LUZIA NAOKO SHINOHARA FURUKAWA
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina
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conferenceObject Chronic Kidney Disease-Associated Frailty is characterized by changes in Muscular Expression of RANKL and FNDC5, which are partially reverted after Parathyroidectomy(2023) DUQUE, Eduardo J.; CRISPILHO, Shirley; OLIVEIRA, Ivone B.; REIS, Luciene M. dos; FURUKAWA, Luzia; TAKAYAMA, Liliam; PEREIRA, Rosa M.; SHINJO, Samuel K.; AVESANI, Carla; JORGETTI, Vanda; ELIAS, Rosilene M.; MOYSES, Rosa M.- Salt intake during pregnancy alters offspring's myocardial structure(2013) ALVES-RODRIGUES, E. N.; VERAS, M. M.; ROSA, K. T.; CASTRO, I. de; FURUKAWA, L. N. S.; OLIVEIRA, I. B.; SOUZA, R. M.; HEIMANN, J. C.Background and Aim: To evaluate the effects of low or high salt intake during pregnancy on left ventricle of adult male offspring. Methods and results: Low-(LS, 0.15%), normal-(NS, 1.3%) or high-salt (HS, 8% NaCl) diet was given to Wistar rats during pregnancy. During lactation all dams received NS as well as the offspring after weaning. To evaluate cardiac response to salt overload, 50% of each offspring group was fed a high-salt (hs, 4% NaCl) diet from the 21st to the 36th week of age (LShs, NShs, HShs). The remaining 50% was maintained on NS (LSns, NSns and HSns). Echocardiography was done at 20 and 30 weeks of age. Mean blood pressure (MBP), histology and left ventricular angiotensin II content (AII) were analyzed at 36 weeks of age. Interventricular septum, left ventricular posterior wall and relative wall thickness increased from the 20th to the 30th week of age only in HShs, cardiomyocyte mean volume was higher in HShs compared to NShs, LShs and HSns. AII and left ventricular fibrosis were not different among groups. Conclusions: HS during pregnancy programs adult male offspring to a blood pressure and angiotensin II independent concentric left ventricular hypertrophy, with no fibrosis, in response to a chronic high-salt intake.
conferenceObject Bone histomorphometric effects of HIV infection and Antiretroviral therapy(2018) RAMALHO, Janaina; MARTINS, Csw; PEREIRA, Rmr; NICKOLAS, Thomas; YIN, Mt; GALVAO, J.; EIRA, Margareth; REIS, Lm; FURUKAWA, Luzia; JORGETTI, Vanda; MOYSES, Rm- Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II AT2 receptor agonist(2019) DOPONA, E. P. B.; ROCHA, V. F.; FURUKAWA, L. N. S.; OLIVEIRA, I. B.; HEIMANN, J. C.Background and aims: Although many studies have reported the effects of AT1 receptor on dietary salt overload, the role of AT2 receptor in this model is far from completely elucidated. The present study aimed to better understand the role of AT2 receptor in cardiac structure alterations in response to chronic high salt intake in rats. Methods and results: Male Wistar rats were fed a normal or high salt diet from weaning until 18 weeks of age. Both groups were subdivided into two groups. Starting at 7 weeks of age, rats were treated with or without compound 21 (0.3 mg/kg/day, n = 16), an AT2 receptor agonist. Metabolics and structural parameters were measured. BP, transverse cardiomyocyte and intersticial fibrose was higher in animals fed with high salt diet compared with normal salt fed animals. Conclusion: Compound 21 prevented the development of cardiac hypertrophy and fibrosis, reduced the increase in blood pressure and prevented the lower weight gain in animals fed a high salt diet.
