Urinary excretion of endothelin-1 (ET-1), transforming growth factor- 1 (TGF- 1) and vascular endothelial growth factor (VEGF165) in paediatric chronic kidney diseases: results of the ESCAPE trial

Grenda, Ryszard; Wühl, Elke; Litwin, Mieczysław; Janas, Roman; Śladowska, Joanna; Arbeiter, Klaus; Berg, Ulla; Afonso, Alberto Caldas; Fischbach, Michel; Mehls, Otto; Sartipy, Peter; Schaefer, Franz

doi:10.1093/ndt/gfm300

Cited by 44 publications

(46 citation statements)

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“…38 O aumento da excreção desses mediadores correlacionou-se com a diminuição da taxa de filtração glomerular (TFG) e foi mais evidente nos pacientes com uropatias obstrutivas, refletindo o impacto da lesão túbulo-intersticial sobre a função renal global. 38 …”

Section: Inflamação E Doença Renal Crônicaunclassified

“…participação de citocinas e quimiocinas em diferentes mecanismos de lesão ao tecido renal. [24][25][26][27][28][29][30][31][32][33][34][35][36][37][38] Especificamente no tecido renal, as citocinas induzem proliferação local de células tubulares e intersticiais, síntese de matriz extracelular, atividade pró-coagulante do endotélio, formação de espécies reativas de oxigênio e aumento da expressão de moléculas de adesão e lípides biologicamente ativos. [24][25][26][27][28][29][30][31] A liberação de citocinas também se relaciona aos efeitos hemodinâmicos e locais da ativação do sistema renina angiotensina (SRA).…”

Section: Citocinas E Quimiocinasunclassified

“…Ref n 38 38 303 11,5 ± 3,9 TGF-β1 Aumento da excreção urinária de TGF-β1 na DRC estágios II-IV Eardley et al 87 …”

Section: Autorunclassified

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Inflamação na doença renal crônica: papel de citocinas

et al. 2011

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Os autores declaram a inexistência de confl itos de interesse. resumoA doença renal crônica (DRC) é um grave problema de saúde pública cuja prevalência tem aumentado nos últimos anos. Apresenta caráter progressivo e está associada à elevada morbidade e mortalidade. Inúmeros fatores estão associados à instalação e progressão da DRC, tais como obesidade, hipertensão arterial e diabetes mellitus. Além desses fatores, existem evidências de inflamação na fisiopatologia da DRC. Diversas citocinas e quimiocinas têm sido detectadas no plasma e urina de pacientes em estágios precoces da DRC e também relacionadas às complicações da doença. A expressão desses mediadores e a lesão renal sofrem interferência de fár-macos como inibidores de enzima conversora de angiotensina (ECA), estatinas e antagonistas de receptores de citocinas. A modulação da resposta imuno-inflamató-ria pode se tornar alvo para tratamento da DRC. O objetivo deste artigo de revisão foi resumir as evidências científicas do papel da inflamação na DRC, destacando-se os efeitos de citocinas e quimiocinas. Palavras-chave: Citocinas. Quimiocinas. Inflamação. Falência renal crônica. abstractChronic kidney disease (CKD) is a serious public health problem whose prevalence has increased in the last few years. Its progression is associated with high morbidity and mortality. Several factors are associated with the onset and progression of CKD, such as obesity, hypertension and diabetes mellitus. Beyond these factors, there is evidence of a pathophysiological role for inflammation in CKD. Several cytokines and chemokines have been detected in the plasma and urine of patients at early stages of CKD, and have also been related to CKD complications. The expression of these mediators and renal injury may be influenced by drugs such as angiotensin-converting enzyme inhibitors, statins and antagonists of cytokine receptors. Modulation of the immune-inflammatory response can become a target for CKD treatment. The aim of this study was to review the scientific evidence on the role of inflammation in CKD, especially the effects of cytokines and chemokines.

