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Introduction: The study aimed to assess reactive oxygen species generation and the expressions of some surface antigens on polymorphonuclear leukocytes (PMNs) in patients on regular hemodialysis (HD) treatment. Materials and Methods: The respiratory burst of PMNs was determined with luminol-dependent chemiluminescence (CL) in resting cells and following N-formyl-methionyl-leucyl-phenylalanine (fMLP), phorbol 12-myristate 13-acetate (PMA), or opsonized zymosan (OZ) stimulation and expressed in arbitrary CL units times assay-time (aUmin). The expressions of CD11b/CD18, CD10, and CD13 receptors were determined with flow cytometry. Results: Basal PMN CL was increased in HD patients to up to 1285129 aUmin compared with 89588 aUmin in healthy controls (p<0.05). The CL of unprimed PMNs increased after fMLP stimulation from 3085746 to 4529808 aUmin, and after OZ stimulation from 129451296 to 146781355 aUmin. PMA-stimulated CL of PMNs was similar to control values. The oxidative burst in PMNs from HD patients and healthy controls was similar in response to TNF-alpha alone. The CL of TNF- alpha-primed PMNs in HD patients was significantly lower than CL measured in healthy controls (p<0.05). The expressions of CD10 and CD13 metalloproteinase receptors were also increased (p<0.05). Although CD11b expression was significantly increased at rest and after fMLP stimulation, the expression of another beta-integrin heterodimer compound, CD18, was not increased. Conclusions: These results provide evidence that TNF- priming of PMNs is down-regulated in HD patients despite constitutive up-regulation of resting cytotoxicity and enhanced expression of adhesion and metalloproteinase receptors.
EN
Introduction: The luminol-enhanced whole blood chemiluminescence (LBCL) assay is a rapid assay for the measurement of reactive oxygen species (ROS) generation by circulating phagocytes. This study's aim was to determine if patients on maintenance hemodialysis (HD) and non-dialyzed patients with chronic renal failure (CRF) have altered LBCL and if dialysis itself affects ROS production in the blood. Materials and Methods: Twenty-six HD patients, 11 non-dialyzed patients with CRF, and 20 gender- and age-matched healthy controls were studied. Resting (rCl) and 210?5 M n-formyl-methionyl-leucyl-phenylalanine-stimulated LBCL (peak chemiluminescence: pCl, total light emission after agonist addition: tCl) calculated per 104 phagocytes present in the 3-l blood samples were measured with a Bio-Orbit? 1251 luminometer at 37?C for 11 min. Results: Prior to the HD session, median rCL, pCL, and tCL were 1.5, 3.0, and 2.8 times higher in HD patients than in healthy controls (p<0.01) and tended to increase at the end of the session. Significant increases in tCl were observed at 30 min and 240 min (end) of HD (1023.5 vs. 1810.6 vs. 2006.8 arbitrary unitss/104 phagocytes, n=9, p<0.05). Median pCl and tCl were 5.0 and 4.3 times higher in non-dialyzed patients with CRF than in healthy controls (p<0.001). However, no significant differences were found between pre- and post-HD LBCL of HD patients and the LBCL of non-dialyzed patients with renal failure. Conclusions: Blood from patients with renal failure generates elevated amounts of oxidants independently of HD treatment. This may add to the understanding of the nature of oxidative stress and suggests the need of antioxidant treatment in these patients.
EN
The paper presents the actual state of knowledge on of in chronic , their and influence of various therapeutic methods (continuous ambualtory peritoneal dialysis, hemodialysis, renal transplantation, erythropoietin therapy).
EN
The arterial hypertension, hyperlipidemia, fluid overload, electrolytic disorders, the presence of arteriovenous fistula and secundary hyperparathyroidism are the most essential causative factors in cardiac pathology of uremic patients. Apart from that, hemodialysis itself is not an indifferent factor. The cardiac consequences consist in prevalence of hypertrophy or dilatation of the heart including valvular annuli or sheer myocardial calcifications and even the aquired heart diseases. Their coexistence with ischaemic heart disease, systolic and especially diastolic dysfunction of the left ventricle may jeopardise life.
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