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Biomedical subjects

J Malyszko

Publications and source records attributed to J Malyszko.

At least 19 recordsLinked to original sources
PubMed2006

Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions.

BACKGROUND/AIMS: The value of neutrophil-gelatinase-associated lipocalin (NGAL), a novel biomarker in the detection of acute renal failure in children after cardiac surgery, has been highlighted in previous studies. The incidence of percutaneous coronary intervention (PCI) increases, which may possibly result in increased incidences of contrast nephropathy, its potentially serious complication. Therefore, the aim of our study was to assess prospectively NGAL in patients undergoing elective PCI in relation to serum creatinine. METHODS: NGAL was assessed in the serum and urine using commercially available kits. RESULTS: We measured urinary and serum NGAL before, and 2, 4, 12, 24 and 48 h after PCI. We found a significant rise in serum NGAL 2 and 4 h after PCI, and a rise in urinary NGAL 4 and 12 h after PCI. Before PCI, serum NGAL was significantly associated with serum creatinine, urea, urinary NGAL, hemoglobin, hematocrit, albumin, age and presence of diabetes. In multivariate analysis, serum creatinine was the only predictor of serum NGAL. Serum NGAL 2 h after PCI correlated with serum creatinine, duration of PCI, HbA1c, hematocrit, hemoglobin and urinary NGAL. In multivariate analysis, the only predictors of serum NGAL 2 h after PCI were serum creatinine, time of PCI and HbA1c. Serum NGAL before PCI was significantly higher in diabetics than in non-diabetics. CONCLUSIONS: NGAL may represent a sensitive early biomarker of renal impairment after PCI. Serum creatinine, duration of PCI, but not type and amount of contrast agent, and appropriate treatment of diabetes, reflected by HbA1c, predict a rise in serum NGAL and kidney function following PCI.

Acute-Phase Proteins↗
PubMed2006

Hepcidin, an acute-phase protein and a marker of inflammation in kidney transplant recipients with and without coronary artery disease.

BACKGROUND: In kidney transplant recipients, endothelial dysfunction and atherosclerosis are almost universal, as are cardiovascular complications. Inflammatory markers have been shown to play a role in the pathogenesis and progression of atherosclerosis, regarded as a chronic inflammatory condition. Iron metabolism is disturbed in chronic inflammatory diseases such as atherosclerosis. Hepcidin, the liver-expressed antimicrobial peptide, LEAP-1, is an acute-phase reactant produced in the liver that displays intrinsic antimicrobial activity. Cross-sectional study was performed to assess possible relations between hepcidin and inflammatory markers in kidney transplant recipients with versus without coronary artery disease (CAD). METHODS: Iron status, complete blood count, creatinine, albumin, and lipids were estimated using standard laboratory methods. Glomerular filtration rate (GFR) was calculated using the MDRD formula. Hepcidin, high-sensitivity C-reactive protein (CRP), IL-6, TNFalpha, and soluble receptor of transferrin were measured using commercially available kits. RESULTS: Kidney transplant recipients with CAD were older, and showed higher hepcidin, hsCRP, IL-6, TNFalpha, sTFR, ferritin, and lower cholesterol levels than did patients without CAD. Univariate analysis of values in kidney transplant recipients showed hepcidin to correlate significantly with total protein, ferritin, time after transplantation, creatinine, eGFR (simplified MDRD), cholesterol, neutrophil count, hsCRP, and IL-6. There were tendencies to correlate with TNFalpha. Multiple regression analysis showed that hepcidin was independently related to GFR, cholesterol, and hsCRP. CONCLUSIONS: Elevated hepcidin values in kidney allograft recipients may be due not only to impaired renal function, but also to a low-grade inflammatory state, as reflected by hepcidin correlations with hsCRP, IL-6, and ferritin.

Adult↗
PubMed2006

Possible relations between thyroid function, endothelium, and kidney and liver function in kidney allograft recipients.

