Navegando por Palavras-chave "acute kidney injury"
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- ItemAcesso aberto (Open Access)Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection(Instituto Oswaldo Cruz, Ministério da Saúde, 2009-12-01) Oliveira, Gabriel Melo De; Masuda, Masako Oya; Rocha, Nazaré N; Schor, Nestor [UNIFESP]; Hooper, Cléber S; Araújo-jorge, Tânia C De; Henriques-pons, Andréa; Instituto Oswaldo Cruz-Fiocruz Laboratório de Biologia Celular; Universidade Federal do Rio de Janeiro Instituto de Biofísica Carlos Chagas Filho; Universidade Federal Fluminense Instituto Biomédico Departamento de Fisiologia e Farmacologia; Universidade Federal de São Paulo (UNIFESP); Centro de Criação de Animais de Laboratório Departamento de Controle de Qualidade AnimalTrypanosoma cruzi infection induces diverse alterations in immunocompetent cells and organs, myocarditis and congestive heart failure. However, the physiological network of disturbances imposed by the infection has not been addressed thoroughly. Regarding myocarditis induced by the infection, we observed in our previous work that Fas-L-/- mice (gld/gld) have very mild inflammatory infiltration when compared to BALB/c mice. However, all mice from both lineages die in the early acute phase. Therefore, in this work we studied the physiological connection relating arterial pressure, renal function/damage and cardiac insufficiency as causes of death. Our results show that a broader set of dysfunctions that could be classified as a cardio/anaemic/renal syndrome is more likely responsible for cardiac failure and death in both lineages. However, gld/gld mice had very early glomerular deposition of IgM and a more intense renal inflammatory response with reduced renal filtration, which is probably responsible for the premature death in the absence of significant myocarditis in gld/gld.
- ItemSomente MetadadadosACE2-angiotensin-(1-7)-Mas axis in renal ischaemia/reperfusion injury in rats(Portland Press Ltd, 2010-11-01) Silveira, Katia D. da; Bosco, Kenia S. Pompermayer; Diniz, Lucio R. L.; Carmona, Adriana Karaoglanovic [UNIFESP]; Cassali, Giovanni D.; Bruna-Romero, Oscar; Sousa, Lirlandia P. de; Teixeira, Mauro M.; Santos, Robson A. S.; Simoes e Silva, Ana C.; Ribeiro Vieira, Maria A.; Universidade Federal de Minas Gerais (UFMG); Universidade Federal de São Paulo (UNIFESP)AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P < 0.01) and renal Ang-(1-7) was decreased substantially (P < 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P < 0.05), AT(1) receptors (P < 0.001) and ACE2 (P < 0.05). At 2 and 4 h of reperfusion, renal ACE activity was reduced (P < 0.05). On the other hand, renal expression of the Mas receptor was greatly increased at 4 h of reperfusion (P < 0.01), which was confirmed by immunohistochemical and Western blot analysis. in conclusion, increased renal expression of the Mas receptor associated with changes in the RAS (renin-angiotensin-system)-related peptidases support an important role for the ACE2 Ang-(1-7) Mas axis in AKI.
