NF-κB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy (2013)
- Authors:
- USP affiliated authors: FANELLI, CAMILLA - FM ; FUJIHARA, CLARICE KAZUE - FM ; ZATZ, ROBERTO - FM ; CÂMARA, NIELS OLSEN SARAIVA - ICB
- Unidades: FM; ICB
- DOI: 10.1152/ajprenal.00491.2012
- Subjects: NEFROPATIAS; TÉCNICAS E PROCEDIMENTOS DE LABORATÓRIO; RIM (PATOLOGIA); RATOS WISTAR; MODELOS ANIMAIS; INSUFICIÊNCIA RENAL ANIMAL
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: American Journal of Physiology. Renal Physiology
- ISSN: 1931-857X
- Volume/Número/Paginação/Ano: v. 305, n. 2, p. F155-F163, 2013
- Este periódico é de assinatura
- Este artigo NÃO é de acesso aberto
- Cor do Acesso Aberto: closed
-
ABNT
OKABE, Cristiene et al. NF-κB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy. American Journal of Physiology. Renal Physiology, v. 305, n. 2, p. F155-F163, 2013Tradução . . Disponível em: https://doi.org/10.1152/ajprenal.00491.2012. Acesso em: 25 set. 2024. -
APA
Okabe, C., Borges, R. L., Almeida, D. C. de, Fanelli, C., Barlette, G. P., Machado, F. G., et al. (2013). NF-κB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy. American Journal of Physiology. Renal Physiology, 305( 2), F155-F163. doi:10.1152/ajprenal.00491.2012 -
NLM
Okabe C, Borges RL, Almeida DC de, Fanelli C, Barlette GP, Machado FG, Arias SCA, Malheiros DMAC, Câmara NOS, Zatz R, Fujihara CK. NF-κB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy [Internet]. American Journal of Physiology. Renal Physiology. 2013 ; 305( 2): F155-F163.[citado 2024 set. 25 ] Available from: https://doi.org/10.1152/ajprenal.00491.2012 -
Vancouver
Okabe C, Borges RL, Almeida DC de, Fanelli C, Barlette GP, Machado FG, Arias SCA, Malheiros DMAC, Câmara NOS, Zatz R, Fujihara CK. NF-κB activation mediates crystal translocation and interstitial inflammation in adenine overload nephropathy [Internet]. American Journal of Physiology. Renal Physiology. 2013 ; 305( 2): F155-F163.[citado 2024 set. 25 ] Available from: https://doi.org/10.1152/ajprenal.00491.2012 - Renoprotective effect of two dosages of Losartan (L) in a model of crhonic kidney disease (CDK) by nitric oxide inhibition and and salt overload
- Losartan (L) and hydrochlorotiazide (H) association (LH) arrests renal inhury in a model of very advanced chronic kidney disease (CKD)
- Losartan (L) and Hydrochlorothiazide (H)Treatment (LH) arrests renal and cardiac injury in advanced chronic kidney disease by mechanisms not entireky dependent on blood pressure
- Furosemide (F) is less effective than hydroclorothiazide (H) as adjuvant to losartan (L) in arresting the nephropathy associated with the 5/6 renal ablation model (NX)
- Associação terapêutica de losartan (L) e hidroclorotiazida (H) previne progressão da lesão renal em modelo de nefropatia crônica resultante da administração de (L) durante a lactação
- Mechanisms of progressive renal injury in adult rats treated with losartan during lactation
- Effects of losartan, in monotherapy or in association with hydrochlorothiazide, in chronic nephropathy resulting from losartan treatment during lactation
- Regression of Albuminuria and Hypertension and Arrest of Severe Renal Injury by a Losartan-Hydrochlorothiazide Association in a Model of Very Advanced Nephropathy
- Combined Losartan (L) and Hydrocholorothyazide (H) treatment (LH) prevents progression of chronic kidney disease (CKD) resulting from L treatment during lactation (LLac)
- Regressão da nefropatia diabética experimental: Ausência de efeito dose resposta de um antagonista da angiotensina II
Informações sobre o DOI: 10.1152/ajprenal.00491.2012 (Fonte: oaDOI API)
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