BACKGROUND: Renal function affects the thyroid gland in many ways. Disturbances in hemostasis and endothelial damage are common complications of kidney disease. Endothelial dysfunction may link these two processes. AIM AND METHODS: This cross-sectional study examined thyroid hormones in relation to markers of endothelial damage and inflammation among 80 kidney allograft recipients and 29 healthy volunteers. Thyroid hormones, markers of endothelial damage (vWF, thrombomodulin, intracellular adhesion molecule [ICAM] vascular adhesion molecule [VCAM], CD146), markers of inflammation (hsCRP), other hemostatic parameters (thrombin-antithrombin complexes [TAT], prothrombin fragments 1 + 2 [F1 + 2], plasmin-antiplasmin complexes, tissue plasminogen activator and its inhibitor, platelet glycoprotein [V-GPV]) as well as P-selectin were measured using commercially available kits. RESULTS: Total T3 was significantly lower among kidney allograft recipients, whereas markers of endothelial dysfunction and inflammation were significantly elevated over controls. In kidney allograft recipients total T3 was independently related to PAI-1, ICAM, and eGFR, whereas free T3 was independently related to thrombomodulin, aspartate, and alanine aminotransferases, hemoglobin, urea, eGFR, dose of cyclosporine and treatment with mycophenolate mofetil/azathioprine. Total T4 was related to aspartate and alanine aminotransferases, dose of cyclosporine, PAI-1, and ICAM. In multiple regression analysis the only correlates of T3 were PAI-1 and ICAM, whereas the only correlates of free T3 were thrombomodulin, aspartate aminotransferase, eGFR, and cyclosporine dose. In healthy volunteers GPV was related only to TSH. CONCLUSIONS: We described novel relations between thyroid hormones and markers of endothelial dysfunction in kidney transplant recipients. In kidney transplant recipients thyroid function metrics were associated with endothelial damage, immunosuppressive treatment, liver and kidney function. Therefore, the relations between thyroid axis and endothelium in kidney allograft recipients merit additional studies.

Adult↗
PubMed2006

Resistin, a new adipokine, is related to inflammation and renal function in kidney allograft recipients.

BACKGROUND: Among patients without chronic kidney disease, resistin, an adipocytokine, has been related to inflammatory markers, coronary artery disease, and cardiovascular disease in the metabolic syndrome. Moreover, resistin up-regulates adhesion molecules. Since inflammation and endothelial cell damage or injury are invariably associated with thrombosis, atherosclerosis, and their major clinical consequences, resistin may play a role to link inflammation and CVD. The aim of this study was to correlate resistin with markers of inflammation and endothelial cell injury in 96 kidney allograft recipients. METHODS: We measured resistin and the following markers of endothelial function/injury: vWF, thrombomodulin, VCAM, hsCRP, tumor necrosis factor alpha (TNFalpha), and interleukin-6 (IL-6). RESULTS: Triglycerides, CRP (assessed by high-sensitivity method), phosphate, creatinine, IL-6, TNFalpha, vWF, prothrombin fragments 1 + 2, and resistin were elevated among kidney transplant recipients compared with the control group. Kidney allograft recipients with coronary artery disease displayed significantly higher resistin levels than those in patients without this complication. Upon univariate analysis resistin levels in kidney allograft recipients were related to hsCRP, IL-6, thrombomodulin, red blood cell count, white blood cell count, platelet count, creatinine, urea, VCAM, CSA, dose and eGFR. Upon multiple regression analysis, resistin was independently related only to creatinine, hsCRP, and white blood cell count in kidney allograft recipients. CONCLUSIONS: The relation of elevated resistin levels to markers of inflammation may represent a novel link between these conditions and adipocytokines. Renal function was a major determinant of elevated resistin in kidney allograft recipients.

Adult↗
PubMed2005

Intima media thickness of common carotid arteries is associated with traditional risk factors and presence of ischaemic heart disease in hemodialysis patients.

