LECTICIA BARBOSA JORGE
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
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
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- Challenges in Diagnosis and Treatment of Systemic Amyloidosis: 10 Years of Experience in a Public Brazilian University Center(2020) SZOR, Roberta Shcolnik; FERNANDES, Fabio; SEGURO, Fernanda S.; LINO, Angelina M.; JORGE, Lecticia B.; MENDONCA, Leonardo O.; FEITOSA, Valkercyo A.; CASTELLI, Jussara B.; REGO, Eduardo M.; JACOMASSI, Mayara; ALVES, Lucas B. O.; MARTINEZ, Gracia; ROCHA, Vanderson
- Atypical presentation of acute post-infectious glomerulonephritis in patients with sickle cell disease: report of two cases(2020) NEVES, Precil Diego Miranda de Menezes; REICHERT, Bernardo Vergara; BRIDI, Ramaiane Aparecida; YU, Luis; DIAS, Cristiane Bitencourt; PINHEIRO, Rafaela Brito Bezerra; TESTAGROSSA, Leonardo de Abreu; CAVALCANTE, Livia Barreira; MALHEIROS, Denise Maria Avancini Costa; JORGE, Lecticia Barbosa; WORONIK, ViktoriaBackgroundSickle cell disease (SCD) is a highly prevalent genetic disease worldwide. In the natural evolution of SCD, glomerular lesions can develop, presenting histopathological patterns of segmental or focal membranoproliferative glomerulosclerosis, with or without thrombotic microangiopathy. We report two cases of acute post-infectious glomerulonephritis (APIGN), with atypical presentations, in patients with SCD.Case presentationCase 1: An 18-year-old female with SCD presented with a 21-day history of progressive oedema, accompanied by dyspnoea, productive cough, fever, and chest pain. Blood tests showed the following: haemoglobin 6.1g/dl; leucocytes 18,820 cells/mm(3); and creatinine 0.49mg/dl. A urine sample evidenced leucocyturia and haematuria. The 24-h proteinuria was 8.99g, serum albumin level was 1.2g/dl, low serum C3 levels and high levels of anti-streptolysin O. Renal biopsy was consistent with APIGN. The patient was treated with diuretic and anti-proteinuric agents, subsequently evolving to reversal of the renal alterations. Case 2: A 12-year-old male with SCD presented with a 20-day history of a non-productive cough and progressive oedema, together with hypertension. The serum creatinine concentration was 0.48mg/dl. A urine sample evidenced leukocyturia and haematuria. The 24-h proteinuria was 12.5g, and the serum albumin level was 2.6g/dl. The levels of C3 and C4 were normal. Renal biopsy revealed APIGN. The patient was treated with diuretic and anti-proteinuric agents, subsequently evolving reversal of the renal alterations.ConclusionsThe presentation of the two cases reported here are not typical of SCD-related kidney injury. Analysis of the renal biopsy specimens elucidated the diagnosis, affecting the prognosis, because that of APIGN is highly favourable, unlike that of nephrotic syndrome associated with SCD glomerulopathy.
- Schistosoma mansoni infection as a trigger to collapsing glomerulopathy in a patient with high-risk APOL1 genotype(2020) NEVES, Precil D.; BRIDI, Ramaiane A.; RAMALHO, Janaina A.; JORGE, Lecticia B.; WATANABE, Elieser H.; WATANABE, Andreia; YU, Luis; WORONIK, Viktoria; PINHEIRO, Rafaela B.; TESTAGROSSA, Leonardo A.; CAVALCANTE, Livia B.; MALHEIROS, Denise M.; DIAS, Cristiane B.; ONUCHIC, Luiz F.Author summary Schistosomiasis mansoni is still a public health problem in Brazil and renal involvement is described. In such cases, a glomerulopathy is the typical manifestation, most often membranoproliferative glomerulonephritis. In the current article, we report a patient with a recent diagnosis of hepatosplenic SM who was admitted for nephrotic syndrome associated with reduced renal function and hypertension. Kidney biopsy established the diagnosis of collapsing glomerulopathy (CG) and molecular genetics investigation identified a high-risk APOL1 genotype (HRG). Of note, HRG has been associated with increased risk to develop CG, and a two-hit model has been proposed for the genesis of this glomerulopathy. According to this model, a HRG represents the increased-susceptibility component, while an infection or other environmental factors could act as triggers for the development of CG. Based on those data and model, our case raises SM infection as a new trigger for this severe form of glomerulopathy. This is the first