Navegando por Palavras-chave "Acute renal failure"
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- ItemSomente MetadadadosAscorbic acid reduces gentamicin-induced nephrotoxicity in rats through the control of reactive oxygen species(Churchill Livingstone, 2014-04-01) Moreira, Miriam A.; Nascimento, Marcos A.; Bozzo, Tatiana A.; Cintra, Alvaro [UNIFESP]; Silva, Sonia M. da [UNIFESP]; Dalboni, Maria Aparecida [UNIFESP]; Mouro, Margaret G.; Higa, Elisa M. S. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Background & aim: Oxidative stress has been implicated in the pathophysiology of many forms of acute renal failure. the aim was examine the effect of vitamin C on oxidative stress and its relationship with nitric oxide on gentamicin-induced nephrotoxicity in rats.Methods: We utilized 32 Wistar rats allocated in four groups of eight animals each: control (CTL), vitamin C (VIT C), gentamicin (GENTA), and GENTA + VIT C; all groups were treated during seven days.Results: Serum urea and creatinine, serum and renal tissue malondialdehyde, blood superoxide anion and hydrogen peroxide in GENTA were increased vs CTL and vs VIT C, and decreased in GENTA + VIT C vs GENTA (all P < 0.05). Serum nitric oxide increased in GENTA vs CTL and vs VIT C, and reduced in GENTA + VII C vs GENTA (P < 0.001). Urinary nitric oxide was reduced in GENTA vs CTL and vs VIT C and increased in GENTA + VIT C vs GENTA (P < 0.001). Severe degeneration of proximal tubules was present in GENTA, but only mild lesions were observed in GENTA + VIT C.Conclusion: This study suggests that VIT C is a valuable tool to protect against GENTA-induced nephrotoxicity, by reducing reactive oxygen species and increasing the nitric oxide. (C) 2013 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.
- ItemAcesso aberto (Open Access)Collagen XVIII/endostatin expression in experimental endotoxemic acute renal failure(Associação Brasileira de Divulgação Científica, 2009-12-01) Cichy, Milene Cristina [UNIFESP]; Rocha, Flavia Gomes de Goes [UNIFESP]; Tristão, Vivian Regina [UNIFESP]; Pessoa, Edson de Andrade [UNIFESP]; Cenedeze, Marcos Antonio [UNIFESP]; Nürmberg Junior, R.; Schor, Nestor [UNIFESP]; Bellini, Maria Helena [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Instituto de Pesquisas Energéticas e Nucleares Centro de Biotecnologia; Faculdades Metropolitanas Unidas Faculdade de Medicina VeterináriaAcute renal failure (ARF) is a frequent complication of Gram-negative sepsis, with a high risk of mortality. Lipopolysaccharide (LPS)-induced ARF is associated with hemodynamic changes that are strongly influenced by the overproduction of nitric oxide (NO) through the cytokine-mediated up-regulation of inducible NO synthase. LPS-induced reductions in systemic vascular resistance paradoxically culminate in renal vasoconstriction. Collagen XVIII is an important component of the extracellular matrix expressed in basement membranes. Its degradation by matrix metalloproteases, cathepsins and elastases results in the formation of endostatin, claimed to have antiangiogenic activity and to be a prominent vasorelaxing agent. We evaluated the expression of endostatin/collagen XVIII in an endotoxemic ARF model. ARF was induced in C57BL/6 mice by intraperitoneal injection of LPS (10 mg/kg) followed by sacrifice 4 and 12 h later. Kidney tissue was the source of RNA and protein and the subject of histological analysis. As early as 4 h after LPS administration, blood urea, creatinine and NO levels were significantly increased compared to control. Endostatin/collagen XVIII mRNA levels were 0.71 times lower than sham-inoculated mice 4 h after LPS inoculation, returning to normal levels 12 h after LPS inoculation. Immunohistological examination revealed that acute injury caused by LPS leads to an increase of endostatin basement membrane staining in association with the decrease of CD31 endothelial basement membrane staining. These results indicate that in the early phase of endotoxemic ARF the endostatin levels were not regulated by gene expression, but by the metabolism of collagen XVIII.