Patients with chronic renal failure are prone to cardiovascular complications. The mechanisms and the assessment of the risk of cardiovascular diseases (CVD) in this population are of interest. The purpose of this study was to investigate the traditional and potential risk factors for the development of CVD and their contribution to ischemic heart disease (IHD) and variation in carotid intima media thickness (IMT) in hemodialyzed patients (HD). Twenty-one chronically HD patients and nineteen healthy volunteers were recruited. Studied parameters were intima-media thickness, body mass index (BMI), mean arterial blood pressure (MAP), hemoglobin, fibrinogen (Fbg), serum lipids, lipoprotein (a) [Lp(a)], total homocysteine (tHcy). Mean carotid IMT, tHcy, Fbg and Lp(a) were higher in HD patients compared to the control group. There were no differences in cholesterol (tCh) and triglycerides between these groups. Patients with ischemic heart disease were older and they had higher values of carotid IMT, tCh, triglycerides, Fbg and Lp(a). There were no differences in MAP, time on dialysis and tHcy between the two subgroups (with vs without IHD). Carotid IMT correlated positively with age (r = 0.68, p = 0.001), BMI (r = 0.50, p = 0.02), tCh (r = 0.58, p < 0.01), LDL- cholesterol (r = 0.55, p = 0.01) and Fbg (r = 0.57, p < 0.01) but not with tHcy or Lp(a) in the patients group. Carotid intima media thickness thus reflects the risk for ischemic heart disease in hemodialyzed patients. Elevated fibrinogen concentration and dyslipidemia influence arterial remodelling.

Carotid Artery Diseases↗
PubMed2005

Correlations between leptin, body composition, bone mineral density, and bone metabolism in kidney transplant recipients.

INTRODUCTION: In kidney transplant recipients leptin levels are often elevated and bone mineral density (BMD) decreased. However, to date there are no about correlations between leptin and BMD in this population. It has been suggested that leptin is a predictor of BMD in postmenopausal women. Moreover, leptin acts as a marker of fat stores. We examined the relationships between leptinemia, some markers of nutritional status, BMD, and bone metabolism in kidney transplant recipients. We also assessed whether leptin was a significant and independent predictor of BMD in this population. METHODS: BMD and fat content (global, percentage, trunk) were measured using dual-energy X-ray absorptiometry in 27 kidney allograft recipients. Markers of bone turnover and leptin were studied using commercially available kits. RESULTS: Leptin correlated with the percentage of body fat, trunk fat, lean body mass, serum creatinine, and urea. Insulin growth factor binding protein 1 was negatively related to waist-hip ratio and global and trunk fat, whereas BMD of the lumbar spine was correlated with the daily dose of prednisone, azathioprine, cyclosporine trough levels, serum calcium, as well as osteoprotegerin level. CONCLUSIONS: Leptin levels are associated with graft function and body fat in kidney allograft recipients. Leptin is not related to nutritional status, BMD, or bone metabolism in kidney allograft recipients, but is associated with the current dosage of immunosuppressants and the serum calcium.

Absorptiometry, Photon↗
PubMed2003

Some aspects of hemostasis in kidney transplant recipients maintained on cyclosporine, azathioprine, and prednisone in comparison to patients treated with cyclosporine and prednisone.

Cyclosporine (CyA) has been implicated to increase cardiovascular morbidity and mortality after renal transplantation. Impairment of the fibrinolytic system is one factor involved in the development of thrombotic complications. The aim of this study was to compare hematological and hemostatic parameters among patients on CyA, azathioprine, and prednisone (n = 31) versus CyA and steroids (n = 14). Using commercially available kits we evaluated thrombin activity as thrombin-antithrombin complexes (TAT), prothrombin fragments (1 + 2), thrombin activatable fibrinolysis inhibitor-(TAFI), TAFI activator, thrombomodulin (TM)-a marker for endothelial cell injury,-plasmin generation (plasmin-antiplasmin complex PAP), a glycoprotein linking coagulation and fibrinolysis. We observed that patients not treated with azathioprine displayed longer prothrombin times and activated partial thromboplastin times; higher fibrinogen, platelet counts and fibrinolytic activity index (FAI); shorter euglobulin clot lysis time; as well as lower thrombin generation markers namely, prothrombin fragments 1 + 2 and thrombin-antithrombin complexes. Although patients in the non-AZA group tended to have been engrafted for a longer time (P =.086), the groups did not differ with regard to age, BMI, erythrocyte count, hematocrit, leukocyte count, creatinine clearance, alanine and asparagine aminotransferase activities mean arterial blood pressure, fibrinogen, TAFI, thrombomodulin, or plasmin-antiplasmin complexes. These findings suggest that kidney transplant recipients on triple therapy are at greater risk of cardiovascular disease than those without azathioprine treatment, despite the lower fibrinolytic activity.

