TY - JOUR
T1 - Detection and characterization of mosaicism in autosomal dominant polycystic kidney disease
AU - HALT Progression of Polycystic Kidney Disease Group, the ADPKD Modifier Study
AU - Hopp, Katharina
AU - Cornec-Le Gall, Emilie
AU - Senum, Sarah R.
AU - te Paske, Iris B.A.W.
AU - Raj, Sonam
AU - Lavu, Sravanthi
AU - Baheti, Saurabh
AU - Edwards, Marie E.
AU - Madsen, Charles D.
AU - Heyer, Christina M.
AU - Ong, Albert C.M.
AU - Bae, Kyongtae T.
AU - Fatica, Richard
AU - Steinman, Theodore I.
AU - Chapman, Arlene B.
AU - Gitomer, Berenice
AU - Perrone, Ronald D.
AU - Rahbari-Oskoui, Frederic F.
AU - Torres, Vicente E.
AU - Harris, Peter C.
N1 - Funding Information:
We thank the families and coordinators for involvement in the study and Andrew Metzger and Timothy Kline (Mayo Clinic). The study was supported by: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant DK058816 (to PCH); the Mayo Clinic Robert M. and Billie Kelley Pirnie Translational Polycystic Kidney Disease Center (DK090728; to VET); an American Society of Nephrology (ASN) Foundation Ben J Lipps Fellowship (to KH); an ASN Kidney Research Fellowship (to EC-LG); the Fulbright Association and the Foundation Monaham (EC-LG); the Zell Family Foundation, and Robert M. and Billie Kelley Pirnie. The HALT-PKD studies were supported by NIDDK cooperative agreements ( DK062410 , DK062408 , DK062402 , DK082230 , DK062411 , and DK062401 ) and National Center for Research Resources General Clinical Research Centers ( RR000039 , RR000585 , RR000054 , RR000051 , RR023940 , RR001032 ) and National Center for Advancing Translational Sciences Clinical and Translational Science Awards (RR025008, TR000454, RR024150, TR00135, RR025752, TR001064, RR025780, TR001082, RR025758, TR001102, RR033179, TR000001). The ADPKD Modifier Study is supported by NIDDK grant DK079856 . We thank the other HALT PKD and/or ADPKD Modifier Investigators as well: A. Yu, F.T. Winklhofer (Kansas University Medical Center, Kansas City, KS), K.Z. Abebe, C.G. Patterson (University of Pittsburgh, Pittsburgh, PA), R.W. Schrier, G.M. Brosnahan (University of Colorado Denver, Aurora, CO), D.C. Miskulin (Tufts University, Boston, MA), W.E. Braun (Cleveland Clinic, Cleveland, OH), P.G. Czarnecki (Brigham and Women’s Hospital, Boston, MA), F.T. Chebib, M.C. Hogan (Mayo Clinic, Rochester, MN), M. Mrug (University of Alabama at Birmingham, Birmingham, AL), Y. Pei, (University of Toronto, Toronto, Ontario, Canada), R. Sandford (University of Cambridge, Cambridge, UK), H. Rennert (The Rogosin Institute, New York, NY), Y. Le Meur (Université de Brest, Brest, France), T. Watnick (University of Maryland, Baltimore, MD), D.J.M. Peter (Leiden University Medical Center, Leiden, The Netherlands), R.T. Gansevoort (University Medical Center Groningen, Groningen, The Netherlands), N. Demoulin (Université Catholique de Louvain, Louvain, Belguim), and O. Devuyst (University Hospital of Zürich, Zurich, Switzerland).