description of a case of CG associated with SM in a patient with an HRG. This case corroborates the interactive role between genetic and environmental factors in the pathogenesis of CG but also identifies SM infection as an additional trigger for its development. Background Schistosoma mansoni schistosomiasis (SM) remains a public health problem in Brazil. Renal involvement is classically manifested as a glomerulopathy, most often membranoproliferative glomerulonephritis or focal and segmental glomerulosclerosis. We report a case of collapsing glomerulopathy (CG) associated with SM and high-risk APOL1 genotype (HRG). Case report A 35-year-old male was admitted for hypertension and an eight-month history of lower-limb edema, foamy urine, and increased abdominal girth. He had a recent diagnosis of hepatosplenic SM, treated with praziquantel, without clinical improvement. Laboratory tests revealed serum creatinine 1.89mg/dL, blood urea nitrogen (BUN) 24mg/dL, albumin 1.9g/dL, cholesterol 531mg/dL, low-density lipoprotein 426mg/dL, platelets 115000/mm(3), normal C3/C4, antinuclear antibody (ANA), rheumatoid factor (RF), and antineutrophil cytoplasmic antibodies (ANCA), negative serologies for hepatitis C virus (HCV) and human immunodeficiency virus (HIV), HBsAg negative and AntiHBc IgG positive, no hematuria or leukocyturia, 24 hour proteinuria 6.56g and negative serum and urinary immunofixation. Kidney biopsy established the diagnosis of CG. A treatment with prednisone was started without therapeutic response, progressing to end-stage kidney disease 19 months later. Molecular genetics investigation revealed an HRG. Conclusions This is the first report of CG associated with SM in the setting of an HRG. This case highlights the two-hit model as a mechanism for CG pathogenesis, where the high-risk APOL1 genotype exerts a susceptibility role and SM infection serves as a trigger to CG.
- Evidences of histologic thrombotic microangiopathy and the impact in renal outcomes of patients with IgA nephropathy(2020) NEVES, Precil Diego Miranda de Menezes; SOUZA, Rafael A.; TORRES, Fabio M.; REIS, Fabio A.; PINHEIRO, Rafaela B.; DIAS, Cristiane B.; YU, Luis; WORONIK, Viktoria; FURUKAWA, Luzia S.; CAVALCANTE, Livia B.; ARAUJO, Stanley de Almeida; WANDERLEY, David Campos; MALHEIROS, Denise M.; JORGE, Lecticia B.Introduction IgA nephropathy (IgAN) is the most common primary glomerulopathy worldwide. According to the Oxford Classification, changes in the kidney vascular compartment are not related with worse outcomes. This paper aims to assess the impact of thrombotic microangiopathy (TMA) in the outcomes of Brazilian patients with IgAN. Materials and methods Analysis of clinical data and kidney biopsy findings from patients with IgAN to assess the impact of TMA on renal outcomes. Results The majority of the 118 patients included were females (54.3%); mean age of 33 years (25;43); hypertension and hematuria were observed in 67.8% and 89.8%, respectively. Median creatinine: 1.45mg/dL; eGFR: 48.8ml/min/1.73m(2); 24-hour proteinuria: 2.01g; low serum C3: 12.5%. Regarding to Oxford Classification: M1: 76.3%; E1: 35.6%; S1: 70.3%; T1/T2: 38.3%; C1/C2: 28.8%. Average follow-up: 65 months. Histologic evidence of TMA were detected in 21 (17.8%) patients and those ones presented more frequently hypertension (100% vs. 61%, p <0.0001), hematuria (100% vs 87.6%, p = 0.0001), worse creatinine levels (3.8 vs. 1.38 mg/dL, p = 0.0001), eGFR (18 vs. 60 ml/min/1.73m(2)), p = 0.0001), low serum C3 (28.5% vs. 10.4%, p = 0.003), lower hemoglobin levels (10.6 vs. 12.7g/dL, p0.001) and platelet counts (207,000 vs. 267,000, p = 0.001). Biopsy findings of individuals with TMA revealed only greater proportions of E1 (68% vs. 32%, p = 0.002). Individuals with TMA were followed for less time (7 vs. 65 months, p<0.0001) since they progressed more frequently to chronic kidney disease (CKD) requiring kidney replacement therapy (KRT) (71.4% vs. 21,6%, p<0.0001). Male sex, T1/T2, and TMA were independently associated with progression to CKD-KRT. Conclusions In this study patients with TMA had worse clinical manifestations and outcomes. In terms of histologic evidence, E1 distinguished patients with TMA from other patients. Further studies are necessary to analyze the impact of vascular lesions on IgAN prognosis.