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Section: Inflamação E Doença Renal Crônicaunclassified

Section: Citocinas E Quimiocinasunclassified

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Inflamação na doença renal crônica: papel de citocinas

et al. 2011

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“…A role for TGF-␤1 is implicated in the deposition of collagen that accompanies the progression of renal disease in rodent models. 34,35 It has also been reported that TGF-␤1 levels are particularly high in pediatric patients with renal insufficiency 36 and in black hypertensives with target organ damage. 2,37 We can find no reports describing an assessment of TGF-␤3 levels in patients with hypertension.…”

Section: Discussionmentioning

confidence: 98%

Chlorthalidone Decreases Platelet Aggregation and Vascular Permeability and Promotes Angiogenesis

2010

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Abstract-Variations in diuretic-mediated inhibition of carbonic anhydrase-dependent chloride transport in platelets and vascular smooth muscle could account for the contrasting efficacy of the thiazide and thiazide-like diuretics in reducing cardiovascular morbidity in patients with hypertension. We assessed platelet carbonic anhydrase activity and catecholamine-induced platelet aggregation in the presence of a thiazide and a "thiazide-like" inhibitor of the sodium-chloride cotransporter. Individual variation in platelet carbonic anhydrase activity correlated with contrasting sensitivity to epinephrine-mediated platelet aggregation. Both chlorthalidone, which potently inhibits platelet carbonic anhydrase, and bendroflumethiazide, which has much less effect on this enzyme, increased the amount of epinephrine needed to induce platelet aggregation when compared with the absence of a diuretic. However, chlorthalidone was significantly more effective than bendroflumethiazide in reducing epinephrine-mediated platelet aggregation. Chlorthalidone also induced marked changes in the number of gene transcripts for two proteins that mediate angiogenesis and vascular permeability, vascular endothelial growth factor C and transforming growth factor-␤3; chlorthalidone and bendroflumethiazide had contrasting effects on the expression of vascular endothelial growth factor C. Chlorthalidone and bendroflumethiazide reduced vascular permeability to albumin, but only chlorthalidone increased angiogenesis. Thiazides and thiazide-like diuretics can comparably reduce blood pressure, but the drugs in this class are not all alike. It can be suggested from our findings that thiazide and thiazide-like diuretics vary in their pleiotropic effects on platelets and in the vasculature, and these differences could explain the contrasting ability of these drugs to reduce cardiovascular morbidity despite comparable reduction in blood pressure. (Hypertension. 2010;56:463-470.)

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“…Substâncias que participam de passos chave da uropatia obstrutiva já foram estudadas com base no mecanismo em que participam: 1) resposta vascular: endotelina-1 , vascular endothelial growth factor VEGF (Grenda et al, 2007); 2) migração de leucócitos: proteína quimiotática de monócitos MCP-1 (Grandaliano et al, 2000;Bartoli et al, 2011;Stephan et al, 2002), interleucinas (Madsen et al, 2012); 3) fatores de crescimento: o fator de crescimento epidermal EGF (Oka et al, 1999;, o insulin-like growth factor-1 IGF-1 (Marshall et al, 1991;Serel et al, 2000) ; 4) disfunção tubular: kidney injury molecule-1 KIM-1 (Wasilewska et al, 2011), N-acetil-ß-D-glucosaminidase, γ-glutamil transferase e fosfatase alcalina (Everaert et al, 1998;Shokeir et al, 2009 ß2-microglobulina (Dommergues et al, 2000).…”

Section: Marcadores De Obstrução Do Trato Urináriounclassified

Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos

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Urinary excretion of endothelin-1 (ET-1), transforming growth factor- 1 (TGF- 1) and vascular endothelial growth factor (VEGF165) in paediatric chronic kidney diseases: results of the ESCAPE trial

Cited by 44 publications

References 29 publications

Inflamação na doença renal crônica: papel de citocinas

Inflamação na doença renal crônica: papel de citocinas

Chlorthalidone Decreases Platelet Aggregation and Vascular Permeability and Promotes Angiogenesis

Avaliação dos valores séricos e urinários de CA 19-9 e TGFbeta1 na obstrução parcial e completa de ureteres em ratos

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