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Susanne Carolinne Penha Ferreira - One of the best experts on this subject based on the ideXlab platform.

  • Detection of renal structures recognized by non-HLA antibodies involved in the humoral rejection in patients with renal transplants
    Universidade de São Paulo, 2008
    Co-Authors: Susanne Carolinne Penha Ferreira
    Abstract:

    O transplante de órgãos é hoje uma opção de tratamento de várias doenças terminais. Apesar de todos os progressos no campo do transplante, o principal problema enfrentado ainda é a rejeição. As principais moléculas responsáveis pela resposta alogeneica e subsequente rejeição ao enxerto, são os antígenos leucocitários humanos (HLA, do inglês Human Leucocyte Antigens). Porém, existem evidências que anticorpos dirigidos a antígenos não-HLA estão associados com rejeição de transplantes. Neste estudo, foi investigada a presença de anticorpos anti-célula endotelial (AACE) em 11 pacientes que perderam seus rins transplantados devido à rejeição humoral irreversível e em 2 com perda por trombose de veia renal. A ausência de anticorpos anti-HLA contra o doador foi verificada antes do transplante, da rejeição e antes e depois da transplantectomia, através da realização de provas cruzadas usando as técnicas mais sensíveis. Anticorpos não-HLA presentes em nove eluatos reagiram com EAHy.926. Eluatos positivos e negativos contra linhagem EAHy.926 foram testados contra cortes histológicos de 6 rins sadios para detecção de quais estruturas renais são reconhecidas por esses anticorpos. A reação foi avaliada pelo método de imunofluorescência indireta. Dos 13 eluatos testados, 4 (isotipo IgG) e 5 (isotipo IgM) reagiram com forte fluorescência nos glomérulos e endotélio arterial, mas não foi verificada reação na cápsula de Bowman e no epitélio tubular. Não foi observado polimorfismo na reatividade dos eluatos. Em onclusão, verificamos que os anticorpos não-HLA têm um importante papel na rejeição humoral. Estes estão reconhecendo antígenos de um sistema provavelmente não-polimórfico nas células de endoteliais presentes, principalmente, nos capilares glomerulares.The transplant of organs is today an option of treatment to several terminal diseases. In spite of all the progress in the field of the transplants, the rejection remains a problem to be solved. The main target molecules for the allogenic response and subsequent allograft rejection are the human leukocyte antigens (HLA). However, there are growing evidences that non-HLA antibodies are associated with transplant rejection. In this study it was investigated the presence of anti-endothelial cell antibodies (AECA) in 11 patients who had early lost their transplanted kidney by irreversible humoral rejection and in 2 ones from renal venal thrombosis. The absence of anti-HLA antibodies against the donor was verified by the negativity of crossmatches performed using the most sensitive assays, at the transplant, at the rejection, and before and after the transplantectomy Antibodies from 9 eluates bound to EAHy.926. Positive and negatives eluates were tested against frozen sections from 6 normal kidneys in order to define the structures to which they were reactive. The reactivity was identified by indirect immunofluorescence method. From 13 eluates evaluated, 4 (isotipe IgG) and 5 (isotipe IgM) reacted to the glomerulus and renal arterial endothelium with intense fluorescence but they did not react to the Bowmans Capsule and tubular epithelium. No polymorphism was observed in eluates reactivity. In conclusion, we have shown that non-HLA antibodies may represent a cause of the humoral rejection. These antibodies are probably recognizing antigens of a nonpolymorphic system in endothelial cells present, mainly, in the glomerular capillaries

Gunnarsson Marika - One of the best experts on this subject based on the ideXlab platform.

