI is possibly due to thrombin appearance during hemodialysis with unfractionated heparin.

Adult↗
PubMed2004

Thrombin activatable fibrinolysis inhibitor (TAFI) and markers of endothelial cell injury in dialyzed patients with diabetic nephropathy.

Patients dialyzed due to diabetic nephropathy are at a higher risk of death due to cardiovascular complications than dialyzed non-diabetic patients. Disturbances in hemostasis may play a role in the vascular complications of diabetes mellitus. It has been postulated that TAFI-thrombin activatable fibrinolysis inhibitor, which couples two opposite systems: coagulation and fibrinolysis, may be involved in the mechanism of vascular endothelial damage in diabetic patients. We assessed: TAFI and TAFIa, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1+2, a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes in diabetic and non-diabetic patients on hemodialyses-HD, peritoneal dialyses-CAPD, patients with chronic renal failure with and without diabetic nephropathy on conservative treatment. Both groups of dialyzed diabetic patients have a higher concentration of markers of ongoing coagulation and TAFI activity when compared to dialyzed non-diabetic patients. Linear regression analysis showed that TAFI concentration was directly related to albumin in HD and CAPD patients without diabetic nephropathy, whereas TAFIa correlated with triglycerides, fibrinogen and leukocytes count in this group. When evaluated separately (HD, CAPD), significant correlations between TAFIa and triglycerides and fibrinogen were found only in diabetic CAPD patients. Multivariate analysis showed no correlation between TAFI and other parameters studied. In conclusion, elevated circulating TAFI and TAFIa might be a new link in the pathogenesis of impaired fibrinolysis in diabetic nephropathy, and thus atherosclerosis progression, particularly in CAPD patients. Hypercoagulable state observed in diabetic patients on conservative treatment and maintained on dialyses may contribute to the higher cardiovascular mortality in this population. In these patients there is also evidence of endothelial injury, and probably secondary activation of the coagulation cascade.

Adult↗
PubMed2004

Thyroid volume and hormone response in the early kidney transplants.

BACKGROUND: Thyroid hormones could affect renal function, and conversely renal function disturbances may affect thyroid function. Disturbances of the thyroid hormone concentration are often connected with thyroid gland enlargement. The aim of study was to estimate the function and morphology of the thyroid and kidney graft after kidney transplantation. As the indicator of thyroid and renal function we have used thyroid gland volume, plasma concentration of T3, reverse rT3, creatinine concentration, and renal arteries RI. MATERIAL/METHODS: Studied group included 17 individuals after kidney transplantation, with stabile graft function. The control group included 18 individuals after various surgical procedures. The estimated parameters were: thyroid volume, renal arteries resistive index, concentrations of creatinine,T3 and rT3.The parameters were controlled before transplantation (surgery), the day after, and at 3rd, 6th and 10th day after surgery. RESULTS: All patients, before and after surgical procedure, were clinically euthyroid. Mean creatinine concentration showed tendency to diminish. Statistical analysis revealed positive correlation between Delta concentration of creatinine and Delta volume of thyroid (R Spearman=0.46, p=0.05). Till the 6th day after transplantation T3 concentration diminished, and at the 10th day presented tendency to rise. We found negative correlation between T3 concentration and renal arteries RI. The rT3 concentration during 10 days after transplantation was above the reference level. CONCLUSIONS: The FT3 level and thyroid volume correlates with kidney transplant function. The supplementary thyroid hormones administration should be considered before and after renal transplantation.

Adult↗
PubMed2004

Bone mineral density and bone metabolism are not related to leptin in hemodialyzed and peritoneally dialyzed uremic patients.

