Anemia – ce este, cum se manifestă şi cum se tratează?

L anemie inflammatoire

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Received Oct 10; Accepted Feb Copyright © de Carvalho et al This is an open access article distributed under the terms of the Creative Commons Attribution Licensewhich permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This article has been cited by other articles in PMC.

Associated Data All relevant data are within the paper and its Supporting Information files. Interested researchers may also ccess the data upon request to: rb.

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Methods The study was performed in patients at ESRD under hemodialysis therapy for more than six months. The patients were divided into three groups according to the genotype. Genomic DNA was extracted from blood cells leukocytes.

Data were analyzed by the software SigmaStat 2. Despite not reaching statistical significance, plasma levels l anemie inflammatoire usCRP were higher in patients carrying the D allele. Our data showed that high levels of PAI-1 are detected when D allele is present, whereas greater interdialytic gain is associated with the presence of I allele.

However, further studies with different experimental designs are necessary to elucidate the mechanisms involved in these associations.

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Diabetes, hypertension, anemia, inflammation, vascular calcification, oxidative stress and alterations of the Renin Angiotensin System L anemie inflammatoire are risk factors for cardiovascular disease CVD in patients under hemodialysis HD [ 2 — 5 ].

The RAS plays a central role in the regulation of blood pressure, hydroelectrolyte homeostasis and renal haemodynamics [ 23 ].

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RAS mediators and enzymes have been linked to the pathogenesis of renal and cardiovascular diseases and also hypertension [ 3 — 5 ]. This polymorphism has been implicated in the development and progression of diabetic nephropathy, although conflicting results have been reported [ 12 — 14 ]. There is substantial evidence that chronic renal and cardiovascular diseases are associated with coagulation disorders, endothelial dysfunction, inflammation and fibrosis [ 1718 ].

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In this regard, several markers of the fibrinolytic system and inflammation, such as D-dimer and C-reactive protein CRP exert a role in the pathogenesis of renal and cardiovascular disorders [ 19 — 21 ]. L anemie inflammatoire serum levels of CRP have been widely considered an important risk factor for atherosclerosis and coronary heart disease [ 22 ].

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D-dimer is the smallest fibrin degradation product. Its plasma levels reflect either increase blood coagulation activation or fibrinolytic action pathway [ 19 ]. Considering fibrogenic markers, the transforming growth factor β1 TGF-β1 is a multifunctional cytokine and key driver of fibrosis. It acts as a regulator of cell proliferation and collagen formation in cardiovascular and renal diseases [ 2324 ].

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Plasminogen activator inhibitor 1 PAI-1a potent regulator of fibrinolysis, has also been involved in several physiopathological processes. Depending on the disease, its overexpression or deficiency may trigger deleterious outcomes [ 25 ]. Patients and Methods Patients This cross-sectional study was performed in patients at ESRD under hemodialysis therapy for more than l anemie inflammatoire months. Among patients, were selected for study and were excluded.

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Exclusion criteria were prescription of oral anticoagulation therapy, patients with acute or chronic hepatic disease, systemic lupus erythematosus, malignant cancer, vasculitis and acute infections, history of renal transplantation, HIV positive, pregnancy and oral contraceptive use in women. Patients required regular hemodialysis sections for 3—4 hours three times a week.

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All HD patients were dialyzed using low-flux polysulphone membranes and high-flow polysulphone membranes with bicarbonate-buffered dialysate. All patients gave signed an informed consent term to participate in the study.

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Assays Blood samples were drawn from hemodialysis vascular access before the beginning of dialysis session at the first session of the week. Blood samples were collected in 0. Samples were aliquoted and stored at °C until analyzed.

Source: Romanian Journal of Rheumatology. Author s : Sabču, Adriana; Boloşiu, H. Hepcidin binds to the cellular iron export channel ferroportin 1 and causes its internalization and degradation and thereby decreases iron efflux from iron exporting tissues into plasma, and also inhibits dietary iron absorption. Hepcidin is modulated by different stimuli, which act as positive or negative regulators.

Briefly, ACE was obtained through one separate reaction, using oligonucleotides. DNA fragment sizes were bp for the D allele and bp for the I allele.

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DNAs vaselina derivata din viermi previously typed individuals were included in each set of analyzed samples as control of enzyme activity Fig 1.