Volume Progression in Polycystic Kidney Disease
Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive enlargement of cyst-filled kidneys. A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume and iothalamate clearance over a three-year period in patients w...
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| Veröffentlicht in: | The New England journal of medicine 2006-05, Vol.354 (20), p.2122-2130 |
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| creator | Grantham, Jared J Torres, Vicente E Chapman, Arlene B Guay-Woodford, Lisa M Bae, Kyongtae T King, Bernard F Wetzel, Louis H Baumgarten, Deborah A Kenney, Phillip J Harris, Peter C Klahr, Saulo Bennett, William M Hirschman, Gladys N Meyers, Catherine M Zhang, Xiaoling Zhu, Fang Miller, John P |
| description | Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive enlargement of cyst-filled kidneys. A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume and iothalamate clearance over a three-year period in patients with ADPKD without azotemia. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume in patients with ADPKD. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal disorder involving a single gene and the fourth leading cause of end-stage renal disease in adults.
1
,
2
Renal cysts contribute to morbidity and can impair the quality of life early in the course of the disease. Pain and gross hematuria are reported in approximately 60 percent of patients.
3
,
4
ADPKD ultimately leads to the destruction of renal parenchyma in more than 50 percent of patients.
5
–
9
Serum creatinine levels rise late in the course of the disease, only after the noncystic parenchyma has incurred serious, irreversible damage. The lack . . . |
| doi_str_mv | 10.1056/NEJMoa054341 |
| format | Article |
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A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume in patients with ADPKD. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal disorder involving a single gene and the fourth leading cause of end-stage renal disease in adults.
1
,
2
Renal cysts contribute to morbidity and can impair the quality of life early in the course of the disease. Pain and gross hematuria are reported in approximately 60 percent of patients.
3
,
4
ADPKD ultimately leads to the destruction of renal parenchyma in more than 50 percent of patients.
5
–
9
Serum creatinine levels rise late in the course of the disease, only after the noncystic parenchyma has incurred serious, irreversible damage. The lack . . .</description><identifier>ISSN: 0028-4793</identifier><identifier>EISSN: 1533-4406</identifier><identifier>DOI: 10.1056/NEJMoa054341</identifier><identifier>PMID: 16707749</identifier><identifier>CODEN: NEJMAG</identifier><language>eng</language><publisher>Boston, MA: Massachusetts Medical Society</publisher><subject>Adult ; Analysis of Variance ; Biological and medical sciences ; Cysts ; Disease Progression ; Female ; General aspects ; Glomerular Filtration Rate ; Humans ; Kidney - pathology ; Kidney - physiopathology ; Kidney diseases ; Kidneys ; Longitudinal Studies ; Magnetic Resonance Imaging ; Male ; Malformations of the urinary system ; Medical sciences ; Mutation ; Nephrology. Urinary tract diseases ; Organ Size ; Polycystic Kidney, Autosomal Dominant - genetics ; Polycystic Kidney, Autosomal Dominant - pathology ; Polycystic Kidney, Autosomal Dominant - physiopathology ; Regression Analysis</subject><ispartof>The New England journal of medicine, 2006-05, Vol.354 (20), p.2122-2130</ispartof><rights>Copyright © 2006 Massachusetts Medical Society. All rights reserved.</rights><rights>2006 INIST-CNRS</rights><rights>Copyright 2006 Massachusetts Medical Society.