MARIANA MOURA NASCIMENTO
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais, Hospital das Clínicas, Faculdade de Medicina
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais, Hospital das Clínicas, Faculdade de Medicina
8 resultados
Resultados de Busca
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- Treatment with beta-blocker nebivolol ameliorates oxidative stress and endothelial dysfunction in tenofovir-induced nephrotoxicity in rats(2022) NASCIMENTO, Mariana Moura; BERNARDO, Desiree Rita Denelle; BRAGANCA, Ana Carolina de; SHIMIZU, Maria Heloisa Massola; SEGURO, Antonio Carlos; VOLPINI, Rildo Aparecido; CANALE, DanieleBackgroundTenofovir disoproxil fumarate (TDF), a widely prescribed component in antiretroviral regimens, has been associated with nephrotoxicity. Nebivolol is a third generation selective beta-1 adrenergic receptor blocker and may protect renal structure and function through the suppression of oxidative stress and enhancement of nitric oxide (NO) synthesis. We aimed to investigate whether nebivolol could be an effective therapeutic strategy to mitigate tenofovir-induced nephrotoxicity. MethodsWe allocated Wistar rats to four groups: control (C), received a standard diet for 30 days; NBV, received a standard diet for 30 days added with nebivolol (100 mg/kg food) in the last 15 days; TDF, received a standard diet added with tenofovir (300 mg/kg food) for 30 days; and TDF+NBV, received a standard diet added with tenofovir for 30 days and nebivolol in the last 15 days. ResultsLong-term exposure to tenofovir led to impaired renal function, induced hypertension, endothelial dysfunction and oxidative stress. Nebivolol treatment partially recovered glomerular filtration rate, improved renal injury, normalized blood pressure and attenuated renal vasoconstriction. Administration of nebivolol contributed to reductions in asymmetric dimethylarginine (ADMA) levels as well as increases in endothelial nitric oxide sintase (eNOS) accompanied by renin-angiotensin-aldosterone system downregulation and decreases in macrophage and T-cells infiltrate. Furthermore, nebivolol was responsible for the maintenance of the adequate balance of thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels and it was associated with reductions in NADPH oxidase (NOX) subunits. ConclusionNebivolol holds multifaceted actions that promote an advantageous option to slow the progression of kidney injury in tenofovir-induced nephrotoxicity.
- Impact of Discontinuing Levofloxacin Prophylaxis on Bloodstream Infections in Neutropenic Hematopoietic Stem Cell Transplantation Patients(2022) GUIMARAES, Thais; BORGES, Igor Carmo; SPADAO, Fernanda de Souza; MARIANO, Livia; NASCIMENTO, Marina de Mattos; HIGASHINO, Hermes; ROSSI, Flavia; ROCHA, Vanderson; COSTA, Silvia FigueiredoMultidrug-resistant pathogens have emerged worldwide. We have driven the hypothesis that the non-use of fluoroquinolone prophylaxis during neutropenia could reduce antibiotic resistance in Gram-negative bacteria that cause bloodstream infections (BSIs) in hematopoietic stem cell transplantation (HSCT) patients and that this change in resistance pattern could lead to an impact on BSI mortality. This is a quasi-experimental study comparing BSI incidence, resistance patterns of bacteria that cause BSI, and BSI mortality when levofloxacin prophylaxis was routine for neutropenic HSCT patients (2016-2018) to when fluoroquinolone prophylaxis was discontinued in our center (2019). Bivariate comparisons and multivariate logistic regression models were used for analyses. A total of 310 HSCTs (66 (21%) allogeneic and 244 (79%) autologous) were performed during the study period. Sixty (19%) patients had BSIs, 30 in each evaluated period. The discontinuation of levofloxacin prophylaxis was associated with an increase in BSI incidence and a decrease in the resistance rates of causative BSI bacteria and in BSI 30-day mortality. The increase in the rate of resistant bacteria causing BSI and in BSI mortality might outweigh the benefits of a decrease in BSI incidence caused by fluoroquinolone prophylaxis in neutropenic HSCT patients. We suggest that the routine use of fluoroquinolone in this context be revisited.
