LUCIA DA CONCEICAO ANDRADE

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Departamento de Clínica Médica, Faculdade de Medicina - Docente
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais, Hospital das Clínicas, Faculdade de Medicina - Líder

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Autor e Coautores FMUSP-HC Normalizados: MARIA HELOISA MASSOLA SHIMIZU ×

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Agora exibindo 1 - 10 de 21
  • article 55 Citação(ões) na Scopus
    Vitamin D Deficiency Aggravates Chronic Kidney Disease Progression after Ischemic Acute Kidney Injury
    (2014) GONCALVES, Janaina Garcia; BRAGANCA, Ana Carolina de; CANALE, Daniele; SHIMIZU, Maria Heloisa Massola; SANCHES, Talita Rojas; MOYSES, Rosa Maria Affonso; ANDRADE, Lucia; SEGURO, Antonio Carlos; VOLPINI, Rildo Aparecido
    Background: Despite a significant improvement in the management of chronic kidney disease (CKD), its incidence and prevalence has been increasing over the years. Progressive renal fibrosis is present in CKD and involves the participation of several cytokines, including Transforming growth factor-beta 1 (TGF-beta 1). Besides cardiovascular diseases and infections, several studies show that Vitamin D status has been considered as a non-traditional risk factor for the progression of CKD. Given the importance of vitamin D in the maintenance of essential physiological functions, we studied the events involved in the chronic kidney disease progression in rats submitted to ischemia/reperfusion injury under vitamin D deficiency (VDD). Methods: Rats were randomized into four groups: Control; VDD; ischemia/reperfusion injury (IRI); and VDD+IRI. At the 62 day after sham or IRI surgery, we measured inulin clearance, biochemical variables and hemodynamic parameters. In kidney tissue, we performed immunoblotting to quantify expression of Klotho, TGF-beta, and vitamin D receptor (VDR); gene expression to evaluate renin, angiotensinogen, and angiotensin-converting enzyme; and immunohistochemical staining for ED1 (macrophages), type IV collagen, fibronectin, vimentin, and alpha-smooth mucle actin. Histomorphometric studies were performed to evaluate fractional interstitial area. Results: IRI animals presented renal hypertrophy, increased levels of mean blood pressure and plasma PTH. Furthermore, expansion of the interstitial area, increased infiltration of ED1 cells, increased expression of collagen IV, fibronectin, vimentin and alpha-actin, and reduced expression of Klotho protein were observed. VDD deficiency contributed to increased levels of plasma PTH as well as for important chronic tubulointerstitial changes (fibrosis, inflammatory infiltration, tubular dilation and atrophy), increased expression of TGF-beta 1 and decreased expression of VDR and Klotho protein observed in VDD+IRI animals. Conclusion: Through inflammatory pathways and involvement of TGF-beta 1 growth factor, VDD could be considered as an aggravating factor for tubulointerstitial damage and fibrosis progression following acute kidney injury induced by ischemia/reperfusion.
  • article 34 Citação(ões) na Scopus
    Vitamin D deficiency aggravates ischemic acute kidney injury in rats
    (2015) BRAGANCA, Ana Carolina de; VOLPINI, Rildo A.; CANALE, Daniele; GONCALVES, Janaina G.; SHIMIZU, Maria Heloisa M.; SANCHES, Talita R.; SEGURO, Antonio C.; ANDRADE, Lucia
    Vitamin D deficiency (VDD) increases the risk of death in hospitalized patients. Renal ischemia/reperfusion injury (IRI) induces acute kidney injury (AKI), which activates cell cycle inhibitors, including p21, a cyclindependent kinase inhibitor and genomic target of 25-hydroxyvitamin D, which is in turn a potent immunomodulator with antiproliferative effects. In this study, we assess the impact of VDD in renal IRI. Wistar rats were divided into groups, each evaluated for 30 days: control (receiving a standard diet); VDD (receiving a vitamin D-free diet); IRI (receiving a standard diet and subjected to 45-min bilateral renal ischemia on day 28); and VDD + IRI (receiving a vitamin D-free diet and subjected to 45-min bilateral renal ischemia on day 28). At 48 h after IRI, animals were euthanized; blood, urine, and kidney tissue samples were collected. Compared with IRI rats, VDD + IRI rats showed a more severe decrease in glomerular filtration rate, greater urinary protein excretion, a higher kidney/body weight ratio and lower renal aquaporin 2 expression, as well as greater morphological damage, characterized by increased interstitial area and tubular necrosis. Our results suggest that the severity of tubular damage in IRI may be associated with downregulation of vitamin D receptors and p21. VDD increases renal inflammation, cell proliferation and cell injury in ischemic AKI.