- ItemAcesso aberto (Open Access)Contribution of CD4+ T cells to the early mechanisms of ischemia- reperfusion injury in a mouse model of acute renal failure(Associação Brasileira de Divulgação Científica, 2007-04-01) Pinheiro, Helady Sanders [UNIFESP]; Câmara, Niels Olsen Saraiva [UNIFESP]; Noronha, Irene Lourdes; Longo-Maugéri, Ieda Maria [UNIFESP]; Franco, Marcello Fabiano de [UNIFESP]; Medina, J.o.a.p. [UNIFESP]; Pacheco-Silva, Alvaro [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal de Juiz de Fora Divisão de Nefrologia; Universidade de São Paulo (USP)Renal ischemia-reperfusion (IR) injury is the major cause of acute renal failure in native and transplanted kidneys. Mononuclear leukocytes have been reported in renal tissue as part of the innate and adaptive responses triggered by IR. We investigated the participation of CD4+ T lymphocytes in the pathogenesis of renal IR injury. Male mice (C57BL/6, 8 to 12 weeks old) were submitted to 45 min of ischemia by renal pedicle clamping followed by reperfusion. We evaluated the role of CD4+ T cells using a monoclonal depleting antibody against CD4 (GK1.5, 50 µ, ip), and class II-major histocompatibility complex molecule knockout mice. Both CD4-depleted groups showed a marked improvement in renal function compared to the ischemic group, despite the fact that GK1.5 mAb treatment promoted a profound CD4 depletion (to less than 5% compared to normal controls) only within the first 24 h after IR. CD4-depleted groups presented a significant improvement in 5-day survival (84 vs 80 vs 39%; antibody treated, knockout mice and non-depleted groups, respectively) and also a significant reduction in the tubular necrosis area with an early tubular regeneration pattern. The peak of CD4-positive cell infiltration occurred on day 2, coinciding with the high expression of ßC mRNA and increased urea levels. CD4 depletion did not alter the CD11b infiltrate or the IFN-g and granzyme-B mRNA expression in renal tissue. These data indicate that a CD4+ subset of T lymphocytes may be implicated as key mediators of very early inflammatory responses after renal IR injury and that targeting CD4+ T lymphocytes may yield novel therapies.
- ItemSomente MetadadadosCritical involvement of Th1-related cytokines in renal injuries induced by ischemia and reperfusion(Elsevier B.V., 2009-06-01) Paiva, Vanessa Nunes de [UNIFESP]; Monteiro, Rebecca M. M. [UNIFESP]; Marques, Vilmar de Paiva; Cenedeze, Marcos Antonio [UNIFESP]; Teixeira, Vicente de P. A.; Reis, Marlene A. dos; Pacheco-Silva, Alvaro [UNIFESP]; Camara, Niels O. S. [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Hosp Israelita Albert Einstein; Univ Fed Triangulo MineiroRenal ischemia and reperfusion injury (IRI) is considered an inflammatory syndrome. To move forward in its pathogenesis, we exploited the role of several cytokines on renal damages triggered by IRI. Specifically to evaluate the role of Th1 immune profile in this system, IL-12, IFN-gamma, and IFN-gamma/IL-12 deficient (KO) mice on C57BL/6 background and their controls were subjected to IRI. in each group, blood and kidney samples were harvested. Renal function was evaluated by serum creatinine and renal morphometric analyses. Gene expression of IL-6 and HO-1 were also investigated by Q-PCR. IFN-gamma KO animals presented the highest impairment in renal function compared to controls. Conversely, IL-12 KO animals were absolutely protected and, in a lesser extent, IFN-gamma/IL-12 KO double knockout was also protected from IRI. Gene expression analyses showed higher expression of HO-1, a cytoprotective gene, and IL-6, a pro-inflammatory cytokine, in IFN-gamma deficient animals subjected to IRI. Our results confirm that Th1 related cytokines such as IL-12 and IFN-gamma are critically involved in renal ischemia and reperfusion injury. (C) 2008 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosEarly modulation of inflammation by mesenchymal stem cell after acute kidney injury(Elsevier B.V., 2009-06-01) Semedo, Patricia [UNIFESP]; Palasio, Carolina G. [UNIFESP]; Oliveira, Cassiano D. [UNIFESP]; Feitoza, Carla Q. [UNIFESP]; Goncalves, Giselle M. [UNIFESP]; Cenedeze, Marcos Antonio [UNIFESP]; Wang, Pamella M. H. [UNIFESP]; Teixeira, Vicente P. A.; Reis, Marlene A.; Pacheco-Silva, Alvaro [UNIFESP]; Saraiva Camara, Niels Olsen [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Triangulo Mineiro Med SchTherapy with stem cells has showed to be promising for acute kidney injury (AKI), although how it works is still controversial. Modulation of the inflammatory response is one possible mechanism. Most of published data relies on early time and whether the protection is still maintained after that is not known. Here, we analyzed whether immune modulation continues after 24 h of reperfusion. MSC were obtained from male Wistar rats. After 3-5 passages, cells were screened for CD73, CD90, CD44, CD45, CD29 and CD 31. in addition, MSC were submitted to differentiation in adipocyte and in osteocyte. AKI was induced by bilaterally clamping of renal pedicles for 60 min. Six hours after injury, MSC (2 x 105 cells) were administered intravenously. MSC-treated animals presented the lowest serum creatinine compared to non-treated animals (24 h: 1.3 +/- 0.21 vs. 3.23 +/- 0.89 mg/dl, p<0.05). the improvement in renal function was followed by a lower expression of IL-1b, IL-6 and TNF-alpha and higher expression of IL-4 and IL-10. However, 48 h after reperfusion, this cytokine profile has changed. the decrease in Th1 cytokines was less evident and IL-6 was markedly up regulated. PCNA analysis showed that regeneration occurs faster in kidney tissues of MSC-treated animals than in controls at 24 h. and also ratio of Bcl-2/Bad was higher at treated animals after 24 and 48 h. Our data demonstrated that the immunomodulatory effects of MSC occur at very early time point, changing the inflammation profile toward a Th2 profile. (C) 2009 Elsevier B.V. All rights reserved.