- ItemSomente MetadadadosAlternative pathways for angiotensin II production as an important determinant of kidney damage in endotoxemia(Amer Physiological Soc, 2016) Rosa, Rodolfo Mattar [UNIFESP]; Colucci, Juliana Almada [UNIFESP]; Yokota, Rodrigo [UNIFESP]; Moreira, Roseli Peres [UNIFESP]; Aragao, Danielle Sanches [UNIFESP]; Ribeiro, Amanda Aparecida [UNIFESP]; Arita, Danielle Yuri [UNIFESP]; Mizuno Watanabe, Ingrid Kazue [UNIFESP]; Palomino, Zaira [UNIFESP]; Cunha, Tatiana Sousa [UNIFESP]; Casarini, Dulce Elena [UNIFESP]Sepsis is an uncontrolled systemic inflammatory response against an infection and a major public health issue worldwide. This condition affects several organs, and, when caused by Gram-negative bacteria, kidneys are particularly damaged. Due to the importance of renin-angiotensin system (RAS) in regulating renal function, in the present study, we aimed to investigate the effects of endotoxemia over the renal RAS. Wistar rats were injected with Escherichia coli lipopolysaccharide (LPS) (4 mg/kg), mimicking the endotoxemia induced by Gram-negative bacteria. Three days after treatment, body mass, blood pressure, and plasma nitric oxide (NO) were reduced, indicating that endotoxemia triggered cardiovascular and metabolic consequences and that hypotension was maintained by NO-independent mechanisms. Regarding the effects in renal tissue, inducible NO synthase (iNOS) was diminished, but no changes in the renal level of NO were detected. RAS was also highly affected by endotoxemia, since renin, angiotensin-converting enzyme (ACE), and ACE2 activities were altered in renal tissue. Although these enzymes were modulated, only angiotensin (ANG) II was augmented in kidneys
- ItemAcesso aberto (Open Access)The effect of hypoxia and reoxygenation in the response of mesangial cells to angiotensin II in vitro(Sociedade Brasileira de Nefrologia, 2013-12-01) Razvickas, Clara Versolato [UNIFESP]; Borges, Fernanda Teixeira [UNIFESP]; Oliveira, Andréia Silva De [UNIFESP]; Schor, Nestor [UNIFESP]; Boim, Mirian Aparecida [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)INTRODUCTION: Mesangial cells (MC) may be involved in the glomerular alterations induced by ischemia/reperfusion injury. OBJECTIVE: To evaluate the response of immortalized MC (IMC) to 30 minutes of hypoxia followed by reoxygenation periods of 30 minutes (H/R30) or 24 hours (H/R24). METHODS: The intracellular calcium concentration ([Ca+2]i) was measured before (baseline) and after adding angiotensin II (AII, 10-5 M) in the presence and absence of glybenclamide (K ATP channel blocker). We estimated the level of intracellular ATP, nitric oxide (NO) and PGE2. RESULTS: ATP concentration decreased after hypoxia and increased after reoxygenation. Hypoxia and H/R induced increases in basal [Ca+2]i. AII induced increases in [Ca+2]i in normoxia (97 ± 9%), hypoxia (72 ± 10%) or HR30 (85 ± 17%) groups, but there was a decrease in the response to AII in group H/R24 since the elevation in [Ca+2]i was significantly lower than in control (61 ± 10%, p < 0.05). Glybenclamide did not modify this response. It was observed a significant increase in NO generation after 24 hours of reoxygenation, but no difference in PGE2 production was observed. Data suggest that H/R injury is characterized by increased basal [Ca+2]i and by an impairment in the response of cells to AII. Results suggest that the relative insensibility to AII may be at least in part mediated by NO but not by prostaglandins or vasodilator K ATP channels. CONCLUSION: H/R caused dysfunction in IMC characterized by increases in basal [Ca+2]i during hypoxia and reduction in the functional response to AII during reoxygenation.