  • article 44 Citação(ões) na Scopus
    Apolipoprotein A-I mimetic peptide 4F attenuates kidney injury, heart injury, and endothelial dysfunction in sepsis
    (2014) MOREIRA, Roberto S.; IRIGOYEN, Maria; SANCHES, Talita R.; VOLPINI, Rildo A.; CAMARA, Niels O. S.; MALHEIROS, Denise M.; SHIMIZU, Maria H. M.; SEGURO, Antonio C.; ANDRADE, Lucia
    Kidney injury, heart injury, and cytokine-induced vascular hyperpermeability are associated with high rates of morbidity and mortality in sepsis. Although the mechanism remains unknown, apolipoprotein A-I (apoA-I) mimetic peptide 4F reduces inflammation and protects HDL levels, which are reduced in sepsis. We hypothesized that 4F also protects kidneys and hearts in a rat model of cecal ligation and puncture (CLP). We divided Wistar rats into groups: sham-operated (control), CLP, and CLP+4F (10 mg/kg body wt ip, 6 h after CLP). At 24 h post-CLP, we evaluated cardiac function, mean arterial pressure (MAP), heart rate (HR), baroreflex sensitivity, total cholesterol, LDL, HDL, serum cytokines, and inulin clearance. We performed immunoblotting for protein regulators of vascular permeability (Slit2 and Robo4) and endothelial nitric oxide synthase (eNOS) in kidney tissue. We evaluated heart mitochondria with electron microscopy. Although there was no difference in MAP, the HR was significantly higher in CLP rats than in control and CLP+4F rats. In CLP+4F rats, baroreflex sensitivity and cardiac function were completely protected from the effects of CLP, as was glomerular filtration; heart mitochondria morphology was improved; sepsis-induced changes in serum cholesterol, LDL, HDL, and apoA-I were less common; all cytokines were lower than in CLP rats; and expression of Slit2, Robo4, and eNOS was completely restored. Administration of 4F inhibits inflammatory responses and strengthens the vascular barrier, protecting kidneys and hearts in an HDL-dependent manner. To determine the extent of the protective effect of 4F, further studies are needed.
  • article 20 Citação(ões) na Scopus
    N-Acetylcysteine Protects Rats with Chronic Renal Failure from Gadolinium-Chelate Nephrotoxicity
    (2012) PEREIRA, Leonardo Victor Barbosa; SHIMIZU, Maria Heloisa Massola; RODRIGUES, Lina Paola Miranda Ruiz; LEITE, Claudia Costa; ANDRADE, Lucia; SEGURO, Antonio Carlos
    The aim of this study was to evaluate the effect of Gd-chelate on renal function, iron parameters and oxidative stress in rats with CRF and a possible protective effect of the antioxidant N-Acetylcysteine (NAC). Male Wistar rats were submitted to 5/6 nephrectomy (Nx) to induced CRF. An ionic - cyclic Gd (Gadoterate Meglumine) was administrated (1.5 mM/KgBW, intravenously) 21 days after Nx. Clearance studies were performed in 4 groups of anesthetized animals 48 hours following Gd-chelate administration: 1 - Nx (n = 7); 2 - Nx+NAC (n = 6); 3 - Nx+Gd (n = 7); 4 - Nx+NAC+Gd (4.8 g/L in drinking water), initiated 2 days before Gd-chelate administration and maintained during 4 days (n = 6). This group was compared with a control. We measured glomerular filtration rate, GFR (inulin clearance, ml/min/kg BW), proteinuria (mg/24 hs), serum iron (mu g/dL); serum ferritin (ng/mL); transferrin saturation (%), TIBC (mu g/dL) and TBARS (nmles/ml). Normal rats treated with the same dose of Gd-chelate presented similar GFR and proteinuria when compared with normal controls, indicating that at this dose Gd-chelate is not nephrotoxic to normal rats. Gd-chelate administration to Nx-rats results in a decrease of GFR and increased proteinuria associated with a decrease in TIBC, elevation of ferritin serum levels, transferrin oversaturation and plasmatic TBARS compared with Nx-rats. The prophylactic treatment with NAC reversed the decrease in GFR and the increase in proteinuria and all alterations in iron parameters and TBARS induced by Gd-chelate. NAC administration to Nx rat did not modify the inulin clearance and iron kinetics, indicating that the ameliorating effect of NAC was specific to Gd-chelate. These results suggest that NAC can prevent Gd-chelate nephrotoxicity in patients with chronic renal failure.