Adult↗
PubMed2003

Thyroid function and morphology in kidney transplant recipients, hemodialyzed, and peritoneally dialyzed patients.

Disturbances in thyroid function are common among patients on renal replacement therapy. The aim of the present study was to compare thyroid stimulating hormone (TSH) and thyroid morphology among patients on hemodialysis (HD), peritoneal dialysis (CAPD), and after kidney transplantation. The study was performed on three groups of patients: 48 transplant recipients (Tx) (receiving cyclosporine, azathioprine, and prednisone); 32 HD, and 26 CAPD patients. The control group included 40 healthy volunteers. Thyroid examinations were performed with a 7.5-MHz probe and the thyroid volume was calculated. Among Tx patients the thyroid volume was 25.16 +/- 12.27mL; 21.60 +/- 10.33mL in HD; 19.70 +/- 8.46 mL in CAPD; and 16.34 +/- 5.46mL in the healthy volunteers. Serum TSH was within the normal range in each group. Goiter was diagnosed in the majority of Tx, most HD patients, and some CAPD patients. Single and multiple nodules were found in 21 Tx, 12 HD, and 2 CAPD patients. Moreover, parathyroid glands were visualized on sonography in 10 Tx, 12 HD, and 8 CAPD subjects. In Tx observed correlations were positive between thyroid volume and creatinine, negative between thyroid volume and TSH. The time after transplantation correlated negatively with TSH. No correlation between TSH, thyroid volume, and time on dialysis was observed. The prevalence in patients on renal replacement therapy was higher than that in the general population. These findings suggest that screening for abnormal thyroid morphology should be performed in kidney patients and that iodide supplementation should be considered in Tx patients.

Adult↗
PubMed2003

Plasma tissue-type plasminogen activator, fibrinogen, and time on dialysis prior to transplantation are related to carotid intima media thickness in renal transplant recipients.

The majority of deaths among patients after renal transplantation is attributed to cardiovascular disease (CVD). Intima media thickness (IMT) of the common carotid artery is related to coronary and cerebrovascular arterial disease. One of the major causes of death due to CVD is acute coronary syndrome, which is precipitated by coronary plaque rupture and subsequent thrombosis. The aim of the study was to evaluate associations between some fibrinolytic factors: antigens of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI-1), and thrombin-activatable fibrinolysis inhibitor (TAFI), and IMT in a population of renal transplant recipients. The study was performed on 33 Caucasian, clinically stable kidney transplant recipients (11 women, mean age 43 years, range 26 to 62 years). All the patients were on triple immunosuppressive regimen (cyclosporine, prednisone, and azathioprine) and had stable graft function (serum creatinine 1.7 +/- 0.7 mg/dL). The mean time since transplantation was 49.9 months (range 4.1 to 131.8 months). In univariate analysis IMT correlated significantly with age (r =.5; P =.001), pulse pressure (PP) (r =.4; P =.05), time on dialysis prior to transplantation (r =.6; P =.001), fibrinogen (r =.4; P =.02), and t-PA (r =.6; P =.001). Multiple regression analysis showed that t-PA antigen concentration (P =.001), fibrinogen (P <.05), and time on dialysis prior to transplantation (P <.05) were positive independent predictors of IMT. These data support the concept of the coincidence of disturbances in fibrinolysis and arterial remodelling in patients after kidney transplantation. On the other hand the study shows that the duration of dialysis therapy before transplantation is detrimental to the arterial vasculature.

Adult↗
PubMed2003

Osteoprotegerin and its correlations with new markers of bone formation and bone resorption in kidney transplant recipients.