BACKGROUND: In chronic renal failure leptin levels are elevated and BMD decreased, however, so far data about correlations between leptin and BMD in dialyzed patients are scarce. It has been suggested that leptin is a predictor of BMD in postmenopausal women. We examined the relationships between leptinemia, BMD and bone metabolism in HD and CAPD patients. We also assessed whether leptin is significant and independent predictor of BMD in dialyzed patients. MATERIAL/METHODS: BMD was measured using dual energy X-ray absorptiometry (DEXA) at lumbar spine and femoral neck in 25 HD and 23 CAPD patients. Markers of bone turnover and leptin were studied using commercially available kits. RESULTS: In femoral neck BMD was significantly higher in CAPD patients, without significant differences in BMD in lumbar spine. There was a negative correlation between BMD at the femoral neck and time on hemodialysis (r= -0.45, p < 0.05). In CAPD patients BMD at the lumbar spine correlated negatively with vitamin D3 (r= -0.54, p < 0.05), osteocalcin (r= 0.54, p < 0 .05), and positively with BMI (r= 0.63, p < 0.01). BMD at the femoral neck correlated positively with BMI (r= 0.59, p < 0.01), and negatively with osteocalcin (r= -0.63, p < 0.05) and time on CAPD (r= -0.52, p < 0.05). Leptin correlate only with cholesterol (r= 0.25, p < 0.05), TSH (r= 0.35, p < 0.01), ss(2) microglobulin (r= 0.32, p < 0.001) and BMD at the femoral neck (r= -0.23, p < 0.05)in all dialyzed (HD and CAPD) patients. CONCLUSIONS: BMD depends on time of renal replacement therapy. Biochemical markers of bone metabolism poorly correlate with BMD and leptin in dialyzed patients. Leptin is not a predictor of BMD in dialyzed patients.

Adult↗
PubMed2004

Effects of coronary artery by-pass grafting on haemostatic factors.

BACKGROUND: Atherogenesis is triggered by functional or structural endothelial injury which leads to humoral and secretion alterations. The haemostatic system plays a significant role in the development of atherosclerosis and its complications, especially acute coronary syndromes. AIM: To assess the effects of coronary artery by-pass grafting (CABG) on some haemostatic factors in patients with stable coronary artery disease (CAD). METHODS: The study group consisted of 45 patients (11 females, 34 males, mean age 60.4+/-9.4 years, range 35-75 years). Endothelial function marker - von Willebrand factor (vWF), and thrombin generation parameters - thrombin-antithrombin complexes (TAT) and prothrombin fragments - F1+2 were measured before as well as 3 days, 7 days and 3 months after CABG. The control group consisted of 33 healthy volunteers (17 females, 16 males, mean age 48.8+/-17.2 years). RESULTS: Serum concentration of vWF as well as TAT and F1+2 levels were significantly higher in the CABG group than in controls. Compared with baseline values, the vWF levels were significantly higher 3 and 7 days after CABG. CONCLUSIONS: There is a hypercoagulability state in patients with CAD who undergo CABG. The use of extracorporeal circulation causes a significant increase in the vWF level which suggests a marked endothelial injury caused by CABG procedure.

Adult↗
PubMed2004

[Role of the hemostatic system in pathogenesis of atherosclerosis as the main etiology of coronary ischemia] [corrected].

Coronary artery disease is a leading cause of mortality in highly developed societies. This occurs in spite of growing therapeutic opportunities. Atherosclerosis begins as a functional or/and structural damage of endothelium, which in turn causes its discontinuation and impairs humoral and secreting function. Haemostasis plays an important role in the progression of atherosclerosis and development of cardiac complications--acute coronary syndromes. Research still continues to determine precisely role of each of haemostasis disorders in increased risk of coronary artery disease and its complications. The aim of this paper is to review the literature data concerning haemostatic risk factors and their role of development of coronary artery disease. Fibrinogen, thrombocytes, factor VII, factor VIII, von Willebrand factor (vWF), thrombomodulin (TM), plasminogen activator inhibitor--type 1 (PAI-1), tissue-plasminogen activator (t-PA) and other haemostatic factors, were described as more or less helpful in estimation of risk of occurrence of coronary artery disease and its cardiovascular complications. Only some of the described hematologic factors were verified so far in large prospective studies, and were recognized as independent risk factors of cardiovascular diseases.

Arteriosclerosis↗
PubMed2004

[Role of the hemostasis in unstable angina pectoris].