- ItemAcesso aberto (Open Access)Effect of cyclooxygenase inhibitors on gentamicin-induced nephrotoxicity in rats(Associação Brasileira de Divulgação Científica, 2004-07-01) Hosaka, E.m.; Santos, Oscar Fernando Pavão dos [UNIFESP]; Seguro, A.c.; Vattimo, M.f.f.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)The frequent use of nonsteroidal anti-inflammatory drugs (NSAID) in combination with gentamicin poses the additional risk of nephrotoxic renal failure. Cyclooxygenase-1 (COX-1) is the main enzyme responsible for the synthesis of renal vasodilator prostaglandins, while COX-2 participates predominantly in the inflammatory process. Both are inhibited by non-selective NSAID such as indomethacin. Selective COX-2 inhibitors such as rofecoxib seem to have fewer renal side effects than non-selective inhibitors. The objective of the present study was to determine whether the combined use of rofecoxib and gentamicin can prevent the increased renal injury caused by gentamicin and indomethacin. Male Wistar rats (250-300 g) were treated with gentamicin (100 mg/kg body weight, ip, N = 7), indomethacin (5 mg/kg, orally, N = 7), rofecoxib (1.4 mg/kg, orally, N = 7), gentamicin + rofecoxib (100 and 1.4 mg/kg, respectively) or gentamicin + indomethacin (100 and 5 mg/kg, respectively, N = 8) for 5 days. Creatinine clearance and alpha-glutathione-S-transferase concentrations were used as markers of renal injury. Animals were anesthetized with ether and sacrificed for blood collection. The use of gentamicin plus indomethacin led to worsened renal function (0.199 ± 0.019 ml/min), as opposed to the absence of a nephrotoxic effect of rofecoxib when gentamicin plus rofexicob was used (0.242 ± 0.011 ml/min). These results indicate that COX-2-selective inhibitors can be used as an alternative treatment to conventional NSAID, especially in situations in which risk factors for nephrotoxicity are present.
- ItemAcesso aberto (Open Access)Incidence, risk factors and prognostic factors of acute renal failure in patients admitted to an intensive care unit(Associação Brasileira de Divulgação Científica, 2006-10-01) Mataloun, Sergio Elia [UNIFESP]; Machado, Flávia Ribeiro [UNIFESP]; Senna, Ana Paula Resque [UNIFESP]; Guimarães, Hélio Penna [UNIFESP]; Amaral, José Luiz Gomes do [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)The objective of the present study was to assess the incidence, risk factors and outcome of patients who develop acute renal failure (ARF) in intensive care units. In this prospective observational study, 221 patients with a 48-h minimum stay, 18-year-old minimum age and absence of overt acute or chronic renal failure were included. Exclusion criteria were organ donors and renal transplantation patients. ARF was defined as a creatinine level above 1.5 mg/dL. Statistics were performed using Pearsons' chi2 test, Student t-test, and Wilcoxon test. Multivariate analysis was run using all variables with P < 0.1 in the univariate analysis. ARF developed in 19.0% of the patients, with 76.19% resulting in death. Main risk factors (univariate analysis) were: higher intra-operative hydration and bleeding, higher death risk by APACHE II score, logist organ dysfunction system on the first day, mechanical ventilation, shock due to systemic inflammatory response syndrome (SIRS)/sepsis, noradrenaline use, and plasma creatinine and urea levels on admission. Heart rate on admission (OR = 1.023 (1.002-1.044)), male gender (OR = 4.275 (1.340-13642)), shock due to SIRS/sepsis (OR = 8.590 (2.710-27.229)), higher intra-operative hydration (OR = 1.002 (1.000-1004)), and plasma urea on admission (OR = 1.012 (0.980-1044)) remained significant (multivariate analysis). The mortality risk factors (univariate analysis) were shock due to SIRS/sepsis, mechanical ventilation, blood stream infection, potassium and bicarbonate levels. Only potassium levels remained significant (P = 0.037). In conclusion, ARF has a high incidence, morbidity and mortality when it occurs in intensive care unit. There is a very close association with hemodynamic status and multiple organ dysfunction.