- ItemAcesso aberto (Open Access)Endothelial, renal and hepatic variables in wistar rats treated with Vancomycin(Academia Brasileira de Ciências, 2014-12-01) Bruniera, Felipe R.; Ferreira, Felipe M.; Savioli, Luiz R.m.; Bacci, Marcelo R.; Feder, David; Pereira, Edimar Cristiano [UNIFESP]; Pedreira, Mavilde da Luz Gonçalves [UNIFESP]; Peterlini, Maria Angélica Sorgini [UNIFESP]; Perazzo, Fábio Ferreira [UNIFESP]; Azzalis, Ligia Ajaime [UNIFESP]; Rosa, Paulo César Pires [UNIFESP]; Junqueira, Virginia Berlanga Campos [UNIFESP]; Sato, Monica A.; Fonseca, Fernando Luiz Affonso [UNIFESP]; Faculdade de Medicina do ABC Departamento de Morfologia Disciplina de Farmacologia; Universidade Federal de São Paulo (UNIFESP)Vancomycin (VCM) is indicated in combat against Gram-positive infections, but it is not considered a first-choice drug because of its adverse effects. It is believed that oxidative stress is the primary mechanism of endothelial injury and the consequent VCM toxicity, which varies from phlebitis to nephrotoxicity. Moreover, dose recommendations, dilution, rates and types of infusion are still controversial. The aim of this study was to determine the effect of different VCM dilutions in endothelial, liver and kidney injuries by biochemical parameters and histopathological analysis. Wistar rats were randomly divided into six groups and subjected to femoral vein cannulation for drug administration. Control groups received 0.9 ml of saline and the others received VCM (10mg/Kg/day) at dilutions of 5.0 and 10.0 mg/mL for 3 and 7 days. Homocysteine, hs-CRP, AST, ALT, GGT, urea, creatinine, lycopene, alpha-tocopherol, beta-carotene and retinol were analyzed. Kidney, liver and cannulated femoral vein fragments were collected.This study showed alterations in ALT which featured hepatotoxicity. However, drug dilutions were not able to show changes in other biochemical parameters. In contrast, kidney and endothelium pathological changes were observed. More studies are needed to characterize VCM induced kidney and endothelium toxicity and biochemical markers able to show such morphological modifications.
- ItemSomente MetadadadosNec-1 Protects against Nonapoptotic Cell Death in Cisplatin-Induced Kidney Injury(Informa Healthcare, 2012-01-01) Tristao, Vivian Regina [UNIFESP]; Goncalves, Paula Fernanda [UNIFESP]; Dalboni, Maria Aparecida [UNIFESP]; Batista, Marcelo Costa [UNIFESP]; Durao, Marcelino de Souza [UNIFESP]; Martins Monte, Julio Cesar [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Background/aims: Necrostatin-1 (Nec-1) inhibits necroptosis, a nonapoptotic cell death pathway. Acute kidney injury (AKI) is a clinical problem of high incidence and mortality. It involves several mechanisms of cell death. We aim to evaluate the effect of Nec-1 in the toxic kidney injury model by cisplatin. Methods: We analyzed the effect of Nec-1 in AKI by cisplatin in human proximal tubule cells by flow cytometry. Results: Our results show that Nec-1 has no effect on apoptosis in renal tubular epithelial cells (Nec-1 + Cis group 13.4 +/- 1.7% vs. Cis group 14.6 +/- 1.4%) (p > 0.05). But, in conditions in which apoptosis was blocked by benzyloxy-carbonyl-Val-Ala-Asp-fluoromethyl ketone (z-VAD-fmk) the use of Nec-1 completely reversed cell viability (Nec-1 + Cis + z-VAD group 72.9 +/- 6.3% vs. Cis group 35.5 +/- 2.2%) (p < 0.05) suggesting that Nec-1 has effect on nonapoptotic cell death (necroptosis). Conclusion: Our findings suggest that the combined use of apoptosis and necroptosis inhibitors can provide additional cytoprotection in AKI. Furthermore, this is the first study to demonstrate that Nec-1 inhibits tubular kidney cell death and restores cell viability via a nonapoptotic mechanism.