Osteoprotegerin (OPG), a natural decoy receptor for osteoclast differentiation factor, is produced by osteoblasts in response to PTH. OPG and its ligand RANKL constitute a complex mediator system involved in the regulation of bone resorption, probably playing an important role in the homeostasis of bone turnover. At present, little is known about the effects of OPG on uremic bone. Successful kidney transplantation reverses many abnormalities of bone metabolism; however, the improvement is often incomplete. The aim of the study was to assess OPG and RANKL concentrations in long-term kidney allograft recipients and their correlations with biochemical markers of bone resorption and formation. The present studies on 48 kidney transplant recipients and 25 healthy volunteers included concentrations of parathormone, osteocalcin, bone-specific alkaline phosphatase, serum CrossLaps, calcidiol, calcitriol, ICTP, PICP, tartrate-resistant acid phosphatase, beta2 microglobulin, IGF-1, IFGBP-1, IGFBP-3, OPG, and RANKL using commercially available kits for measurements. Among kidney transplant recipients OPG and RANKL did not differ between transplant patients and healthy volunteers, whereas other markers of bone formation and resorption were significantly higher in the former group. OPD was related to age, time on dialysis prior transplantation, urea, platelet count, CSA dose, azathioprine dose, 25(OH)D(3), TRAP, IGF-1, IGFBP-3, whereas RANKL was related to leukocyte count, CSA concentration and dose, urine DPD, and beta2 microglobulin content. In healthy volunteers OPG correlated only with CrossLaps, whereas RANKL correlated only with osteocalcin and TRAP. Correlations between OPG, IGF system components, and some markers of bone metabolism may indicate the role of OPG/RANKL system in the pathogenesis of bone metabolism disturbances following renal transplantation.

Adult↗
PubMed2003

Thrombin-activatable fibrinolysis inhibitor in kidney transplant recipient with dyslipidemia.

Kidney transplant recipients are not only prone to dyslipidemia but also have a high risk of cardiovascular death. Impairment of the fibrinolytic system is thought to be one factor playing a role in development of thrombotic complications. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a glycoprotein, linking coagulation and fibrinolysis. The purpose of this study was to assess TAFI concentrations and activities in renal transplant recipients stratified based upon serum cholesterol values above 220 mg/dL or below 200 mg/dL. The groups did not differ regarding age, creatinine clearance, BMI, time after transplantation, albumin, fibrinogen, thrombomodulin, or PAP. Additionally, we evaluated thrombin activity (thrombin-antithrombin complex TAT, prothrombin fragments 1 + 2); TAFI activator; thrombomodulin (TM), catalyzer of TAFI activation; and the degree of plasmin generation (plasmin-antiplasmin complex PAP) using commercially available kits. In patients with hyperlipidemia significantly higher TAFI concentrations and activities may contribute to prolonged ECLT and lowered fibrinolytic activity index (FAI). Increased levels of F1 + 2 and TAT were observed in hypercholesterolemic patients, indicating enhanced thrombin generation. Elevated TAFI concentration, and activities and enhanced thrombin generation observed in hypercholesterolemic kidney transplant recipients may contribute to hypofibrinolysis and progression of atherosclerosis in this group of patients.

Adult↗
PubMed2002

Markers of endothelial cell injury and thrombin activatable fibrinolysis inhibitor in nephrotic syndrome.

Thromboembolic complications are often seen in patients with nephrotic syndrome. Markers of endothelial cell injury [thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule, thrombin activatable fibrinolysis inhibitor (TAFI), protein Z, vascular endothelial growth factor, markers of thrombin and plasmin generation] were studied in 22 patients with nephrotic syndrome. All these parameters studied, except protein Z and D-dimers, were significantly higher in patients with nephrotic syndrome, whereas protein Z was significantly lower when compared with the healthy volunteers. None of the endothelial cell markers (thrombomodulin, P-selectin, E-selectin, intracellular adhesion molecule, vascular cell adhesion molecule), thrombin and plasmin generation markers (thrombin-antithrombin complexes, prothrombin fragments 1 + 2, plasmin-antiplasmin complexes, D-dimers), protein C, protein Z, vascular endothelial growth factor, and TAFI concentration and activity were directly correlated with the level of proteinuria, albumin, cholesterol, triglycerides or creatinine, except significant positive correlations between TAFI activity and serum creatinine, E-selectin and albumin as well as negative correlations between plasmin-antiplasmin complexes and proteinuria. In these patients, there is evidence of endothelial cell injury and probably secondary activation of the coagulation cascade. Elevated circulating TAFI antigen and activity might be a new link in the pathogenesis of impaired fibrinolysis and the progression of atherosclerosis in nephrotic syndrome. Protein Z deficiency might also contribute to the enhanced risk of thromboembolic complications in nephrotic syndrome.