conferenceObject A SINGLE DOSE OF LITHIUM PROTECTS AGAINST RENAL INJURY FOLLOWING BILATERAL URETERAL OBSTRUCTION(2022) SHIMIZU, Maria Heloisa Massola; VOLPINI, Rildo Aparecido; BRAGANCA, Ana Carolina de; NASCIMENTO, Mariana Moura; BERNARDO, Desiree; CANALE, Daniele; SEGURO, Antonio CarlosconferenceObject OBESITY ASSOCIATED WITH VITAMIN D DEFICIENCY IMPAIRS RENAL FUNCTION, HAEMODYNAMICS, METABOLIC PARAMETERS AND AGGRAVATES THE RENAL MORPHOLOGICAL DAMAGE IN RATS SUBMITTED TO ISCHAEMIA-REPERFUSION INJURY(2022) BERNARDO, Desiree; BRAGANCA, Ana Carolina de; SHIMIZU, Maria Heloisa Massola; SEGURO, Antonio Carlos; NASCIMENTO, Mariana Moura; CANALE, Daniele; VOLPINI, Rildo AparecidoconferenceObject TREATMENT WITH NEBIVOLOL AMELIORATES RENOVASCULAR ALTERATIONS AND OXIDATIVE STRESS IN TENOFOVIR-INDUCED NEPHROTOXICITY IN RATS(2022) NASCIMENTO, Mariana Moura; BERNARDO, Desiree; BRAGANCA, Ana Carolina de; SHIMIZU, Maria Heloisa Massola; SEGURO, Antonio Carlos; VOLPINI, Rildo Aparecido; CANALE, DanieleconferenceObject Male Mice Heterozygous LSD1 Knockout Gene Prevented the Effect of High Sodium Intake on Renal Fibrosis and AT1 Conformational Status(2019) NASCIMENTO, Mariana Moura; KATAYAMA, Isis Akemi; POJOGA, Luminita H.; HEIMANN, Joel Claudio- Administration of a single dose of lithium ameliorates rhabdomyolysis-associated acute kidney injury in rats(2023) SHIMIZU, Maria Heloisa Massola; VOLPINI, Rildo Aparecido; BRAGANCA, Ana Carolina de; NASCIMENTO, Mariana Moura; BERNARDO, Desiree Rita Denelle; SEGURO, Antonio Carlos; CANALE, DanieleRhabdomyolysis is characterized by muscle damage and leads to acute kidney injury (AKI). Clinical and experimental studies suggest that glycogen synthase kinase 3 beta (GSK3 beta) inhibition protects against AKI basically through its critical role in tubular epithelial cell apoptosis, inflammation and fibrosis. Treatment with a single dose of lithium, an inhibitor of GSK3 beta, accelerated recovery of renal function in cisplatin and ischemic/reperfusion-induced AKI models. We aimed to evaluate the efficacy of a single dose of lithium in the treatment of rhabdomyolysis-induced AKI. Male Wistar rats were allocated to four groups: Sham, received saline 0.9% intraperitoneally (IP); lithium (Li), received a single IP injection of lithium chloride (LiCl) 80 mg/kg body weight (BW); glycerol (Gly), received a single dose of glycerol 50% 5 mL/kg BW intramuscular (IM); glycerol plus lithium (Gly+Li), received a single dose of glycerol 50% IM plus LiCl IP injected 2 hours after glycerol administration. After 24 hours, we performed inulin clearance experiments and collected blood / kidney / muscle samples. Gly rats exhibited renal function impairment accompanied by kidney injury, inflammation and alterations in signaling pathways for apoptosis and redox state balance. Gly+Li rats showed a remarkable improvement in renal function as well as kidney injury score, diminished CPK levels and an overstated decrease of renal and muscle GSK3 beta protein expression. Furthermore, administration of lithium lowered the amount of macrophage infiltrate, reduced NF kappa B and caspase renal protein expression and increased the antioxidant component MnSOD. Lithium treatment attenuated renal dysfunction in rhabdomyolysis-associated AKI by improving inulin clearance and reducing CPK levels, inflammation, apoptosis and oxidative stress. These therapeutic effects were due to the inhibition of GSK3 beta and possibly associated with a decrease in muscle injury.
- The association between obesity and vitamin D deficiency modifies the progression of kidney disease after ischemia/reperfusion injury(2022) BERNARDO, Desiree Rita Denelle; CANALE, Daniele; NASCIMENTO, Mariana Moura; SHIMIZU, Maria Heloisa Massola; SEGURO, Antonio Carlos; BRAGANCA, Ana Carolina de; VOLPINI, Rildo AparecidoAcute kidney injury (AKI) alters renal hemodynamics, leading to tubular injury, activating pathways of inflammation, proliferation, and cell death. The initial damage caused to renal tissue after an ischemia/reperfusion (I/R) injury exerts an important role in the pathogenesis of the course of AKI, as well as in the predisposition to chronic kidney disease. Vitamin D deficiency has been considered a risk factor for kidney disease and it is associated with tubulointerstitial damage, contributing to the progression of kidney disease. Obesity is directly related to diabetes mellitus and hypertension, the main metabolic disorders responsible for the progression of kidney disease. Furthermore, the expansion of adipose tissue is described as an important factor for increased secretion of pro-inflammatory cytokines and their respective influence on the progression of kidney disease. We aimed to investigate the influence of vitamin D deficiency and obesity on the progression of renal disease in a murine model of renal I/R. Male Wistar rats underwent renal I/R surgery on day 45 and followed until day 90 of the protocol. We allocated the animals to four groups according to each diet received: standard (SD), vitamin D-depleted (VDD), high fat (HFD), or high fat vitamin D-depleted (HFDV). At the end of 90 days, we observed almost undetectable levels of vitamin D in the VDD and HFDV groups. In addition, HFD and HFDV groups presented alterations in the anthropometric and metabolic profile. The combination of vitamin D deficiency and obesity contributed to alterations of functional and hemodynamic parameters observed in the HFDV group. Moreover, this combination favored the exacerbation of the inflammatory process and the renal expression of extracellular matrix proteins and phenotypic alteration markers, resulting in an enlargement of the tubulointerstitial compartment. All these changes were associated with an increased renal expression of transforming growth factor beta and reduced expression of the vitamin D receptor. Our results show that the synergistic effect of obesity and vitamin D deficiency exacerbated the hemodynamic and morphological changes present in the evolution of renal disease induced by I/R.