  • article 0 Citação(ões) na Scopus
    N-acetylcysteine attenuates renal alterations induced by senescence in the rat (vol 48, pg 298, 2013)
    (2013) SHIMIZU, M. H.; VOLPINI, R. A.; BRAGANCA, A. C. de; CAMPOS, R.; CANALE, D.; SANCHES, T. R.; ANDRADE, L.; SEGURO, A. C.
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    VITAMIN D DEFICIENCY AGGRAVATES TENOFOVIR INDUCED METABOLIC SYNDROME AND RENAL FAILURE
    (2013) CANALE, Daniele; BRAGANCA, Ana Carolina de; GONCALVES, Janana; SHIMIZU, Maria Helosa M.; VOLPINI, Rildo A.; ANDRADE, Lucia; SEGURO, Antonio Carlos
    Introduction and Aims:Vitamin D deficiency (VDD) is highly prevalent among HIV-infected individuals. Tenofovir disoproxil fumarate (TDF), a widely used component of antiretroviral regimens for HIV treatment, has been associated with comorbidities, some of which have been attributed to renal toxicity and metabolic syndrome. The aim of the study was to investigate the effect of VDD on TDF treated rats. Methods:Wistar rats were randomly divided into four groups: control (C, n = 9), receiving a standard diet for 60 days; VDD (n = 6), receiving a free-vitamin D diet for 60 days; TDF (n = 9), receiving a standard diet for 60 days with the addition of TDF (50 mg/kg food) for the last 30 days; and VDD+TDF (n = 7) received a free-vitamin D diet for 60 days with the addition of TDF (50 mg/kg food) for the last 30 days. We measured inulin clearance (GFR, mL/min/100g); blood pressure (BP, mmHg), renal blood flow and calculated renal vascular resistance (RVR, mmHg/mL/min); serum levels of 25-hydroxyvitamin D (25(OH)D, ng/mL), cholesterol (mg/dL) and triglycerides (mg/dL); urinary sodium excretion (UVNa,mEq/24h). In renal tissue, we immunoblotted for angiotensin II (AII), endothelial nitric oxide synthase (eNOS) and vitamin D receptor (VDR). Data are expressed as mean ± SEM. Results:Vitamin D levels were similar in C (15.4±1 ng/mL) and TDF (14.8±1.3 ng/mL) groups and <1.5 ng/mL in VDD groups. Body weight, water intake and food ingestion were not different among the 4 groups. Treatment with TDF led to impaired renal function, hypertension, higher RVR and dyslipidemia. Administration of TDF also increased protein expression of AII and VDR. Association of TDF and VDD exacerbates TDF nephrotoxicity, as well as metabolic syndrome. Furthermore, VDD+TDF group showed urinary sodium retention. The increased VDR protein expression in TDF groups may represent a compensatory effect to decrease renal injury. Conclusions:VDD aggravates renovascular effects and TDF-induced renal failure at least in part due to the involvement of renin-angiotensin-aldosterone system. Therefore, the assessment of vitamin D is important in HIV patients receiving TDF.
