Browsing by Author "Rodrigues, B"
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- Anemia na goença renal crónicaPublication . Rodrigues, B
- Atypical renal presentation of antiphospholipid syndromePublication . Gaspar, A; Manso, RT; Pereira, F; Cunha, L; Inchaustegui, L; Serra, A; Rodrigues, B; Correia, PAntiphospholipid syndrome (APS) is a systemic autoimmune disease which can occur as a primary disease or in association with other autoimmune diseases, the most frequent being Systemic Lupus Erythematosus (SLE). Although renal manifestations of SLE are well known, antiphospholipid syndrome renal manifestations such as antiphospholipid syndrome nephropathy and glomerulopathies have yet to be better characterized. The authors present the case of a 39 -year -old Caucasian woman with antiphospholipid syndrome diagnosis and a previous history of deep venous thrombosis and intermittent polyarthralgia, who was referred to a nephrology consultation for proteinuria and microscopic haematuria with preserved renal function. The renal biopsy showed a pattern of membranous glomerulopathy and thrombotic microangiopathy in association with antiphospholipid syndrome nephropathy. This case report illustrates a complex clinical and anatomopathological case of a 39 - year -old woman with a previous antiphospholipid syndrome diagnosis who presented with unspecific manifestations such as proteinuria and microscopic haematuria and preserved renal function. The histological findings alert us to the range of possible renal manifestations of APS and the need to better characterize these patients by preforming renal biopsy.
- Candida species contamination of preservation fluid-outcome of renal transplantation in 6 patientsPublication . Rodrigues, B; Natário, A; Vizinho, R; Jorge C, C; Weigert, A; Martinho, A; Toscano, C; Marques, T; Machado, DBACKGROUND: Fungal infections are a rare but important cause of morbidity and mortality in kidney transplantation. Fungal contamination of the kidney preservation fluid may, sometimes, be the cause of these infections. However, the clinical consequences of fungal contamination of this fluid are not completely understood and literature on this topic is controversial. The purpose of this study was to determine the incidence of preservation fluid contamination by fungi and its clinical consequences. METHODS: From June 2010 to September 2011, a prospective cohort analysis was conducted at our center, enrolling all patients who received a renal allograft and whose perfusion fluid was analyzed for microbiology sterility. Patients with perfusion fluids positive for fungi were further studied: the patients' status was assessed during regular visits and data were recorded, including clinical characteristics, infections, graft function, immunosuppressive regimen and outcomes. RESULTS: Microbiologic, cultures of 70 kidney perfusion fluids using specific mycologic media, obtained from 74 cadaveric renal transplants (4 fluids were unsuitable for analysis), were evaluated. Six samples were positive for yeasts (8.6%), with 4 isolates of Candida albicans and 2 isolates of Candida glabrata. Four patients had no evidence of fungal infection during the follow-up period (median 321 days); conversely, 2 patients developed severe mycotic vascular complications leading to transplantectomy. CONCLUSIONS: Perfusion fluid contamination by fungi is an elusive situation that can lead either to an unremarkable clinical course or to graft loss life-threatening situations. Routine culture of kidney perfusion fluid is critical for prompt diagnosis and early implementation of appropriate treatment.
- Cystatin C as a marker of acute kidney injury in the emergency departmentPublication . Soto, K; Coelho, S; Rodrigues, B; Martins, H; Frade, F; Lopes, S; Cunha, L; Papoila, A; Devarajan, PBACKGROUND AND OBJECTIVES: The diagnosis of acute kidney injury (AKI) is usually based on changes in serum creatinine, which is a poor marker of early renal dysfunction. The discriminative and predictive abilities of serum and urinary cystatin C were examined for the prediction of AKI. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this prospective cohort study, serum and urinary cystatin C were serially measured in a heterogeneous group of patients (n = 616) presenting to a tertiary care emergency department. The primary outcome was AKI, classified according to RIFLE and AKIN criteria. The secondary outcome was an adjudication based on clinical criteria to AKI, prerenal azotemia, chronic kidney disease (CKD), and normal kidney function. RESULTS: Patients were adjudicated to have AKI in 21.1%, prerenal azotemia in 25.8%, CKD in 2.4%, and normal kidney function in 50.7%. For the diagnosis of AKI, the discriminatory ability of urinary creatinine and cystatin C was marginal. Both serum cystatin C and serum creatinine (at presentation and 6 hours later) showed high discriminatory ability for the diagnosis of AKI. However, only serum cystatin C attained a significant early predictive power (Hosmer-Lemeshow P value > 0.05). Serum cystatin C could differentiate between AKI and prerenal azotemia, but not between AKI and CKD. CONCLUSIONS: Serum cystatin C is an early, predictive biomarker of AKI, which outperforms serum creatinine in the heterogeneous emergency department setting. However, neither biomarker discriminated between AKI and CKD. Additional biomarkers continue to be needed for improved specificity in the diagnosis of community-acquired AKI.
