CLEONICE DA SILVA
Índice h a partir de 2011
4
Projetos de Pesquisa
Unidades Organizacionais
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
3 resultados
Resultados de Busca
Agora exibindo 1 - 3 de 3
- Hyperbaric Oxygen Therapy Induces Kidney Protection in an Ischemia/Reperfusion Model in Rats(2012) RAMALHO, R. J.; OLIVEIRA, P. S. T. de; CAVAGLIERI, R. C.; SILVA, C.; MEDEIROS, P. R. B.; MARTINI FILHO, D.; POLI-DE-FIGUEIREDO, L. F.; NORONHA, I. L.Ischemia/reperfusion (I/R) injury remains a major cause of graft dysfunction, which impacts short- and long-term follow-up. Hyperbaric oxygen therapy (HBO), through plasma oxygen transport, has been currently used as an alternative treatment for ischemic tissues. The aim of this study was to analyze the effects of HBO on kidney I/R injury model in rats, in reducing the harmful effect of I/R. The renal I/R model was obtained by occluding bilateral renal pedicles with nontraumatic vascular clamps for 45 minutes, followed by 48 hours of reperfusion. HBO therapy was delivered an hypebaric chamber (2.5 atmospheres absolute). Animals underwent two sessions of 60 minutes each at 6 hours and 20 hours after initiation of reperfusion. Male Wistar rats (n = 38) were randomized into four groups: sham, sham operated rats; Sham+HBO, sham operated rats exposed to HBO; I/R, animals submitted to I/R; and I/R+HBO, I/R rats exposed to HBO. Blood, urine, and kidney tissue were collected for biochemical, histologic, and immunohistochemical analyses. The histopathological evaluation of the ischemic injury used a grading scale of 0 to 4. HBO attenuated renal dysfunction after ischemia characterized by a significant decrease in blood urea nitrogen (BUN), serum creatinine, and proteinuria in the I/R+HBO group compared with I/R alone. In parallel, tubular function was improved resulting in significantly lower fractional excretions of sodium and potassium. Kidney sections from the I/R plus HBO group showed significantly lower acute kidney injury scores compared with the I/R group. HBO treatment significantly diminished proliferative activity in I/R (P < .05). There was no significant difference in macrophage infiltration or hemoxygenase-1 expression. In conclusion, HBO attenuated renal dysfunction in a kidney I/R injury model with a decrease in BUN, serum creatinine, proteinuria, and fractional excretion of sodium and potassium, associated with reduced histological damage.
conferenceObject Hyperbaric Oxygen Therapy Induces Kidney Protection in the Ischemia/Reperfusion Model(2012) RAMALHO, R. J.; OLIVEIRA, P. S. T.; CAVAGLIERI, R. C.; SILVA, C.; MEDEIROS, P. R. B.; MARTINI-FILHO, D.; POLI-DE-FIGUEIREDO, L. F.; NORONHA, I. L.conferenceObject Podocyte Injury in Membranous and Proliferative Lupus Nephritis: Distinct Underlying Mechanisms?(2012) REZENDE, Gabriela M.; VIANA, Vilma S. T.; MALHEIROS, Denise M.; LEON, Elaine P.; BORBA, Eduardo F.; SILVA, Neila A. S.; NORONHA, Irene L.; SILVA, Cleonice; BONFA, EloisaBackground/Purpose: Lupus nephritis (LN) is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE) with proteinuria being the predominant common manifestation and may therefore reflect podocyte injury. Podocytes are highly specialized cells that have a relevant role in the glomerular filtration barrier and alteration in the expression of their biomarkers has been shown to be associated with podocyte dysfunction in some glomerulopathies. A systematic analysis of podocyte-associated molecules encom-passing different subcellular compartments was performed in a large series of LN biopsies. Expression of Wilms tumor protein (WT1), Synaptopodin (Synpo) and glomerular epithelial protein 1 (GLEPP1) with nuclear, cytoplasmic and membrane distribution respectively, were evaluated attempting to identify if podocyte phenotype is distinct in proliferative and membranous nephritis. Possible association of molecular expression alterations with long term proteinuria severity and outcome in lupus was also investigated. Methods: Immunohistochemistry analysis was performed using monoclonal antibodies to WT1, Synpo and GLEPP1 proteins in 52 biopsies from patients with lupus nephritis fulfilling the revised ACR criteria for SLE. Demographic, clinical and laboratorial data at the time of biopsy were analyzed. Results: Thirty-nine (75%) biopsies were classified as proliferative LN and thirteen (25%) as pure membranous class V. Immunohistochemistry analysis in normal kidney revealed preserved staining of WT1, Synpo and GLEPP1 podocyte biomarkers along the capillary walls. Preserved and concomitant WT1 and Synpo staining was observed in a significant higher frequency in pure class V biopsies than in proliferative LN (69.23 vs. 2.56%, p 0.0001). Likewise, preserved GLEPP1 expression was also more frequent in pure class V LN (53.85 vs. 2.86%, p 0.0002). Proteinuria and serum albumin levels at the time of biopsy did not statistically differ in the two groups (p 0.87 and p 0.41) whereas in the mean long-term follow-up of four years a tendency of lower proteinuria (p 0.050) was observed in those patients with biopsies expressing preserved WT1/Synpo staining. Conclusion: This is the first study comparing proliferative and membranous lupus nephritis which evaluated simultaneously the expression of proteins in different subcellular podocyte compartments and provided novel evidence of preserved podocyte structural architecture predominantly in membranous lesions which may account for a better long term outcome of patients with this LN histological class. These findings suggest possible different underlying mechanisms for proteinuria in both conditions.