Hereditär nefrit hos bullterrier i Sverige
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,...
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| Formato: | L3 |
| Lenguaje: | sueco Inglés |
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SLU/Dept. of Animal Environment and Health (until 231231)
2007
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| Materias: |
| _version_ | 1855571810819506176 |
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| author | Gunnarsson, Marika |
| author_browse | Gunnarsson, Marika |
| author_facet | Gunnarsson, Marika |
| author_sort | Gunnarsson, Marika |
| collection | Epsilon Archive for Student Projects |
| description | 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. |
| format | L3 |
| id | RepoSLU11118 |
| institution | Swedish University of Agricultural Sciences |
| language | swe Inglés |
| publishDate | 2007 |
| publishDateSort | 2007 |
| publisher | SLU/Dept. of Animal Environment and Health (until 231231) |
| publisherStr | SLU/Dept. of Animal Environment and Health (until 231231) |
| record_format | eprints |
| spelling | RepoSLU111182017-09-28T08:51:33Z Hereditär nefrit hos bullterrier i Sverige Gunnarsson, Marika hereditär nefrit bullterrier basalmembran kollagen glomeruli elektronmikroskopi ultrastruktur lamellering fotutskott histopatologi ärftlig njursjukdom ljusmikroskopi persisterande proteinuri urinprotein urinkreatinin typ IV 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. SLU/Dept. of Animal Environment and Health (until 231231) 2007 L3 swe eng https://stud.epsilon.slu.se/11118/ |
| spellingShingle | hereditär nefrit bullterrier basalmembran kollagen glomeruli elektronmikroskopi ultrastruktur lamellering fotutskott histopatologi ärftlig njursjukdom ljusmikroskopi persisterande proteinuri urinprotein urinkreatinin typ IV Gunnarsson, Marika Hereditär nefrit hos bullterrier i Sverige |
| title | Hereditär nefrit hos bullterrier i Sverige |
| title_full | Hereditär nefrit hos bullterrier i Sverige |
| title_fullStr | Hereditär nefrit hos bullterrier i Sverige |
| title_full_unstemmed | Hereditär nefrit hos bullterrier i Sverige |
| title_short | Hereditär nefrit hos bullterrier i Sverige |
| title_sort | hereditär nefrit hos bullterrier i sverige |
| topic | hereditär nefrit bullterrier basalmembran kollagen glomeruli elektronmikroskopi ultrastruktur lamellering fotutskott histopatologi ärftlig njursjukdom ljusmikroskopi persisterande proteinuri urinprotein urinkreatinin typ IV |