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c547t-c34f71bf313aa605f6e8eb09eba52546b142299ac084355efa621fb1fd1d52af3</citedby><cites>FETCH-LOGICAL-c547t-c34f71bf313aa605f6e8eb09eba52546b142299ac084355efa621fb1fd1d52af3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.nejm.org/doi/pdf/10.1056/NEJMoa054341$$EPDF$$P50$$Gmms$$H</linktopdf><linktohtml>$$Uhttps://www.nejm.org/doi/full/10.1056/NEJMoa054341$$EHTML$$P50$$Gmms$$H</linktohtml><link.rule.ids>314,776,780,2746,2747,26080,27901,27902,52357,54039</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17767922$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16707749$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Grantham, Jared J</creatorcontrib><creatorcontrib>Torres, Vicente E</creatorcontrib><creatorcontrib>Chapman, Arlene B</creatorcontrib><creatorcontrib>Guay-Woodford, Lisa M</creatorcontrib><creatorcontrib>Bae, Kyongtae T</creatorcontrib><creatorcontrib>King, Bernard F</creatorcontrib><creatorcontrib>Wetzel, Louis H</creatorcontrib><creatorcontrib>Baumgarten, Deborah A</creatorcontrib><creatorcontrib>Kenney, Phillip J</creatorcontrib><creatorcontrib>Harris, Peter C</creatorcontrib><creatorcontrib>Klahr, Saulo</creatorcontrib><creatorcontrib>Bennett, William M</creatorcontrib><creatorcontrib>Hirschman, Gladys N</creatorcontrib><creatorcontrib>Meyers, Catherine M</creatorcontrib><creatorcontrib>Zhang, Xiaoling</creatorcontrib><creatorcontrib>Zhu, Fang</creatorcontrib><creatorcontrib>Miller, John P</creatorcontrib><creatorcontrib>CRISP Investigators</creatorcontrib><title>Volume Progression in Polycystic Kidney Disease</title><title>The New England journal of medicine</title><addtitle>N Engl J Med</addtitle><description>Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive enlargement of cyst-filled kidneys. A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume and iothalamate clearance over a three-year period in patients with ADPKD without azotemia. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume in patients with ADPKD. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal disorder involving a single gene and the fourth leading cause of end-stage renal disease in adults.
1
,
2
Renal cysts contribute to morbidity and can impair the quality of life early in the course of the disease. Pain and gross hematuria are reported in approximately 60 percent of patients.
3
,
4
ADPKD ultimately leads to the destruction of renal parenchyma in more than 50 percent of patients.
5
–
9
Serum creatinine levels rise late in the course of the disease, only after the noncystic parenchyma has incurred serious, irreversible damage. The lack . . .</description><subject>Adult</subject><subject>Analysis of Variance</subject><subject>Biological and medical sciences</subject><subject>Cysts</subject><subject>Disease Progression</subject><subject>Female</subject><subject>General aspects</subject><subject>Glomerular Filtration Rate</subject><subject>Humans</subject><subject>Kidney - pathology</subject><subject>Kidney - physiopathology</subject><subject>Kidney diseases</subject><subject>Kidneys</subject><subject>Longitudinal Studies</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Malformations of the urinary system</subject><subject>Medical sciences</subject><subject>Mutation</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Organ Size</subject><subject>Polycystic Kidney, Autosomal Dominant - genetics</subject><subject>Polycystic Kidney, Autosomal Dominant - pathology</subject><subject>Polycystic Kidney, Autosomal Dominant - physiopathology</subject><subject>Regression Analysis</subject><issn>0028-4793</issn><issn>1533-4406</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpt0DtPwzAUBWALgWgpbMwoQsBEqN-OR1TKs0AHYLUc10apkrjYzZB_T1AjFSHucpdP514dAI4RvEKQ8fHL9PHZa8gooWgHDBEjJKUU8l0whBBnKRWSDMBBjEvYDaJyHwwQF1AIKodg_OHLprLJPPjPYGMsfJ0UdTL3ZWvauC5M8lQsatsmN0W0OtpDsOd0Ge1Rv0fg_Xb6NrlPZ693D5PrWWoYFevUEOoEyh1BRGsOmeM2szmUNtcMM8pzRDGWUhuYUcKYdZpj5HLkFmjBsHZkBC42uavgvxob16oqorFlqWvrm6i4kBmTMOvg6R-49E2ou98UxkQSTjjs0OUGmeBjDNapVSgqHVqFoPppUf1useMnfWaTV3axxX1tHTjvgY5Gly7o2hRx64To_uvOj8DZxlVVVLVdVv_f-wZUaYN_</recordid><startdate>20060518</startdate><enddate>20060518</enddate><creator>Grantham, Jared J</creator><creator>Torres, Vicente