  • article 59 Citação(ões) na Scopus
    Effects of Continuous Erythropoietin Receptor Activator in Sepsis-Induced Acute Kidney Injury and Multi-Organ Dysfunction
    (2012) RODRIGUES, Camila E.; SANCHES, Talita R.; VOLPINI, Rildo A.; SHIMIZU, Maria H. M.; KURIKI, Patricia S.; CAMARA, Niels O. S.; SEGURO, Antonio C.; ANDRADE, Lucia
    Background: Despite advances in supportive care, sepsis-related mortality remains high, especially in patients with acute kidney injury (AKI). Erythropoietin can protect organs against ischemia and sepsis. This effect has been linked to activation of intracellular survival pathways, although the mechanism remains unclear. Continuous erythropoietin receptor activator (CERA) is an erythropoietin with a unique pharmacologic profile and long half-life. We hypothesized that pretreatment with CERA would be renoprotective in the cecal ligation and puncture (CLP) model of sepsis-induced AKI. Methods: Rats were randomized into three groups: control; CLP; and CLP+CERA (5 mu g/kg body weight, i.p. administered 24 h before CLP). At 24 hours after CLP, we measured creatinine clearance, biochemical variables, and hemodynamic parameters. In kidney tissue, we performed immunoblotting-to quantify expression of the Na-K-2Cl cotransporter (NKCC2), aquaporin 2 (AQP2), Toll-like receptor 4 (TLR4), erythropoietin receptor (EpoR), and nuclear factor kappa B (NF-kappa B)-and immunohistochemical staining for CD68 (macrophage infiltration). Plasma interleukin (IL)-2, IL-1 beta, IL-6, IL-10, interferon gamma, and tumor necrosis factor alpha were measured by multiplex detection. Results: Pretreatment with CERA preserved creatinine clearance and tubular function, as well as the expression of NKCC2 and AQP2. In addition, CERA maintained plasma lactate at normal levels, as well as preserving plasma levels of transaminases and lactate dehydrogenase. Renal expression of TLR4 and NF-kappa B was lower in CLP+CERA rats than in CLP rats (p<0.05 and p<0.01, respectively), as were CD68-positive cell counts (p<0.01), whereas renal EpoR expression was higher (p<0.05). Plasma levels of all measured cytokines were lower in CLP+CERA rats than in CLP rats. Conclusion: CERA protects against sepsis-induced AKI. This protective effect is, in part, attributable to suppression of the inflammatory response.
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    VITAMIN D DEFICIENCY IS ASSOCIATED WITH DOWNREGULATION OF KLOTHO AND DEVELOPMENT OF FIBROSIS IN A MURINE MODEL OF RENAL ISCHEMIA/REPERFUSION INJURY
    (2013) GONCALVES, Janaina G.; CANALE, Daniele; BRAGANCA, Ana Carolina de; SHIMIZU, Maria Heloisa M.; MOYSES, Rosa Maria A.; ANDRADE, Lucia; SEGURO, Antonio C.; VOLPINI, Rildo A.
    Introduction and Aims:Vitamin D deficiency (VDD) is highly prevalent in chronic kidney disease (CKD) patients. Ischemia/reperfusion-Acute Kidney Injury (IR-AKI) is considered a risk factor for CKD progression. Previous studies suggests that activation of the renin-angiotensin-aldosterone system (RAAS) and VDD could be involved in reduction of Klotho expression, an early marker of stage 1 CKD. The aim of this study was to investigate the effect of VDD on klotho expression and fibrosis development in a model of IR-AKI. Methods:Male Wistar rats (180-200g) were randomly divided into four groups (n=8 each): control (C) and ischemic (IR) fed a standard diet; VDD and VDD+IR, fed a free-vitamin D diet. On day 28, IR and VDD+IR rats were submitted to 45-minute clamping of both renal arteries. On day 90, we measured inulin clearance (GFR); Mean arterial blood pressure (MAP), renal blood flow (RBF) and calculated renal vascular resistance (RVR). We also measured serum levels of 25-hydroxyvitamin D (25(OH)D, ng/mL) and proteinuria. In renal tissue, we immunoblotted for klotho and performed imunohistochemical assay for collagen IV and fibronectin. We estimated fibrosis by fractional interstitial area (FIA) and fibronectin/collagen IV expression by score ranging from 0 to 4 according to the extension of staining. Data are expressed as mean ± SEM. Table 1. Hemodynamic and biochemical data and fractional interstitial area, Western Blot and Immunohistochemical studies. Results:Vitamin D levels were similar in C (15.4±1) and IR (15±0.6) groups and <1.5 ng/mL in VDD groups. GFR, RBF and RVR were not different among the studied groups. MAP was markedly elevated in VDD, IR and VDD+IR groups, reflecting a possible interaction on RAAS. Also, VDD, IR and VDD+IR groups showed larger areas of fibrosis and higher scores for fibronectin and collagen IV and decreased levels of klotho. Conclusions:The increased proteinuria/fibrosis and fibronectin/collagen IV expression in VDD+IR rats suggests progressive renal injury. Downregulation of klotho expression is a possible marker of chronification. Our study shows a very plausible role of VDD in this pathway as a potential stimulus for fibrosis.