  • Hereditär nefrit hos bullterrier i Sverige
    SLU Dept. of Animal Environment and Health, 2007
    Co-Authors: Gunnarsson Marika
    Abstract:

    Bull terrier hereditary nephritis is caused by a mutation that leads to an inadequate synthesis of collagen type IV, which is an important component in the basement membranes. The inheritance of the mutation is autosomal dominant in bull terriers and progression to renal failure takes variable time, from several months to ten years. Proteinuria is the first clinical sign of the disease and the diagnosis is confirmed by transmission electron microscopy of renal tissue where typical ultrastructural changes in the glomerular basement membrane (GBM), thickening and multilaminar splitting are found. This study was performed in order to find out the occurrence of hereditary nephritis in bull terriers in Sweden through examination of urine samples and renal tissue and comparisons with how the disease is described in the literature. Urine samples from 76 Swedish bull terriers were collected and examined for proteinuria. Dogs in heat or pregnancy were excluded. Three dogs had persistent proteinuria which was defined as a urinary protein creatinine ratio >0,5 in at least two urine samples taken at least one month apart, and in one of them a renal biopsy was performed. Renal tissue for light and transmission electron microscopy from nine bullterriers that had been euthanized/died earlier because of renal disease were also evaluated. In accordance with earlier studies the light microscopic changes found were non-specific and not diagnostic. Common lesions were fetal glomeruli (in adult dogs), larger glomerular tufts, adhesions between capillaries and Bowmans Capsule, mesangial thickening, thickened and mineralized basement membranes, glomerular sclerosis, periglomerular fibrosis, cystic dilatation of Bowmans Capsules with glomerular atrophy and protein content in the tubules. The ultrastructural abnormalities corresponded well to those described as specific for hereditary nephritis in earlier studies, including thickening and multilaminar splitting of the GBM. These changes in the GBM were seen in all the seven dogs that could be evaluated with electron microscopy. The results suggest that hereditary nephritis occurs in the bull terrier breed in Sweden and that the disease can be diagnosed by clinical symptoms and light microscopy together with transmission electron microscopy. Urine specimens from a greater number of dogs, especially from suspected families, would further increase the knowledge about how widespread hereditary nephritis amongst bull terriers is in Sweden.Hereditär nefrit hos bullterrier orsakas av en mutation som leder till att kollagen typ IV, vilket är en viktig komponent i basalmembran, inte bildas på ett normalt sätt. Mutationen nedärvs autosomalt dominant hos bullterrier och progression till total njursvikt sker efter varierande lång tid, från flera månader till tio år. Proteinuri är det första kliniska tecknet på sjukdomen och diagnosen ställs genom transmissionselektronmikroskopi av njurvävnad där man ser typiska ultrastrukturella förändringar på det glomerulära basalmembranet (GBM), förtjockning och lamellering. Den här studien genomfördes för att ta reda på förekomsten av hereditär nefrit hos bullterrier i Sverige genom undersökningar av urinprover och njurvävnad samt jämförelser med hur sjukdomen beskrivits i litteraturen. Urinprover från 76 svenska bullterriers samlades in och analyserades avseende proteininnehåll. Hundar i löp och dräktighet uteslöts. Tre hundar hade persisterande proteinuri vilket definierades som en urinprotein/kreatininkvot >0,5 i minst två provtagningar med minst en månads mellanrum, och en av dessa blev aktuell för njurbiopsi. Tidigare insamlad njurvävnad för ljusmikroskopi och transmissionselektronmikroskopi från nio bullterriers som avlivats/självdött på grund av njursjukdom bedömdes också. De ljusmikroskopiska fynden är ospecifika och inte diagnostiska vid hereditär nefrit men de fynd som tidigare beskrivits kunde även hittas i snitten från de bullterriers som ingick i studien. Vanliga förändringar var kvarstående fetala glomeruli (hos vuxna hundar), förstorade glomeruli, adhesioner mellan kapillärer och Bowmans kapsel, ökning av mesangiellt matrix, förtjockade och mineraliserade basalmembran, skleroserade glomeruli, periglomerulär fibros, cystiskt dilaterade Bowmans kapslar med atrofierade glomeruli samt proteininnehåll i tubuli. De ultrastrukturella fynden överensstämde också med de som angivits som specifika i litteraturen, det vill säga förtjockning och lamellering av GBM. Dessa GBMförändringar sågs hos alla de sju hundar som kunde bedömas med elektronmikroskopi. Resultaten tyder på att hereditär nefrit förekommer hos bullterrier i Sverige och att sjukdomen kan diagnosticeras med hjälp av klinisk bild och ljusmikroskopi tillsammans med transmissionselektronmikroskopi. Prover från ett större antal hundar och framförallt från misstänkta familjer skulle ytterligare öka kunskapen om utbredningen av hereditär nefrit hos bullterrier i Sverige

Michelle M. Kett - One of the best experts on this subject based on the ideXlab platform.