Haemostasis plays an important role in the development of cardiac complications--acute coronary syndromes. The thrombus formation in coronary arteries, related to unstable atherosclerotic plaque rupture is the basic pathogenesis of acute coronary syndromes. The balance between coagulation and fibrinolytic system influences on ruptured atherosclerotic plaque and following acute coronary syndrome. Critical narrow or total occlusion of the coronary artery could be a consequence of this interaction. Researches are continued to determine precisely role of haemostasis disorders in unstable angina pectoris. The aim of this paper is to review the literature data concerning haemostatic risk factors in unstable angina pectoris. Fibrinogen, thrombocytes, factor VIII, von Willebrand factor (vWF), thrombomodulin (TM), plasminogen activator inhibitor--type 1 (PAI-1), tissue-plasminogen activator (t-PA) and other haemostatic factors, play more or less essential role in unstable angina pectoris. However further investigations are needed to determine their utility and to search for new and better haemostatic factors of acute coronary syndromes.

Angina, Unstable↗
PubMed2004

[Techniques for creating hemodialysis fistulas].

Hemodialysis is the primary method of renal replacement therapy. To conduct hemodialysis therapy, an effective vascular access is necessary. The authors describe basic types of surgically created accesses for hemodialysis and their complications. Peripheral blood vessels are listed by order in which they are used for access creation.

Arteriovenous Shunt, Surgical↗
PubMed2004

[Cardiovascular risk factors in dialyzed patients].

Cardiovascular complications are the main cause of mortality and morbidity among patients on dialyses. The aim of the work was to assess the effect of the type of renal replacement therapy on the risk factors and cardiovascular complication in dialyzed patients. The studies were performed retrospectively on 90 hemodialyzed and 49 peritoneally dialyzed patients. Risk factors of cardiovascular diseases as well as serum lipids, complete blood count, serum albumin, fibrinogen, C-reactive protein, calcium, phosphates, PTH, systolic, diastolic, mean blood pressure, left ventricular hypertrophy. Hemodialyzed patients were more anemic, longer on renal replacement therapy, with higher albumin, phosphates, lower fibrinogen, cholesterol, LDL, triglycerides, calcium, systolic and diastolic blood pressure than peritoneally dialyzed patients. Left ventricular hypertrophy more frequently found in hemodialyzed patients than in peritoneally dialyzed patients. In peritoneally dialyzed patients glucose load into the peritoneum, dyslipidemia and hiperfibrinogenemia may further contribute at the cardiovascular complications. In hemodialyzed patients anemia, left ventricular hypertrophy and ischemic heart disease is more frequent than in peritoneally dialyzed patients.

Adult↗
PubMed2003

Endothelial cell injury markers in chronic renal failure on conservative treatment and continuous ambulatory peritoneal dialysis.

AIM: In chronic renal failure in dialyzed patients vascular damage is frequently observed and it is probable that disturbances in fibrinolytic activity and endothelial dysfunction may play a role in vascular complications such as stroke or ischemic heart disease. There have been a few data concerning hemostasis in chronic renal failure. Since hemostatic disturbances in nephrotic syndrome mimick those observed in patients maintained on chronic ambulatory peritoneal dialyses (CAPD), the aim of the study was to assess adhesion molecules (P-selectin, E-selectin, ICAM, VCAM and markers of endothelial cell injury), von Willebrand factor, thrombomodulin, and TFPI (tissue factor pathway inhibitor) in CAPD patients as well as in subjects with chronic renal failure (CRF) treated conservatively. METHODS: The studies were performed on 23 CAPD patients, 24 patients with nephrotic syndrome and 24 sex- and age-matched healthy volunteers. TFPI total, full length, truncated, von Willebrand factor, trombomodulin, P-selectin, E-selectin, ICAM, VCAM and vascular endothelial growth factor (VEGF) and its receptor sFlt3 were assayed using commercially available kits. We evaluated also thrombin activity (thrombin-antithrombin complexes (TAT), prothrombin fragments 1 and 2) and the degree of plasmin generation. RESULTS: In CAPD and CRF patients, concentrations of the adhesion molecules P-selectin, E-selectin, ICAM and VCAM were significantly higher when compared to the control group. Concentrations of total, free and truncated TFPI were significantly higher in CAPD and CRF patients when compared to the healthy volunteers. Concentrations of 'classical' markers of endothelial cell injury, von Willebrand factor and thrombomodulin, were significantly higher in CAPD and CRF patients when compared to the control group. In CAPD patients, VCAM and thrombomodulin were significantly elevated when compared to the CRF patients. CONCLUSIONS: The elevated levels of adhesion molecules in CAPD patients probably reflect inadequate clearance as well as enhanced synthesis/release. They may also indicate endothelial cell injury as well as elevated levels of von Willebrand factor and trombomodulin and increased ICAM and VCAM in CAPD patients. Our studies indicate that in renal failure patients, particularly on CAPD, there is evidence of endothelial cell injury and a high degree of hypercoagulation relative to healthy subjects. It may lead to fibrin deposition in the vascular wall, thrombus formation, and development and progression of atherosclerosis with its complications.