- Plasma NGAL for the diagnosis of AKI in patients admitted from the emergency department settingPublication . Soto, K; Papoila, A; Coelho, S; Bennett, M; Ma, Q; Rodrigues, B; Fidalgo, P; Frade, F; Devarajan, PBACKGROUND AND OBJECTIVES: The purpose of this study was to determine the accuracy of plasma neutrophil gelatinase-associated lipocalin as a marker of AKI in patients admitted from the emergency department. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this prospective cohort study, patients (n=616) admitted from the emergency department from March to November of 2008 were classified according to clinical criteria as AKI, transient azotemia, stable CKD, and normal function. Plasma neutrophil gelatinase-associated lipocalin was measured serially. A logistic regression model using clinical characteristics was fitted to the data, and a second model included discretized plasma neutrophil gelatinase-associated lipocalin. Performance of the models was evaluated by Hosmer-Lemeshow goodness-of-fit test, area under the receiver operating characteristic curve, net reclassification improvement, integrated discrimination improvement, and predictiveness curve. RESULTS: Twenty-one percent of patients were classified as AKI; the highest median levels of plasma neutrophil gelatinase-associated lipocalin were in the AKI group (146-174 ng/ml at various time points) and increased with AKI severity (207-244 ng/ml for Acute Kidney Injury Network classification stage>2). The discriminative ability of plasma neutrophil gelatinase-associated lipocalin for AKI diagnosis (area under the curve, 0.77-0.82 at various time points) improved with higher grades of severity (area under the curve, 0.85-0.89 for AKIN>2). Plasma neutrophil gelatinase-associated lipocalin discriminated AKI from normal function and transient azotemia (area under the curve, 0.85 and 0.73, respectively). Patients were classified into three grades of AKI risk according to plasma neutrophil gelatinase-associated lipocalin levels (low, moderate [i.e., the gray zone], and high). Patients with plasma neutrophil gelatinase-associated lipocalin in the high-risk category displayed a 10-fold greater risk of AKI (odds ratio, 9.8; 95% confidence interval, 5.6 to 16.9). The addition of plasma neutrophil gelatinase-associated lipocalin to the clinical model yielded a net reclassification improvement of 94.3% and an integrated discrimination improvement of 0.122. CONCLUSION: Plasma neutrophil gelatinase-associated lipocalin is an accurate biomarker for prediction of AKI in patients admitted from the emergency department. This work proposes a three-grade classification of AKI risk based on plasma neutrophil gelatinase-associated lipocalin levels.
- Poliangeíte microscópica: evolução clínica de um doentePublication . Faustino, A; Faria, A; Carvalho, F; Rodrigues, B; Correia, P; Louro, F
- Síndrome de Churg-StraussPublication . Rodrigues, B; Araújo, JMA síndrome de Churg-Strauss é uma vasculite ANCA-associada de pequenos e médios vasos. As manifestações clínicas mais comuns são eosinofilia marcada, asma, sinusite crónica, infiltrados pulmonares, cardiomiopatia, queixas gastrointestinais e mononeurite multiplex. Os anticorpos Anti-MPO (anti-mieloperoxidade), pANCA (com padrão de imunoflurescência perinuclear) encontram-se presentes em 38-59% dos casos. O envolvimento cardíaco é uma importante causa de morbilidade e a principal causa de mortalidade no síndrome de Churg-Strauss. Histologicamente caracteriza-se por uma vasculite necrotizante eosinofílica. O tratamento é baseado na corticoterapia e em fármacos imunosupressores (ciclofosfamida e azatioprina) sendo determinado de acordo com critérios de prognóstico. A remissão completa ocorre em cerca de 90% dos casos, sendo as recaídas frequentes (25% dos casos).
- The risk of chronic kidney disease and mortality are increased after community-acquired acute kidney injury.Publication . Soto, K; Campos, P; Pinto, I; Rodrigues, B; Frade, F; Papoila, AL; Devarajan, PWe investigated whether community-acquired acute kidney injury encountered in a tertiary hospital emergency department setting increases the risk of chronic kidney disease (CKD) and mortality, and whether plasma biomarkers could improve the prediction of those adverse outcomes. In a prospective cohort study, we enrolled 616 patients at admission to the emergency department and followed them for a median of 62.1 months. Within this cohort, 130 patients were adjudicated as having acute kidney injury, 159 transient azotemia, 15 stable CKD, and 312 normal renal function. Serum cystatin C and plasma neutrophil gelatinase-associated lipocalin (NGAL) were measured at index admission. After adjusting for clinical variables, the risk of developing CKD stage 3, as well as the risk of death, were increased in the acute kidney injury group (hazard ratio [HR], 5.7 [95% confidence interval, 3.8-8.7] and HR, 1.9 [95% confidence interval, 1.3-2.8], respectively). The addition of serum cystatin C increased the ability to predict the risk of developing CKD stage 3, and death (HR, 1.5 [1.1-2.0] and 1.6 [1.1-2.3], respectively). The addition of plasma NGAL resulted in no improvement in predicting CKD stage 3 or mortality (HR, 1.0 [0.7-1.5] and 1.2 [0.8-1.8], respectively). The risk of developing CKD stage 3 was also significantly increased in the transient azotemia group (HR, 2.4 [1.5-3.6]). Thus, an episode of community acquired acute kidney injury markedly increases the risk of CKD, and moderately increases the risk of death. Our findings highlight the importance of follow-up of patients with community acquired acute kidney injury, for potential early initiation of renal protective strategies.
- Utilidade do exame de urina como ferramenta diagnósticaPublication . Rodrigues, B