- Treatment of Human Immunodeficiency Virus Infection With Tenofovir Disoproxil Fumarate-Containing Antiretrovirals Maintains Low Bone Formation Rate, But Increases Osteoid Volume on Bone Histomorphometry(2019) RAMALHO, Janaina; MARTINS, Carolina Steller Wagner; GALVAO, Juliana; FURUKAWA, Luzia N.; DOMINGUES, Wagner V.; OLIVEIRA, Ivone B.; REIS, Luciene M. dos; PEREIRA, Rosa M. R.; NICKOLAS, Thomas L.; YIN, Michael T.; EIRA, Margareth; JORGETTI, Vanda; MOYSES, Rosa M. A.Bone mineral density (BMD) loss is a known complication of human immunodeficiency virus (HIV) infection and its treatment, particularly with tenofovir disoproxil fumarate (TDF)-containing antiretroviral regimens. Although renal proximal tubular dysfunction and phosphaturia is common with TDF, it is unknown whether BMD loss results from inadequate mineralization. We evaluated change in BMD by dual-energy X-ray absorptiometry (DXA) and bone histomorphometry by tetracycline double-labeled transiliac crest biopsies in young men living with HIV before (n = 20) and 12 months after (n = 16) initiating TDF/lamivudine/efavirenz. We examined relationships between calciotropic hormones, urinary phosphate excretion, pro-inflammatory and pro-resorptive cytokines, and bone remodeling-related proteins with changes in BMD and histomorphometry. Mean age was 29.6 +/- 5.5 years, with mean CD4 + T cell count of 473 +/- 196 cells/mm(3). At baseline, decreased bone formation rate and increased mineralization lag time were identified in 16 (80%) and 12 (60%) patients, respectively. After 12 months, we detected a 2% to 3% decrease in lumbar spine and hip BMD by DXA. By histomorphometry, we observed no change in bone volume/total volume (BV/TV) and trabecular parameters, but rather, increases in cortical thickness, osteoid volume, and osteoblast and osteoclast surfaces. We did not observe significant worsening of renal phosphate excretion or mineralization parameters. Increases in PTH correlated with decreased BMD but not histomorphometric parameters. Overall, these data suggest abnormalities in bone formation and mineralization occur with HIV infection and are evident at early stages. With TDF-containing antiretroviral therapy (ART), there is an increase in bone remodeling, reflected by increased osteoblast and osteoclast surfaces, but a persistence in mineralization defect, resulting in increased osteoid volume. (c) 2019 American Society for Bone and Mineral Research
- Advanced Glycation End Products and Bone Metabolism in Patients with Chronic Kidney Disease(2023) QUADROS, Kelcia R. S.; ROZA, Noemi A. V.; FRANCA, Renata A.; ESTEVES, Andre B. A.; BARRETO, Joaquim; DOMINGUEZ, Wagner V.; FURUKAWA, Luzia N. S.; CARAMORI, Jacqueline Teixeira; SPOSITO, Andrei C.; OLIVEIRA, Rodrigo Bueno deAdvanced glycation end products (AGEs) accumulation may be involved in the progression of CKD-bone disorders. We sought to determine the relationship between AGEs measured in the blood, skin, and bone with histomorphometry parameters, bone protein, gene expression, and serum biomarkers of bone metabolism in patients with CKD stages 3 to 5D patients. Serum levels of AGEs were estimated by pentosidine, glycated hemoglobin (A1c), and N-carboxymethyl lysine (CML). The accumulation of AGEs in the skin was estimated from skin autofluorescence (SAF). Bone AGEs accumulation and multiligand receptor for AGEs (RAGEs) expression were evaluated by immunohistochemistry; bone samples were used to evaluate protein and gene expression and histomorphometric analysis. Data are from 86 patients (age: 51 +/- 13 years; 60 [70%] on dialysis). Median serum levels of pentosidine, CML, A1c, and SAF were 71.6 pmol/mL, 15.2 ng/mL, 5.4%, and 3.05 arbitrary units, respectively. AGEs covered 3.92% of trabecular bone and 5.42% of the cortical bone surface, whereas RAGEs were expressed in 0.7% and 0.83% of trabecular and cortical bone surfaces, respectively. AGEs accumulation in bone was inversely related to serum receptor activator of NF-KB ligand/parathyroid hormone (PTH) ratio (R = -0.25; p = 0.03), and RAGE expression was negatively related to serum tartrate-resistant acid phosphatase-5b/PTH (R = -0.31; p = 0.01). Patients with higher AGEs accumulation presented decreased bone protein expression (sclerostin [1.96 (0.11-40.3) vs. 89.3 (2.88-401) ng/mg; p = 0.004]; Dickkopf-related protein 1 [0.064 (0.03-0.46) vs. 1.36 (0.39-5.87) ng/mg; p = 0.0001]; FGF-23 [1.07 (0.4-32.6) vs. 44.1 (6-162) ng/mg; p = 0.01]; and osteoprotegerin [0.16 (0.08-2.4) vs. 6.5 (1.1-23.7) ng/mg; p = 0.001]), upregulation of the p53 gene, and downregulation of Dickkopf-1 gene expression. Patients with high serum A1c levels presented greater cortical porosity and Mlt and reduced osteoblast surface/bone surface, eroded surface/bone surface, osteoclast surface/bone surface, mineral apposition rate, and adjusted area. Cortical thickness was negatively correlated with serum A1c (R = -0.28; p = 0.02) and pentosidine levels (R = -0.27; p = 0.02). AGEs accumulation in the bone of CKD patients was related to decreased bone protein expression, gene expression changes, and increased skeletal resistance to PTH; A1c and pentosidine levels were related to decreased cortical thickness; and A1c levels were related to increased cortical porosity and Mlt.