- ItemSomente MetadadadosUrinary alpha-GST and pi-GST for prediction of dialysis requirement or in-hospital death in established acute kidney injury(Informa Healthcare, 2011-12-01) Seabra, Victor F. [UNIFESP]; Perianayagam, Mary C.; Tighiouart, Hocine; Liangos, Orfeas; Santos, Oscar F. P. dos [UNIFESP]; Jaber, Bertrand L.; St Elizabeths Med Ctr; Tufts Univ; Universidade Federal de São Paulo (UNIFESP); Tufts Med Ctr; Klinikum CoburgContext: Urinary alpha-glutathione S-transferase (alpha-GST) and pi-glutathione S-transferase (pi-GST) are promising proximal and distal tubular leakage markers for early detection of acute kidney injury (AKI).Objective: To examine the performance of these markers for predicting the composite of dialysis requirement or in-hospital death in patients with an established diagnosis of AKI.Materials and methods: Prospective cohort study of 245 adults with AKI. A single urinary alpha-GST and pi-GST measurement was obtained at time of nephrology consultation.Results: Overall, urinary pi-GST performed better than alpha-GST for prediction of dialysis requirement (AUC 0.59 vs. 0.56), and the composite outcome (AUC 0.58 vs. 0.56). in subgroup analyses, pi-GST displayed better discrimination for prediction of dialysis requirement in patients with baseline eGFR < 60 mL/min/1.73 m(2) (AUC 0.61) and oliguria (AUC 0.72). Similarly, alpha-GST performed better in patients with stage-1 (AUC 0.66) and stage-2 AKI (AUC 0.80).Conclusions: in patients with an established diagnosis of AKI, a single urinary pi-GST measurement performed better than alpha-GST at predicting dialysis requirement or death, but neither marker had good prognostic discrimination.
- ItemSomente MetadadadosThe use of regional citrate anticoagulation for continuous venovenous hemodiafiltration in acute kidney injury(Lippincott Williams & Wilkins, 2008-11-01) Durao, Marcelino S. [UNIFESP]; Monte, Julio C. M. [UNIFESP]; Batista, Marcelo C. [UNIFESP]; Oliveira, Moacir; Lizuka, Llson J.; Santos, Bento F. [UNIFESP]; Pereira, Virgilio G.; Cendoroglo, Miguel [UNIFESP]; Santos, Oscar F. P. [UNIFESP]; Hosp Israelita Albert Einstein; Universidade Federal de São Paulo (UNIFESP)Objective. Continuous renal replacement therapy is commonly used in the treatment of acute kidney injury. Although the optimal anticoagulation system is not well defined, citrate has emerged as the most promising method. We evaluated the data of 143 patients with acute kidney injury subjected to citrate-based continuous venovenous hemodiafiltration.Design: Retrospective cohort study.Setting. Intensive care unit of tertiary care private hospital.Patients. Patients with acute kidney injury treated from February 2004 to July 2006.Interventions: None.Measurements and Main Results: the main cause of acute kidney injury was sepsis (58%). the mean dialysis dose was 36.6 mL/kg/hr allowing for excellent metabolic control (last tests: creatinine, 1.1 mg/dL; urea, 46 mg/dL). No significant bleeding, severe electrolyte, or calcium disorders were observed. of the 418 filters used, almost 28,000 hrs of treatment, hemofilter patency was 68% at 72 hrs. Hospital mortality was 59%, and 22% of survivors were dialysis-dependent at the time of discharge. Within our sample, we identified 21 patients with liver failure (mean prothrombin time index, 21% vs. 67%, p < 0.001). This group presented with a lesser median systemic ionized calcium level (1.06 vs. 1.12 mmol/L, p < 0.001) and similar mean total calcium level (8.5 vs. 8.6 mg/dL, not significant), compared with patients without liver failure. These subjects also showed acidemia (median pH, 7.31 vs. 7.40, p < 0.001); however, they exhibited higher levels of lactate (median 29 vs. 16 mg/dL, p < 0.001), chloride (mean 109 vs. 107 mEq/L, p = 0.045) and had a trend to higher mortality rate (76% vs. 56%).Conclusions. Besides a trend toward higher mortality rate observed in the group with liver failure, we found that citrate-based continuous venovenous hemodialfiltration allowed an effective dialysis dose and reasonable filter patency. (Crit Care Med 2008; 36:3024-3029)