  • article 59 Citação(ões) na Scopus
    N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation
    (2012) CAMPOS, Renata; SHIMIZU, Maria Heloisa Massola; VOLPINI, Rildo Aparecido; BRAGANCA, Ana Carolina de; ANDRADE, Lucia; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; OLIVO, Clarice; CANALE, Daniele; SEGURO, Antonio Carlos
    Campos R, Shimizu MH, Volpini RA, de Bragan a AC, Andrade L, Lopes FD, Olivo C, Canale D, Seguro AC. N-acetylcysteine prevents pulmonary edema and acute kidney injury in rats with sepsis submitted to mechanical ventilation. Am J Physiol Lung Cell Mol Physiol 302: L640-L650, 2012. First published January 20, 2012; doi: 10.1152/ajplung.00097.2011.-Sepsis is a common cause of acute kidney injury (AKI) and acute lung injury. Oxidative stress plays as important role in such injury. The aim of this study was to evaluate the effects that the potent antioxidant N-acetylcysteine (NAC) has on renal and pulmonary function in rats with sepsis. Rats, treated or not with NAC (4.8 g/l in drinking water), underwent cecal ligation and puncture (CLP) 2 days after the initiation of NAC treatment, which was maintained throughout the study. At 24 h post-CLP, renal and pulmonary function were studied in four groups: control, control + NAC, CLP, and CLP + NAC. All animals were submitted to low-tidal-volume mechanical ventilation. We evaluated respiratory mechanics, the sodium cotransporters Na-K-2Cl (NKCC1) and the alpha-subunit of the epithelial sodium channel (alpha-ENaC), polymorphonuclear neutrophils, the edema index, oxidative stress (plasma thiobarbituric acid reactive substances and lung tissue 8-isoprostane), and glomerular filtration rate. The CLP rats developed AKI, which was ameliorated in the CLP + NAC rats. Sepsis-induced alterations in respiratory mechanics were also ameliorated by NAC. Edema indexes were lower in the CLP + NAC group, as was the wet-to-dry lung weight ratio. In CLP + NAC rats, alpha-ENaC expression was upregulated, whereas that of NKCC1 was downregulated, although the difference was not significant. In the CLP + NAC group, oxidative stress was significantly lower and survival rates were significantly higher than in the CLP group. The protective effects of NAC (against kidney and lung injury) are likely attributable to the decrease in oxidative stress, suggesting that NAC can be useful in the treatment of sepsis.
  • article 17 Citação(ões) na Scopus
    N-acetylcysteine attenuates renal alterations induced by senescence in the rat
    (2013) SHIMIZU, Maria Heloisa M.; VOLPINI, Rildo A.; BRAGANCA, Ana Carolina de; CAMPOS, Renata; CANALE, Daniele; SANCHES, Talita R.; ANDRADE, Lucia; SEGURO, Antonio C.
    The aim of this study was to evaluate the effects of N-acetylcysteine (NAC) on renal function, as well as on sodium and water transporters, in the kidneys of aged rats. Normal, 8-month-old male Wistar rats were treated (n = 6) or not (n = 6) with NAC (600 mg/L in drinking water) and followed for 16 months. At the end of the follow-up period, we determined inulin clearance, serum thiobarbituric acid reactive substances (TBARS), serum cholesterol, and urinary phosphate excretion. In addition, we performed immunohistochemical staining for p53 and for ED-1-positive cells (macrophages/monocytes), together with Western blotting of kidney tissue for NKCC2, aquaporin 2 (AQP2), urea transporter A1 (UT-A1) and Klotho protein. At baseline, the two groups were similar in terms of creatinine clearance, proteinuria, cholesterol, and TBARS. At the end of the follow-up period, NAC-treated rats presented greater inulin clearance and reduced proteinuria, as well as lower serum cholesterol, serum TBARS, and urinary phosphate excretion, in comparison with untreated rats. In addition, NAC-treated rats showed upregulated expression of NKCC2, AQP2, and UT-A1; elevated Klotho protein expression, low p53 expression, and few ED-1 positive cells. In conclusion, we attribute these beneficial effects of NAC (the significant improvements in inulin clearance and in the expression of NKCC2, AQP2, and UT-A1) to its ability to decrease oxidative stress, inhibit p53 expression, minimize kidney inflammation, and stimulate Klotho expression.