RESUMO
OBJECTIVES:: Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor ß1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor ß1 and monocyte chemoattractant protein-1 expression in these patients. METHODS:: Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. (1). The immunohistochemical detection of Transforming growth factor ß1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105. RESULTS:: Transforming growth factor ß1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor ß1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001). CONCLUSION:: Transforming growth factor ß1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.
Assuntos
Quimiocina CCL2/metabolismo , Glomerulonefrite por IGA/metabolismo , Vasculite por IgA/metabolismo , Túbulos Renais/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Adolescente , Criança , Pré-Escolar , Feminino , Fibrose , Glomerulonefrite por IGA/patologia , Humanos , Vasculite por IgA/patologia , Túbulos Renais/patologia , Masculino , PrognósticoRESUMO
OBJECTIVES: Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor β1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in these patients. METHODS: Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. (1). The immunohistochemical detection of Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105. RESULTS: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor β1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001). CONCLUSION: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.
Assuntos
Humanos , Masculino , Feminino , Pré-Escolar , Criança , Adolescente , Vasculite por IgA/metabolismo , Quimiocina CCL2/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Glomerulonefrite por IGA/metabolismo , Túbulos Renais/metabolismo , Prognóstico , Vasculite por IgA/patologia , Fibrose , Glomerulonefrite por IGA/patologia , Túbulos Renais/patologiaRESUMO
Haemophilus influenzae biogroup aegyptius (H. aegyptius) is the etiological agent of Brazilian purpuric fever (BPF), a recently described pediatric disease that is often fatal. The vascular destruction that occurs in this disease is a distinctive trait, and little is known about the mechanism(s) of the overwhelming purpura fulminans that causes the high mortality associated with this pediatric infection. Iron is an essential micronutrient for nearly all living cells, and the mechanisms used by bacteria to acquire and internalize iron are often associated with virulence. Therefore, the focus of our studies is the molecular characterization of the iron uptake system used by H. aegyptius. Specifically, we are investigating the high-affinity transferrin binding proteins in the bacterial outer membrane, components of ABC transporter systems, and a possible regulatory mechanism for the genes encoding these proteins. A detailed understanding of the molecular nature of the regulatory genetic components and proteins involved in the acquisition of iron will broaden the knowledge of the pathogenesis of the disease caused by H. aegyptius and will also lead to a better understanding of the nature of other infections that affect the vascular system.
Assuntos
Haemophilus influenzae/genética , Vasculite por IgA/microbiologia , Ferro/metabolismo , Receptores da Transferrina/genética , Proteínas de Bactérias/genética , Proteínas de Bactérias/metabolismo , Clonagem Molecular , Previsões , Haemophilus influenzae/metabolismo , Vasculite por IgA/genética , Vasculite por IgA/metabolismo , Receptores da Transferrina/metabolismo , Transferrina/metabolismoRESUMO
Twenty-nine children with typical Schönlein-Henoch purpura (SHP) were tested at the initial phase of the disease for respiratory function. Of the 29 patients, 28 had a decrease of lung transfer for carbon monoxide (TLCO) as measured by a steady-state method. Lung volumes and blood gas values were normal; slight radiologic signs of interstitial lung involvement were observed in 18 of 26 patients. There was a decrease in TLCO to 56.8% of normal values for height and gender and to 58.5% when normal values were volume-adjusted to functional residual capacity. In 19 of 25 patients, TLCO measurements were performed at 3-month intervals during follow-up. In all cases, normalization of TLCO values was observed only after complete clinical recovery from SHP. All children with persisting symptoms, even limited to microscopic hematuria or slight proteinuria, had low TLCO values. In one patient low TLCO during follow-up preceded a late relapse of SHP in the form of acute nephritic disease with characteristic IgA deposits on renal biopsy. We conclude that low TLCO in SHP is probably related to alteration of the alveolar-capillary membrane by circulating immune complexes. This noninvasive technique may be useful in diagnosis, and during the follow-up of the disease as an early indicator of reactivation.