E</creator><creator>Chapman, Arlene B</creator><creator>Guay-Woodford, Lisa M</creator><creator>Bae, Kyongtae T</creator><creator>King, Bernard F</creator><creator>Wetzel, Louis H</creator><creator>Baumgarten, Deborah A</creator><creator>Kenney, Phillip J</creator><creator>Harris, Peter C</creator><creator>Klahr, Saulo</creator><creator>Bennett, William M</creator><creator>Hirschman, Gladys N</creator><creator>Meyers, Catherine M</creator><creator>Zhang, Xiaoling</creator><creator>Zhu, Fang</creator><creator>Miller, John P</creator><general>Massachusetts Medical Society</general><scope>IQODW</scope><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>0TZ</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K0Y</scope><scope>LK8</scope><scope>M0R</scope><scope>M0T</scope><scope>M1P</scope><scope>M2M</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20060518</creationdate><title>Volume Progression in Polycystic Kidney Disease</title><author>Grantham, Jared J ; Torres, Vicente E ; Chapman, Arlene B ; Guay-Woodford, Lisa M ; Bae, Kyongtae T ; King, Bernard F ; Wetzel, Louis H ; Baumgarten, Deborah A ; Kenney, Phillip J ; Harris, Peter C ; Klahr, Saulo ; Bennett, William M ; Hirschman, Gladys N ; Meyers, Catherine M ; Zhang, Xiaoling ; Zhu, Fang ; Miller, John P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c547t-c34f71bf313aa605f6e8eb09eba52546b142299ac084355efa621fb1fd1d52af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Analysis of Variance</topic><topic>Biological and medical sciences</topic><topic>Cysts</topic><topic>Disease Progression</topic><topic>Female</topic><topic>General aspects</topic><topic>Glomerular Filtration Rate</topic><topic>Humans</topic><topic>Kidney - pathology</topic><topic>Kidney - physiopathology</topic><topic>Kidney diseases</topic><topic>Kidneys</topic><topic>Longitudinal Studies</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Malformations of the urinary system</topic><topic>Medical sciences</topic><topic>Mutation</topic><topic>Nephrology. 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A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume and iothalamate clearance over a three-year period in patients with ADPKD without azotemia. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
A magnetic-resonance–based method was used to determine the rates of change in total kidney volume and cyst volume in patients with ADPKD. Higher rates of kidney enlargement were associated with more rapid decreases in renal function.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal disorder involving a single gene and the fourth leading cause of end-stage renal disease in adults.
1
,
2
Renal cysts contribute to morbidity and can impair the quality of life early in the course of the disease. Pain and gross hematuria are reported in approximately 60 percent of patients.
3
,
4
ADPKD ultimately leads to the destruction of renal parenchyma in more than 50 percent of patients.
5
–
9
Serum creatinine levels rise late in the course of the disease, only after the noncystic parenchyma has incurred serious, irreversible damage. The lack . . .</abstract><cop>Boston, MA</cop><pub>Massachusetts Medical Society</pub><pmid>16707749</pmid><doi>10.1056/NEJMoa054341</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; New England Journal of Medicine |
| subjects | Adult Analysis of Variance Biological and medical sciences Cysts Disease Progression Female General aspects Glomerular Filtration Rate Humans Kidney - pathology Kidney - physiopathology Kidney diseases Kidneys Longitudinal Studies Magnetic Resonance Imaging Male Malformations of the urinary system Medical sciences Mutation Nephrology. Urinary tract diseases Organ Size Polycystic Kidney, Autosomal Dominant - genetics Polycystic Kidney, Autosomal Dominant - pathology Polycystic Kidney, Autosomal Dominant - physiopathology Regression Analysis |
| title | Volume Progression in Polycystic Kidney Disease |
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