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: ANTONIO CARLOS SEGURO ×

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  • 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.
  • conferenceObject
    IMPACT OF DIFFERENT METHODS OF RENAL REPLACEMENT THERAPY IN WEIL SYNDROME
    (2015) CLETO, Sergio; MALAQUE, Ceila; RODRIGUES, Camila; SZTAJNBOK, Jaques; SEGURO, Antonio; ANDRADE, Lucia
  • 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 8 Citação(ões) na Scopus
    Renal Tubular Dysfunction in Sickle Cell Disease
    (2013) SILVA JUNIOR, Geraldo B.; VIEIRA, Ana Patricia F.; BEM, Amanda X. Couto; ALVES, Marilia P.; MENESES, Gdayllon C.; MARTINS, Alice M. C.; SANCHES, Talita R.; ANDRADE, Lucia C.; SEGURO, Antonio C.; LIBORIO, Alexandre B.; DAHER, Elizabeth F.
    Background/Aims: Kidney abnormalities are one of the main chronic complications of sickle cell disease (SCD). The aim of this study is to investigate the occurrence of renal tubular abnormalities among patients with SCD. Methods: This is a prospective study with 26 SCD adult patients in Brazil. Urinary acidification and concentration tests were performed using calcium chloride (CaCl2), after a 12h period of water and food deprivation. Fractional excretion of sodium (FENa), transtubular potassium gradient (TTKG) and solute free water reabsorption (TcH2O) were calculated. The SCD group was compared to a group of 15 healthy volunteers (control group). Results: Patient`s average age and gender were similar to controls. Urinary acidification deficit was found in 10 SCD patients (38.4%), who presented urinary pH > 5.3 after CaCl2 test. Urinary osmolality was significantly lower in SCD patients (355 +/- 60 vs. 818 +/- 202mOsm/kg, p= 0.0001, after 12h period water deprivation). Urinary concentration deficit was found in all SCD patients (100%). FENa was higher among SCD patients (0.75 +/- 0.3 vs. 0.55 +/- 0.2%, p= 0.02). The TTKG was higher in SCD patients (5.5 +/- 2.5 vs. 3.0 +/- 1.5, p= 0.001), and TcH2O was lower (0.22 +/- 0.3 vs. 1.1 +/- 0.3L/day, p= 0.0001). Conclusions: SCD is associated with important kidney dysfunction. The main abnormalities found were urinary concentrating and incomplete distal acidification defect. There was also an increase in the potassium transport and decrease in water reabsorption, evidencing the occurrence of distal tubular dysfunction.
  • conferenceObject
    TUBULOGLOMERULAR EVALUATION IN VISCERAL LEISHMANIASIS BEFORE AND AFTER TREATMENT WITH PENTAVALENT ANTIMONIAL
    (2014) OLIVEIRA, Michelle J. C.; SILVA JUNIOR, Geraldo; SAMPAIO, Aline M.; MONTENEGRO, Barbara; ALVES, Marilia P.; HENN, Guilherme A. L.; ROCHA, Hermano A. L.; MENESES, Gdayllon C.; MARTINS, Alice M. C.; SANCHES, Talita R.; ANDRADE, Lucia C.; SEGURO, Antonio C.; LIBORIO, Alexandre B.; DAHER, Elizabeth F.
  • article 73 Citação(ões) na Scopus
    Effects of Brazilian green propolis on proteinuria and renal function in patients with chronic kidney disease: a randomized, double-blind, placebo-controlled trial
    (2019) SILVEIRA, Marcelo Augusto Duarte; TELES, Flavio; BERRETTA, Andressa A.; SANCHES, Talita R.; RODRIGUES, Camila Eleuterio; SEGURO, Antonio Carlos; ANDRADE, Lucia
    BackgroundChronic kidney disease (CKD) is a public health problem worldwide, and proteinuria is a well-established marker of disease progression in CKD patients. Propolis, a natural resin produced by bees from plant materials, has anti-inflammatory, immunomodulatory, and anti-oxidant properties, as well as having been shown to have an antiproteinuric effect in experimental CKD. The aim of this study was to evaluate the impact of Brazilian green propolis extract on proteinuria reduction and the changes in the estimated glomerular filtration rate (eGFR).MethodsThis was a randomized, double-blind, placebo-controlled study including patients with CKD caused by diabetes or of another etiology, 18-90years of age, with an eGFR of 25-70ml/min per 1.73m(2) and proteinuria (urinary protein excretion >300mg/day) or micro- or macro-albuminuria (urinary albumin-to-creatinine ratio>30mg/g or>300mg/g, respectively). We screened 148 patients and selected 32, randomly assigning them to receive 12months of Brazilian green propolis extract at a dose of 500mg/day (n=18) or 12months of a placebo (n=14).ResultsAt the end of treatment, proteinuria was significantly lower in the propolis group than in the placebo group695mg/24h (95% CI, 483 to 999) vs. 1403mg/24h (95% CI, 1031 to 1909); P=0.004independent of variations in eGFR and blood pressure, which did not differ between the groups during follow-up. Urinary monocyte chemoattractant protein-1 was also significantly lower in the propolis group than in the placebo group58pg/mg creatinine (95% CI, 36 to 95) vs. 98pg/mg creatinine (95% CI, 62 to 155); P=0.038.ConclusionsBrazilian green propolis extract was found to be safe and well tolerated, as well as to reduce proteinuria significantly in patients with diabetic and non-diabetic CKD.Trial Registration.(ClinicalTrials.gov number NCT02766036. Registered: May 9, 2016).
  • 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.
  • article 6 Citação(ões) na Scopus
    High Cholesterol Feeding May Induce Tubular Dysfunction Resulting in Hypomagnesemia
    (2012) FAVARO, Vanessa F.; OSHIRO-MONREAL, Fabiola M.; BRAGANCA, Ana Carolina de; ANDRADE, Lucia; SEGURO, Antonio Carlos; HELOU, Claudia M. B.
    Background/Aims: Hypomagnesemia may induce hypercholesterolemia, but the contrary has not been described yet. Thus, magnesium homeostasis was evaluated in rats fed a cholesterol-enriched diet for 8 days. This study has a relevant clinical application if hypomagnesemia, due to hypercholesterolemia, is confirmed in patients with long-term hypercholesterolemia. Methods: Both hypercholesterolemic (HC) and normocholesterolemic rats (NC) were divided into sets of experiments to measure hemodynamic parameters, physiological data, maximum capacity to dilute urine (C-H2O), variations (Delta) in [Ca2+](i) and the expression of transporter proteins. Results: HC developed hypomagnesemia and showed high magnesuria in the absence of hemodynamic abnormalities. However, the urinary sodium excretion and C-H2O in HC was similar to NC. On the other hand, the responses to angiotensin II by measuring Delta [Ca2+](i) were higher in the thick ascending limb of Henle's loop (TAL) of HC than NC. Moreover, high expression of the cotransporter NKCC2 was found in renal outer medulla fractions of HC. Taken together, the hypothesis of impairment in TAL was excluded. Actually, the expression of the epithelial Mg2+ channel in renal cortical membrane fractions was reduced in HC. Conclusion: Impairment in distal convoluted tubule induced by hypercholesterolemia explains high magnesuria and hypomagnesemia observed in HC.