- ItemSomente MetadadadosA role for regulatory T cells in renal acute kidney injury(Elsevier B.V., 2009-05-01) Monteiro, Rebecca M. M. [UNIFESP]; Camara, Niels O. S. [UNIFESP]; Rodrigues, Mauricio M. [UNIFESP]; Tzelepis, Fanny [UNIFESP]; Damiao, Marcio J. [UNIFESP]; Cenedeze, Marcos A. [UNIFESP]; Teixeira, Vicente de Paula A.; Reis, Marlene A. dos; Pacheco-Silva, Alvaro [UNIFESP]; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP); Hosp Albert EinsteinIschemia reperfusion injury (IRI) is a potential contributor for the development of chronic allograft nephropathy. T cells are important mediators of injury, even in the absence of alloantigens. We performed a depletion of TCD4(+)CTLA4(+)Foxp3(+) cells with anti-CD25(PC61), a treatment with anti-GITR (DTA-1) and rat-IgG, followed by 45 min of ischemia and 24/72 h of reperfusion, and then analyzed blood urea, kidney histopathology and gene expression in kidneys by QReal Time PCR. After 24 h of reperfusion, depletion of TCD4(+)CTLA4(+)Foxp3(+) cells reached 30.3%(spleen) and 67.8%(lymph nodes). 72 h after reperfusion depletion reached 43.1%(spleen) and 90.22%(lymph nodes) and depleted animals presented with significantly poorer renal function, while DTA-1 (anti-GITR)-treated ones showed a significant protection, all compared to serum urea from control group (IgG: 150.10 +/- 50.04; PC61: 187.23 +/- 31.38; DTA-1: 64.53 +/- 25.65, mg/dL, p<0.05). These data were corroborated by histopathology. We observed an increase of HO-1 expression in animals treated with DTA-1 at 72 h of reperfusion with significant differences. Thus, our results suggest that PC61 (anti-CD25) mAb treatment is deleterious, while DTA-1 (anti-GITR) mAb treatment presents a protective role in the renal IRI, indicating that some regulatory populations of T cells might have a role in IRI. (C) 2009 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosTransplantation With Kidneys Retrieved From Deceased Donors With Acute Renal Failure(Lippincott Williams & Wilkins, 2013-02-27) Klein, Rodrigo [UNIFESP]; Galante, Nelson Zocoler [UNIFESP]; Sandes-Freitas, Taina Veras de [UNIFESP]; Franco, Marcello Fabiano de [UNIFESP]; Tedesco-Silva, Helio [UNIFESP]; Medina-Pestana, Jose Osmar [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Hosp Rim & HipertensaoBackground. the discard rate of kidneys recovered from deceased donors with acute renal failure (ARF) is higher compared with those without ARF mainly due to the uncertainty regarding short-term and long-term outcomes.Methods. We retrospectively analyzed 1-year patient, graft, and rejection-free survivals and renal function of transplantations performed with kidneys recovered from deceased donors with or without ARF, defined as serum creatinine level of more than 1.5 mg/dL. We performed multivariable analysis to evaluate whether ARF was an independent risk factor associated with inferior outcomes.Results. of a total of 1518 patients, 253 received kidneys from expanded-criteria donors (ECD; with ARF [n=116] and without ARF [n=137]) and 1265 from standard-criteria donors (SCD; with ARF [n=369] and without ARF [n=896]). the incidence of delayed graft function was higher in ECD (68.1% vs. 58.4%; P=0.072) and SCD (69.9% vs. 50.6%; P<0.001) recipients of kidneys with ARF compared with those without ARF, respectively. At 1 year, patient, graft, and rejection-free survivals were not statistically different in SCD or ECD recipients with or without ARF. Renal function at 1 year was similar in recipients of ECD (41.9 +/- 26.3 vs. 40.1 +/- 21.7 mL/min; P=0.565) or SCD (50.9 +/- 29.9 vs. 53.6 +/- 28.5 mL/min; P=0.131) kidneys with and without ARF, respectively. Compared with kidneys without ARF, receiving a kidney allograft with ARF was not associated with increased risk of death, graft lost, or inferior renal function 1 year after transplantation.Conclusion. in this cohort of patients, kidneys from deceased donors with ARF provided graft survival and renal function comparable with kidneys from donors without ARF 1 year after transplantation.