- Schistosomiasis-associated glomerulopathy: Clinical aspects, pathological characteristics, and renal outcomes(2020) NEVES, Precil Diego Miranda de Menezes; JORGE, Lecticia Barbosa; CAVALCANTE, Livia Barreira; MALHEIROS, Denise; WORONIK, Viktoria; DIAS, Cristiane BitencourtBackground: In Brazil, schistosomiasis is caused only by Schistosoma mansoni, occurring in the northeastern and southeastern regions. Schistosomiasis primarily affects the liver and gastrointestinal tract, although the kidneys can also be affected, mainly in the form of glomerulopathics. Here, we describe the characteristics of patients with schistosomiasis-associated glomerulopathies, including treatment and renal outcomes. Materials and methods: This was a retrospective analysis of patients diagnosed with schistosomiasis-associated glomerulopathy between 2002 and 2017. Clinical, biochemical, and histopathological (kidney biopsy) data were evaluated. Results: Of the 24 patients evaluated, 19 (79.1%) were male and 16 (66.4%) were White. The mean age was 38.58 +/- 9.83 years. We observed the hepatosplenic form of schistosomiasis in 15 patients (68.1%). nephrotic-nephritic syndrome in 13 (54.1%), hematuria in 20 (83.3%), and hypertension in 18 (75.0%). Renal histology showed a predominance of membranoproliferative pattern (n = 17/70.8%). On immunolluorescence, 19 patients (82.6%) showed immunoglobulin M (IgM) expression, 10 (43.4%) showed IgM+IgG expression, and 1(4.3%) showed a ""full house"" pattern. The median follow-up time was 59.70 months, by the end of which 9 patients (37.5%) had developed end-stage renal disease (ESRD). Baseline serum creatinine was higher among the patients who developed ESRD than among those who did not (1.99 +/- 1.08 vs. 1.34 +/- 0.46 mg/dL, p = 0.05). Conclusion: Our study is one of the rare clinical studies on schistosomiasis-associated glomerulopathy with a long follow-up and renal endpoints, showing that one third of our patients, independent of their histological form, progress to dialysis.
- Renal Outcomes in Brazilian Patients with Immunoglobulin A Nephropathy and Cellular Crescentic Lesions(2020) NEVES, Precil Diego Miranda de Menezes; PINHEIRO, Rafaela Bezerra Brito; DIAS, Cristiane Bitencourt; YU, Luis; TESTAGROSSA, Leonardo de Abreu; CAVALCANTE, Livia Barreira; MALHEIROS, Denise Maria Avancini Costa; JORGE, Lecticia Barbosa; WORONIK, ViktoriaBackground and Aim: Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulopathy. The Oxford classification was recently updated to include crescents as markers of poor prognosis. The aim of this study was to evaluate the impact of cellular crescents on the prognosis of patients with IgAN in Brazil. Methods: This was a single-centre retrospective analysis of medical records and renal biopsies in patients with IgAN. The renal biopsy findings were classified according to the revised Oxford classification: mesangial hypercellularity, endocapillary hypercellularity (E), segmental glomerulosclerosis (S), tubular atrophy or interstitial fibrosis (T), and crescent formation (C). We evaluated a composite outcome (progression to end-stage renal disease or creatinine doubling). We performed analyses between the patients with crescents in the renal biopsy specimen (C1/C2 group) and those without such crescents (C0 group). Results: We evaluated 111 patients, of whom 72 (65.0%) were women, 80 (72.0%) self-identified as White, 73 (65.6%) were hypertensive, and 95 (85.6%) had haematuria. The distribution of patients according to cellular crescentic lesions was: C0, 80 (72%); C1, 27 (24.4%); C2, 4 (3.6%). The composite outcome was observed in 33 (29.72%) of the 111 patients. In comparison with the C0 group, the C1/C2 group had higher proportions of patients with hypertension (p = 0.04), haematuria (p = 0.03), worse serum creatinine (p = 0.0007), and worse estimated glomerular filtration rate (p = 0.0007). The C1/C2 group also had higher proportions of patients in whom the biopsy specimen was classified as E1 (p = 0.009), S1 (p = 0.001), or T1/T2 (p = 0.03), In addition, the mean follow-up period was shorter in the C1/C2 group (p < 0.0001). Furthermore, the composite outcome was observed in a greater proportion of patients and in a shorter length of time in the C1/C2 group than in the C0 group (p = 0.002 and p = 0.0014, respectively). In a Cox regression analysis, the independent risk factors for the composite outcome had Oxford classifications of S1, T1/T2, and C1/C2. Conclusion: Oxford classification findings of S1, T1/T2, or C1/C2 were independent risk factors for the composite outcome, corroborating previous studies.