  • Typical histological features of kidneys of wildtype (WT) and GDNF HET mice fed control (CONT) or high fat (HFF) diet.
    2013
    Co-Authors: Seshini Gurusinghe, Russell D. Brown, Xiaochu Cai, Chrishan S. Samuel, Sharon D. Ricardo, Merlin C. Thomas, Michelle M. Kett
    Abstract:

    Panels A-F: High power images of typical glomeruli stained with periodic acid-Schiff (PAS). Glomeruli of WT-CONT (A) and HET-CONT (B) appeared normal with no differences in PAS positive staining. Glomeruli of WT-HFF mice showed glomerular hypertrophy (C) and some presented with glomerulosclerosis (D). Kidneys of HET-HFF mice contained very large glomeruli (E) and glomeruli with glomerulosclerosis (F). Bar = 100 um. Panels G-J: Fluorescent micrographs of collagen IV (Red) immunostaining. Collagen IV immunostaining in control WT (G) and HET (H) kidneys presented as a fine matrix localized to basement membranes of renal tubules, Bowmans Capsule and the intra and extraglomerular mesangium. In obese WT (I) and HET (J) kidneys, the accumulation of collagen IV protein was present and localized to the tubulointerstitium associated with expansion of the interstitial space (arrow). More extensive collagen IV was also evident in the glomerulointerstitium surrounding the glomerular Bowman’s Capsule.

Hull R. - One of the best experts on this subject based on the ideXlab platform.

  • Presence of the Dr receptor in normal human tissues and its possible role in the pathogenesis of ascending urinary tract infection.
    1
    Co-Authors: Nowicki B., Truong L., Moulds J., Hull R.
    Abstract:

    The Dr hemagglutinin of uropathogenic Escherichia coli recognizes the Dra blood group antigen, a component of the IFC or Cromer-related blood group complex. The present report used the Dr hemagglutinin to demonstrate location of the Dr receptor in selected human tissues and to evaluate the possible use of this lectin as a tissue marker recognizing sites sensitive for bacterial colonization. It was found that the Dr receptor was expressed in different parts of the digestive, urinary, genital, and respiratory tracts, and skin. Intense staining by Dr hemagglutinin was shown in colonic, bronchial, and endometrial glands, and skin eccrine sweat glands. Structures of the urinary tract showing strong fluorescence were renal tubular basement membrane, Bowmans' Capsule, and transitional epithelium. The role of Dra antigen as receptor for adhesion for Dr-positive E. coli in ascending colonization of urinary tract and the possible importance of Dra in human pathology is discussed

Seshini Gurusinghe - One of the best experts on this subject based on the ideXlab platform.

  • Typical histological features of kidneys of wildtype (WT) and GDNF HET mice fed control (CONT) or high fat (HFF) diet.
    2013
    Co-Authors: Seshini Gurusinghe, Russell D. Brown, Xiaochu Cai, Chrishan S. Samuel, Sharon D. Ricardo, Merlin C. Thomas, Michelle M. Kett
    Abstract:

    Panels A-F: High power images of typical glomeruli stained with periodic acid-Schiff (PAS). Glomeruli of WT-CONT (A) and HET-CONT (B) appeared normal with no differences in PAS positive staining. Glomeruli of WT-HFF mice showed glomerular hypertrophy (C) and some presented with glomerulosclerosis (D). Kidneys of HET-HFF mice contained very large glomeruli (E) and glomeruli with glomerulosclerosis (F). Bar = 100 um. Panels G-J: Fluorescent micrographs of collagen IV (Red) immunostaining. Collagen IV immunostaining in control WT (G) and HET (H) kidneys presented as a fine matrix localized to basement membranes of renal tubules, Bowmans Capsule and the intra and extraglomerular mesangium. In obese WT (I) and HET (J) kidneys, the accumulation of collagen IV protein was present and localized to the tubulointerstitium associated with expansion of the interstitial space (arrow). More extensive collagen IV was also evident in the glomerulointerstitium surrounding the glomerular Bowman’s Capsule.