Adult↗
PubMed2002

Simvastatin and markers of endothelial function in patients undergoing continuous ambulatory peritoneal dialysis.

Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) are prone to dyslipidemia and have a high risk of cardiovascular death. The aim of this study was to assess the effects of a 6-month treatment with simvastatin (10 mg at bedtime) on markers of endothelial cell injury in 12 hypercholesterolemic CAPD patients. Cholesterol and low-density lipoprotein cholesterol fell significantly after 1 month of therapy. Simvastatin treatment significantly decreased concentrations of vascular cell adhesion molecule and intracellular adhesion molecule after 3 and 6 months of the therapy, respectively. Thrombomodulin decreased significantly after 6 months of the treatment, whereas von Willebrand's factor, P-selectin and E-selectin remained unaltered during simvastatin therapy. Simvastatin, an effective hypolipemic agent, favorably affects endothelial function and may potentially slow the progression of atherosclerosis and confer protection from thrombotic complications in patients with hypercholesterolemia undergoing CAPD.

Biomarkers↗
PubMed2001

Accumulation of toxic products degradation of kynurenine in hemodialyzed patients.

In patients that developed a chronic renal failure the augmentation in tryptophan degradation is reflected in the increase in plasma metabolites of kynurenine pathway. Hemodialysis is one of therapeutic approaches that significantly reduce all plasma kynurenine metabolites in uremic patients. In spite of haemodialysis, plasma concentration of kynurenine, kynurenic acid, 3-hydroxykynurenine, anthranilic acid, xanthurenic acid and quinolinic acid were still elevated in uremic patients in comparison with healthy volunteers. These data shows significant disturbances in kynurenine metabolism in uremic patients. Accumulation of these substances in uremic blood is capable to account for certain uremic symptoms.

Female↗
PubMed2001

A possible role of thrombin-activatable fibrinolysis inhibitor in disturbances of fibrinolytic system in renal transplant recipients.

BACKGROUND: Cardiovascular disease (CVD) is a major cause of death in renal transplant recipients (RTR). Suppression of fibrinolysis plays a role in the progression of atherosclerosis. Accelerated progression of atherosclerosis and fibrinolytic system suppression has been observed in RTR. Despite many years of intensive research, the reason for impaired fibrinolysis in this patient population is not fully understood. Thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently discovered glycoprotein combining coagulation and fibrinolysis. This study was conducted to evaluate concentrations of TAFI, markers of thrombin generation, endothelial injury, and some standard laboratory parameters in RTR receiving triple immunosuppressive drug regimen. METHODS: The study was performed in 29 stable, non-diabetic kidney transplant recipients treated with cyclosporin A, azathioprine, and prednisone and in 18 age- and sex-matched healthy volunteers. Soluble thrombomodulin (sTM), prothrombin fragments F1+2 (F1+2), thrombin--antithrombin complexes (TAT), plasmin--antiplasmin complexes (PAP), and TAFI were measured with commercially available kits. RESULTS: The RTR group had significantly higher plasma levels of TAT, F1+2, sTM and TAFI than the healthy volunteers. There were no differences in PAP concentrations between the two groups. Plasma sTM correlated inversely with creatinine clearance, body mass index, haemoglobin, and albumin. Plasma TAT level was positively associated with total cholesterol. TAFI antigen influenced negatively PAP antigen concentration. CONCLUSIONS: On the basis of our research, we concluded that elevated circulating TAFI antigen might be a new link in the pathogenesis of impaired fibrinolysis in RTR, and thus atherosclerosis progression. In the patient group there is also evidence of endothelial injury, followed by secondary activation of the coagulation cascade. Hypercholesterolaemia in RTR is associated with enhanced thrombin activity.

Adult↗