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    Wyświetlanie 1-3 z 3
    Tytuł:
    Aliskiren reduces albuminuria after kidney transplantation
    Autorzy:
    Tylicki, Leszek
    Debska-Slizien, Alicja
    Lizakowski, Slawomir
    Przybylska, Milena
    Heleniak, Zbigniew
    Renke, Marcin
    Chamienia, Andrzej
    Biedunkiewicz, Bogdan
    Rutkowski, Przemyslaw
    Małgorzewicz, Sylwia
    Rutkowski, Boleslaw
    Powiązania:
    https://bibliotekanauki.pl/articles/1038634.pdf
    Data publikacji:
    2017
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    albuminuria
    aliskiren
    kidney transplantation
    renoprotection
    Opis:
    Background: The renoprotective effects of the direct renin inhibitor, aliskiren, in renal transplant recipients have been supposed, but not finally proven. We performed an exploratory double-blind, losartan controlled, cross-over study to evaluate the influence of aliskiren, direct renin inhibitor, on albuminuria and other surrogate markers of kidney injury in patients after renal transplantation. The safety of this therapy was also evaluated. Method: 16 of 18 patients (12 M, 4 F), 48.3 ± 9.0 years, 57.7 ± 9.1 months after kidney transplantation, with hypertension and stable serum creatinine 1.4 ± 0.08 mg/dl without proteinuria, completed the protocol. Each patient underwent two 8-week treatment periods (one with 150 mg of aliskiren, and one with 50 mg of losartan) in random order, allowing an 8-week placebo washout between them. Results: There were no differences in albuminuria, transforming growth factor β-1 and 15-F2t-isoprostanes urine excretion between aliskiren and losartan. Creatinine serum level, eGFR, 24 h systolic and 24 h diastolic blood pressure were stable through the study. There were no differences in haemoglobin and potassium serum concentration between studied drugs. Conclusion: Aliskiren decreases albuminuria in renal transplant recipients with clinically minimal side effects. The effect does not differ from that of losartan.
    Źródło:
    Acta Biochimica Polonica; 2017, 64, 2; 221-226
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Red blood cell and plasma glutathione peroxidase activities and selenium concentration in patients with chronic kidney disease: A review
    Autorzy:
    Zachara, Bronisław
    Gromadzińska, Jolanta
    Wąsowicz, Wojciech
    Zbróg, Zbigniew
    Powiązania:
    https://bibliotekanauki.pl/articles/1041155.pdf
    Data publikacji:
    2006
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    hemodialysis
    selenium
    kidney transplantation
    glutathione peroxidase
    chronic kidney disease
    antioxidants
    plasma
    Opis:
    The metabolism of oxygen in aerobic organisms leads to generation of reactive oxygen species (ROS). These entities are able to oxidize almost all classes of macromolecules, including proteins, lipids and nucleic acids. The physiological level of ROS is usually regulated by antioxidant defense mechanisms. There are at least three groups of antioxidant enzymes: superoxide dismutases, catalases and glutathione peroxidases (GSH-Pxs) which neutralize ROS. The trace elements (copper, zinc and selenium) bound to the active sites of the above listed enzymes play an important role in the antioxidant defense system. In mammals, a major function of selenium (Se) and Se-dependent GSH-Pxs is to protect cells from oxidative stress. Selenium concentrations and GSH-Px activities are altered in blood components of chronic kidney disease (CKD) patients. The Se level is frequently lower than in healthy subjects and the concentration very often decreases gradually with advancing stage of the disease. Studies on red cell GSH-Px activity in CKD patients reported its values significantly lower, significantly higher and lower or higher, but not significantly as compared with healthy subjects. On the other hand, all authors who studied plasma GSH-Px activity have shown significantly lower values than in healthy subjects. The degree of the reduction decreases gradually with the progression of the disease. High inverse correlations were seen between plasma GSH-Px activity and creatinine level. A gradual decrease in plasma GSH-Px activity in CKD patients is due to the fact that this enzyme is synthesized predominantly in the kidney and thus the impairment of this organ is the cause of the enzyme's lower activity. Se supplementation to CKD patients has a slightly positive effect in the incipient stage of the disease, but usually no effect was observed in end-stage CKD. Presently, kidney transplantation is the only treatment that may restore plasma Se level and GSH-Px activity in patients suffering from end-stage CKD. A few studies have shown that in kidney recipients, plasma Se concentration and GSH-Px activity are restored to normal values within a period of 2 weeks to 3 months following surgery and thus it can be acknowledged that Se supplementation to those patients has a positive effect on plasma GSH-Px activity.
    Źródło:
    Acta Biochimica Polonica; 2006, 53, 4; 663-677
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Renal tubular acidosis - underrated problem?
    Autorzy:
    Golembiewska, Edyta
    Ciechanowski, Kazimierz
    Powiązania:
    https://bibliotekanauki.pl/articles/1039734.pdf
    Data publikacji:
    2012
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    molecular pathophysiology
    kidney transplantation
    renal tubular acidosis
    gene mutations
    Opis:
    Renal tubular acidosis (RTA) is a hyperchloremic metabolic acidosis characterized by a normal anion gap and normal (or near normal) glomerular filtration rate in the absence of diarrhoea. Inherited isolated forms of renal tubular acidosis are not common. However, they can also be a part of a more generalized tubule defect, like in Fanconi syndrome. In recent years more and more gene mutations have been found which are associated with RTA (mutations in the gene SLC4A4, encoding a Na+-HCO3- cotransporter (NBC-1); in the gene SLC4A1, encoding Cl-/HCO3- exchanger (AE1); in the gene ATP6B1, encoding B1 subunit of H+-ATPase; in the gene CA2 encoding carbonic anhydrase II; and others) and allow better understanding of underlying processes of bicarbonate and H+ transport. Isolated renal tubular acidosis can be frequently acquired due to use of certain drug groups, autoimmune disease or kidney transplantation. As the prevalence of acquired forms of RTA is common, new therapeutic options for the currently used supplementation of oral alkali, are awaited.
    Źródło:
    Acta Biochimica Polonica; 2012, 59, 2; 213-217
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-3 z 3

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