Adult↗
PubMed2003

Thyroid function and incidentalomas in kidney transplant recipients.

BACKGROUND: Ultrasound (US) is currently the best method for detecting thyroid nodules, especially those less than 1 cm in diameter, known as 'incidentaloma'. The ultimate diagnosis of non-palpable masses is done by fine-needle aspiration biopsy (FNAB), especially sonographically controlled (S-FNAB). Because of the increasing prevalence of thyroid nodules in Poland, it is essential to assess the nodules for FNAB and S-FNAB, especially in persons at high risk for thyroid carcinoma (patients after transplant with immunosuppression, persons with endemic goiter). MATERIAL/METHODS: Prospective sonographic, color Doppler and power Doppler tests of the thyroid were performed in 44 kidney allograft recipients. The TSH level and urine iodide level was assessed in each patient. The control group included 35 healthy volunteers. RESULTS: TSH levels were normal. The urine iodide concentration was over 30 mg/100 ml in 5 cases. In the rest of the group and in the controls it was below 30 mg/100 ml. In each case the thyroid was enlarged when compared to volunteers. There were thyroid nodules in 19 cases, single in 6 cases and multiple in 13. Of these nodules, 31 were smaller than 1 cm, 20 nodules were 1-2 cm in diameter, and none was greater than 2 cm. Nodules were classified according to whether or not there was flow within the nodule with eventual perinodular flow. FNAB revealed malignancies in 5 cases (nodules with flow). CONCLUSIONS: Goiter was observed in all patients after thyroid transplant. In five of 44 cases malignancies were detected. In patients after transplant the US picture and the TSH and iodide levels should be checked.

Adult↗
PubMed2003

[Thrombin activatable fibrinolysis o inhibitor-TAFI- in dialyzed patients with diabetic nephropathy].

Patients with end-stage renal disease dialyzed due to diabetic nephropathy are at higher risk of death due to cardiovascular complications than dialyzed non-diabetic patients. Disturbances in hemostasis may play a role in the vascular complications of diabetes mellitus. It has been postulated that TAFI-Thrombin Activatable Fibrinolysis Inhibitor, newly described glycoprotein, couples two opposite systems: coagulation and fibrinolysis. The aim of the work was to study TAFI concentration in hemodialyzed and peritoneally dialyzed diabetic and non-diabetic patients. We assessed: TAFI concentration, markers of ongoing coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2 (markers of TAFI activation), a marker of ongoing fibrinolysis: plasmin-antiplasmin complexes, a marker of TAFI cataliser to TAFIa-thrombomodulin using commercially available kits. All four groups studied did not differ in regard to fibrinogen, thrombomodulin, plasmin-antiplasmin complexes, and TAFI concentration. Both groups of dialyzed diabetic patients have higher concentration of markers of ongoing coagulation when compared to dialyzed non-diabetic patients. Hypercoagulable state observed in dialyzed diabetic patients may contribute to the higher cardiovascular mortality in these population.

Adult↗