Focal and segmental glomerulosclerosis
An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form...
Gespeichert in:
| Veröffentlicht in: | Cellular and molecular life sciences : CMLS 2006-11, Vol.63 (21), p.2506-2511 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2511 |
|---|---|
| container_issue | 21 |
| container_start_page | 2506 |
| container_title | Cellular and molecular life sciences : CMLS |
| container_volume | 63 |
| creator | Daskalakis, N Winn, M P |
| description | An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm. |
| doi_str_mv | 10.1007/s00018-006-6171-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11136043</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2044086991</sourcerecordid><originalsourceid>FETCH-LOGICAL-c456t-61961aeb696f35f2720001aa2d4a005ffc11ead1f541554beea5648ed37af65b3</originalsourceid><addsrcrecordid>eNqFkU1LAzEQhoMotlZ_gBcpHnpbncnX7p5EilVB8KLgLWR3k7olu6mbrtB_b2qLXxdPkyHPvLwzLyGnCBcIkF4GAMAsAZCJxBST9R4ZIqeQ5JDi_u4tM_oyIEchLCIsMioPyQBlLigIPiSTmS-1G-u2Ggczb0y7it3c-cZ0vfOhdKbzoQ7H5MBqF8zJro7I8-zmaXqXPDze3k-vH5KSC7mKLnKJ2hQyl5YJS1O6cag1rbgGENaWiEZXaAVHIXhhjBaSZ6ZiqbZSFGxErra6y75oTFVGP512atnVje7Wyuta_f5p61c19-8KEZkEzqLCZKfQ-bfehJVq6lAa53RrfB-UzJBSCtm_IAXJMGcQwfM_4ML3XRvPoBiXGcvTTwi3UBnvFTpjvzwjqE1YahuWimGpTVhqHWfOfi77PbFLh30A7YiPaA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>346839730</pqid></control><display><type>article</type><title>Focal and segmental glomerulosclerosis</title><source>MEDLINE</source><source>SpringerLink Journals</source><source>PubMed Central</source><creator>Daskalakis, N ; Winn, M P</creator><creatorcontrib>Daskalakis, N ; Winn, M P</creatorcontrib><description>An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm.</description><identifier>ISSN: 1420-682X</identifier><identifier>EISSN: 1420-9071</identifier><identifier>DOI: 10.1007/s00018-006-6171-y</identifier><identifier>PMID: 16952054</identifier><language>eng</language><publisher>Switzerland: Springer Nature B.V</publisher><subject>Genetics ; Genome, Human - genetics ; Glomerulosclerosis, Focal Segmental - pathology ; Human Genome & Diseases: Review ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Kidney diseases ; Membrane Proteins - genetics ; Mutation - genetics ; Transplants & implants ; TRPV Cation Channels - genetics</subject><ispartof>Cellular and molecular life sciences : CMLS, 2006-11, Vol.63 (21), p.2506-2511</ispartof><rights>Birkhäuser Verlag, Basel 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-61961aeb696f35f2720001aa2d4a005ffc11ead1f541554beea5648ed37af65b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136043/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11136043/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16952054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Daskalakis, N</creatorcontrib><creatorcontrib>Winn, M P</creatorcontrib><title>Focal and segmental glomerulosclerosis</title><title>Cellular and molecular life sciences : CMLS</title><addtitle>Cell Mol Life Sci</addtitle><description>An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm.</description><subject>Genetics</subject><subject>Genome, Human - genetics</subject><subject>Glomerulosclerosis, Focal Segmental - pathology</subject><subject>Human Genome & Diseases: Review</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Kidney diseases</subject><subject>Membrane Proteins - genetics</subject><subject>Mutation - genetics</subject><subject>Transplants & implants</subject><subject>TRPV Cation Channels - genetics</subject><issn>1420-682X</issn><issn>1420-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkU1LAzEQhoMotlZ_gBcpHnpbncnX7p5EilVB8KLgLWR3k7olu6mbrtB_b2qLXxdPkyHPvLwzLyGnCBcIkF4GAMAsAZCJxBST9R4ZIqeQ5JDi_u4tM_oyIEchLCIsMioPyQBlLigIPiSTmS-1G-u2Ggczb0y7it3c-cZ0vfOhdKbzoQ7H5MBqF8zJro7I8-zmaXqXPDze3k-vH5KSC7mKLnKJ2hQyl5YJS1O6cag1rbgGENaWiEZXaAVHIXhhjBaSZ6ZiqbZSFGxErra6y75oTFVGP512atnVje7Wyuta_f5p61c19-8KEZkEzqLCZKfQ-bfehJVq6lAa53RrfB-UzJBSCtm_IAXJMGcQwfM_4ML3XRvPoBiXGcvTTwi3UBnvFTpjvzwjqE1YahuWimGpTVhqHWfOfi77PbFLh30A7YiPaA</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Daskalakis, N</creator><creator>Winn, M P</creator><general>Springer Nature B.V</general><general>Birkhäuser-Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20061101</creationdate><title>Focal and segmental glomerulosclerosis</title><author>Daskalakis, N ; Winn, M P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-61961aeb696f35f2720001aa2d4a005ffc11ead1f541554beea5648ed37af65b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Genetics</topic><topic>Genome, Human - genetics</topic><topic>Glomerulosclerosis, Focal Segmental - pathology</topic><topic>Human Genome & Diseases: Review</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Kidney diseases</topic><topic>Membrane Proteins - genetics</topic><topic>Mutation - genetics</topic><topic>Transplants & implants</topic><topic>TRPV Cation Channels - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Daskalakis, N</creatorcontrib><creatorcontrib>Winn, M P</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cellular and molecular life sciences : CMLS</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Daskalakis, N</au><au>Winn, M P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Focal and segmental glomerulosclerosis</atitle><jtitle>Cellular and molecular life sciences : CMLS</jtitle><addtitle>Cell Mol Life Sci</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>63</volume><issue>21</issue><spage>2506</spage><epage>2511</epage><pages>2506-2511</pages><issn>1420-682X</issn><eissn>1420-9071</eissn><abstract>An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm.</abstract><cop>Switzerland</cop><pub>Springer Nature B.V</pub><pmid>16952054</pmid><doi>10.1007/s00018-006-6171-y</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1420-682X |
| ispartof | Cellular and molecular life sciences : CMLS, 2006-11, Vol.63 (21), p.2506-2511 |
| issn | 1420-682X 1420-9071 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11136043 |
| source | MEDLINE; SpringerLink Journals; PubMed Central |
| subjects | Genetics Genome, Human - genetics Glomerulosclerosis, Focal Segmental - pathology Human Genome & Diseases: Review Humans Intracellular Signaling Peptides and Proteins - genetics Kidney diseases Membrane Proteins - genetics Mutation - genetics Transplants & implants TRPV Cation Channels - genetics |
| title | Focal and segmental glomerulosclerosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T03%3A27%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Focal%20and%20segmental%20glomerulosclerosis&rft.jtitle=Cellular%20and%20molecular%20life%20sciences%20:%20CMLS&rft.au=Daskalakis,%20N&rft.date=2006-11-01&rft.volume=63&rft.issue=21&rft.spage=2506&rft.epage=2511&rft.pages=2506-2511&rft.issn=1420-682X&rft.eissn=1420-9071&rft_id=info:doi/10.1007/s00018-006-6171-y&rft_dat=%3Cproquest_pubme%3E2044086991%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=346839730&rft_id=info:pmid/16952054&rfr_iscdi=true |