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Wyświetlanie 1-3 z 3
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:
EUCOMMIA ULMOIDES OLIV. EXTRACT REGULATES AGE-INDUCED INJURY IN TUBULAR ENDOTHELIAL CELLS VIA THE RAGE-NRF2 PATHWAY
Autorzy:
Hur, Jinyoung
Do, Moon Ho
Kim, Mina
Choi, Jiwon
Kim, Yoonsook
Ha, Sang Keun
Powiązania:
https://bibliotekanauki.pl/articles/895476.pdf
Data publikacji:
2019-08-30
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
diabetic nephropathy
advanced glycation end product
nuclear factor erythroid 2-related factor 2
Eucommia ulmoides
Opis:
The leaves, stems, and bark of Eucommia ulmoides Oliv. (EU), also known as Du-Zhong, have traditionally been used to cure various diseases, such as liver, kidney, and muscle diseases, in Asia. Despite evidence for protective effects against renal complications, its precise effects and mechanisms of action are unclear. In this study, the effects of EU on advanced glycation end products (AGEs)-induced renal disease and its mechanism were examined. NRK 52E normal rat kidney tubular epithelial cells were treated with AGEs and an EU extract. Expression levels of TGF-β1, an indicator of renal cell damage, and catalase, an antioxidant marker, were examined. Nuclear factor-E2-related factor 2 (Nrf2), kelch-like ECH-associated protein 1 (keap1), and p65 regulation were examined to identify additional antioxidant mechanisms related to renal cell apoptosis and AGEs-induced renal cell damage. The effects of EU on mitogen-activated protein kinase (MAPK), Akt, and phosphoinositide 3-kinase (PI3K), which are involved in apoptosis, were also examined. TGF-β1 expression increased in response to AGEs and decreased by additional treatment with EU. Additionally, EU increased the expression of catalase. We found that EU increased Nrf2, keap1, and p65 and regulated the expression of RAGE (receptor for AGEs) and its downstream target Sirt1. EU also regulated the AGEs-altered phosphorylation of apoptosis factors. Based on these findings, we concluded that EU regulates AGEs-induced renal cell damage via antioxidant and apoptosis-related mechanisms.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 4; 683-690
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-3 z 3

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