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Wyszukujesz frazę "Renke, Marcin" wg kryterium: Autor


Wyświetlanie 1-4 z 4
Tytuł:
Atorvastatin improves tubular status in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study
Autorzy:
Renke, Marcin
Tylicki, Leszek
Rutkowski, Przemysław
Neuwelt, Alexander
Larczyński, Wojciech
Ziętkiewicz, Marcin
Aleksandrowicz, Ewa
Łysiak-Szydłowska, Wiesława
Rutkowski, Bolesław
Powiązania:
https://bibliotekanauki.pl/articles/1040322.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
proteinuria
kidney
tubular injury
chronic kidney disease
Atorvastatin
Opis:
Background. There is evidence that dyslipidemia is associated with chronic kidney disease (CKD) and it has been implicated in the progression of renal damage. Optimal management of dyslipidemia should therefore lead to renal benefits. A number of experimental models demonstrate a beneficial effect of statins in ameliorating renal damage. However, the exact mechanism by which statins protect against renal damage remains unclear. Methods. In a placebo-controlled, randomized, cross-over study we evaluated the influence of atorvastatin (ATO) 40 mg/day added to the renin-angiotensin-aldosterone systeme (RAAS) blockade on proteinuria and surrogate biomarkers of tubular damage or injury in 14 non-diabetic patients with proteinuria (0.4-1.8 g per 24 h) with normal or declined kidney function (eGFR 55-153 ml/min). In the eight-week run-in period, therapy using angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: ATO/washout/placebo or placebo/washout/ATO. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. The primary end point of this study was a change in proteinuria measured as 24-h urine protein excretion (DPE). Secondary end points included urine N-acetyl-β-d-glucosaminidase (NAG) and α1-microglobulin (α1m) excretion. Results. The ATO therapy significantly reduced urine excretion of α1m (p=0.033) and NAG (p=0.038) as compared to placebo. There were no differences in proteinuria, blood pressure, eGFR and serum creatinine between the ATO and placebo groups. Conclusion. Atorvastatin treatment is safe and improves biomarkers of tubular damage or injury in non-diabetic patients with CKD.
Źródło:
Acta Biochimica Polonica; 2010, 57, 4; 547-552
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Effect of pentoxifylline on proteinuria, markers of tubular injury and oxidative stress in non-diabetic patients with chronic kidney disease - placebo controlled, randomized, cross-over study
Autorzy:
Renke, Marcin
Tylicki, Leszek
Rutkowski, Przemysław
Knap, Narcyz
Ziętkiewicz, Marcin
Neuwelt, Alexander
Aleksandrowicz, Ewa
Łysiak-Szydłowska, Wiesława
Woźniak, Michał
Rutkowski, Bolesław
Powiązania:
https://bibliotekanauki.pl/articles/1040438.pdf
Data publikacji:
2010
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
pentoxifylline
oxidative stress
kidney
chronic kidney disease
proteinuria
tubular injury
Opis:
Background: Inhibition of the renin-angiotensin-aldosterone system (RAAS) with angiotensin converting enzyme inhibitors (ACEI) and/or angiotensin II subtype 1 receptor antagonists (ARB) is a common strategy used in the management of patients with chronic kidney disease (CKD). However, there is no universal therapy that can stop progression of CKD. Pentoxifylline (PTE) is a non-specific phosphodiesterase inhibitor with anti-inflammatory properties. It has been reported to have promising effects in CKD treatment. Methods: In a placebo-controlled, randomized, cross-over study we evaluated the influence of PTE (1200 mg/day) added to RAAS blockade on proteinuria, surrogate markers of tubular injury and oxidative stress-dependent products in 22 non-diabetic patients with proteinuria (0.4-4.3 g per 24h) with normal or declined kidney function [eGFR 37-178 mL/min]. In an eight-week run-in period, therapy using ACEI and/or ARB was adjusted to achieve a blood pressure below 130/80 mm Hg. Next, patients were randomly assigned to one of two treatment sequences: PTE/washout/placebo or placebo/washout/PTE. Clinical evaluation and laboratory tests were performed at the randomization point and after each period of the study. Results: The PTE therapy reduced proteinuria (by 26%) as compared to placebo. There were no differences in α1-microglobulin, urine excretion of N-acetyl-β-d-glucosaminidase (NAG), hsCRP, the urinary excretion of 15-F2t-isoprostane, blood pressure (BP), eGFR and serum creatinine between the PTE and placebo groups. Conclusion: Pentoxifylline may decrease proteinuria in non-diabetic patients with CKD.
Źródło:
Acta Biochimica Polonica; 2010, 57, 1; 119-123
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
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:
Immune response against HtrA proteases in children with cutaneous mastocytosis
Autorzy:
Renke, Joanna
Kędzierska-Mieszkowska, Sabina
Lange, Magdalena
Nedoszytko, Bogusław
Liberek, Anna
Plata-Nazar, Katarzyna
Renke, Marcin
Wenta, Tomasz
Żurawa-Janicka, Dorota
Skórko-Glonek, Joanna
Lipińska, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1038382.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
HtrA proteases
children
cutaneous mastocytosis
mast cells
Opis:
Mast cells play an important role in both, the innate and adaptive immunity, however, clonal proliferation of abnormal mast cells in various organs leads to mastocytosis. A skin variant of the disease, cutaneous mastocytosis (CM) is the most frequent form of mastocytosis in children. HtrA proteases are modulators of important cellular processes, including cell signaling and apoptosis, and are related to development of several pathologies. The above and the observation that mast cells constitutively release the HtrA1 protein, prompted us to investigate a possible involvement of the HtrA proteins in pediatric CM. Levels of the serum autoantibodies (IgG) against the recombinant HtrA proteins (HtrA1-4) in children with CM (n=36) and in healthy controls (n=62) were assayed. Anti-HtrA IgGs were detected using enzyme linked immunosorbent assay (ELISA) and Western-blotting. In the CM sera, levels of the anti-HtrA1 and anti-HtrA3 autoantibodies were significantly increased when compared to the control group, while the HtrA protein levels were comparable. No significant differences in the anti-HtrA2 IgG level were found; for the anti-HtrA4 IgGs lower levels in CM group were revealed. In healthy children, the IgG levels against the HtrA1, -3 and -4 increased significantly with the age of children; no significant changes were observed for the anti-HtrA2 IgG. Our results suggest involvement of the HtrA1 and HtrA3 proteins in pediatric CM; involvement of the HtrA4 protein is possible but needs to be investigated further. In healthy children, the autoantibody levels against HtrA1, -3 and -4, but not against HtrA2, increase with age.
Źródło:
Acta Biochimica Polonica; 2018, 65, 3; 471-478
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-4 z 4

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