Funding Information:
We thank the families and coordinators for involvement in the study and Andrew Metzger and Timothy Kline (Mayo Clinic). The study was supported by: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) grant DK058816 (to PCH); the Mayo Clinic Robert M. and Billie Kelley Pirnie Translational Polycystic Kidney Disease Center (DK090728; to VET); an American Society of Nephrology (ASN) Foundation Ben J Lipps Fellowship (to KH); an ASN Kidney Research Fellowship (to EC-LG); the Fulbright Association and the Foundation Monaham (EC-LG); the Zell Family Foundation, and Robert M. and Billie Kelley Pirnie. The HALT-PKD studies were supported by NIDDK cooperative agreements (DK062410, DK062408, DK062402, DK082230, DK062411, and DK062401) and National Center for Research Resources General Clinical Research Centers (RR000039, RR000585, RR000054, RR000051, RR023940, RR001032) and National Center for Advancing Translational Sciences Clinical and Translational Science Awards (RR025008, TR000454, RR024150, TR00135, RR025752, TR001064, RR025780, TR001082, RR025758, TR001102, RR033179, TR000001). The ADPKD Modifier Study is supported by NIDDK grant DK079856. We thank the other HALT PKD and/or ADPKD Modifier Investigators as well: A. Yu, F.T. Winklhofer (Kansas University Medical Center, Kansas City, KS), K.Z. Abebe, C.G. Patterson (University of Pittsburgh, Pittsburgh, PA), R.W. Schrier, G.M. Brosnahan (University of Colorado Denver, Aurora, CO), D.C. Miskulin (Tufts University, Boston, MA), W.E. Braun (Cleveland Clinic, Cleveland, OH), P.G. Czarnecki (Brigham and Women's Hospital, Boston, MA), F.T. Chebib, M.C. Hogan (Mayo Clinic, Rochester, MN), M. Mrug (University of Alabama at Birmingham, Birmingham, AL), Y. Pei, (University of Toronto, Toronto, Ontario, Canada), R. Sandford (University of Cambridge, Cambridge, UK), H. Rennert (The Rogosin Institute, New York, NY), Y. Le Meur (Universit? de Brest, Brest, France), T. Watnick (University of Maryland, Baltimore, MD), D.J.M. Peter (Leiden University Medical Center, Leiden, The Netherlands), R.T. Gansevoort (University Medical Center Groningen, Groningen, The Netherlands), N. Demoulin (Universit? Catholique de Louvain, Louvain, Belguim), and O. Devuyst (University Hospital of Z?rich, Zurich, Switzerland).
Publisher Copyright:
© 2019 International Society of Nephrology
PY - 2020/2
Y1 - 2020/2
N2 - Autosomal dominant polycystic kidney disease (ADPKD) is an inherited, progressive nephropathy accounting for 4-10% of end stage renal disease worldwide. PKD1 and PKD2 are the most common disease loci, but even accounting for other genetic causes, about 7% of families remain unresolved. Typically, these unsolved cases have relatively mild kidney disease and often have a negative family history. Mosaicism, due to de novo mutation in the early embryo, has rarely been identified by conventional genetic analysis of ADPKD families. Here we screened for mosaicism by employing two next generation sequencing screens, specific analysis of PKD1 and PKD2 employing long-range polymerase chain reaction, or targeted capture of cystogenes. We characterized mosaicism in 20 ADPKD families; the pathogenic variant was transmitted to the next generation in five families and sporadic in 15. The mosaic pathogenic variant was newly discovered by next generation sequencing in 13 families, and these methods precisely quantified the level of mosaicism in all. All of the mosaic cases had PKD1 mutations, 14 were deletions or insertions, and 16 occurred in females. Analysis of kidney size and function showed the mosaic cases had milder disease than a control PKD1 population, but only a few had clearly asymmetric disease. Thus, in a typical ADPKD population, readily detectable mosaicism by next generation sequencing accounts for about 1% of cases, and about 10% of genetically unresolved cases with an uncertain family history. Hence, identification of mosaicism is important to fully characterize ADPKD populations and provides informed prognostic information.
AB - Autosomal dominant polycystic kidney disease (ADPKD) is an inherited, progressive nephropathy accounting for 4-10% of end stage renal disease worldwide. PKD1 and PKD2 are the most common disease loci, but even accounting for other genetic causes, about 7% of families remain unresolved. Typically, these unsolved cases have relatively mild kidney disease and often have a negative family history. Mosaicism, due to de novo mutation in the early embryo, has rarely been identified by conventional genetic analysis of ADPKD families. Here we screened for mosaicism by employing two next generation sequencing screens, specific analysis of PKD1 and PKD2 employing long-range polymerase chain reaction, or targeted capture of cystogenes. We characterized mosaicism in 20 ADPKD families; the pathogenic variant was transmitted to the next generation in five families and sporadic in 15. The mosaic pathogenic variant was newly discovered by next generation sequencing in 13 families, and these methods precisely quantified the level of mosaicism in all. All of the mosaic cases had PKD1 mutations, 14 were deletions or insertions, and 16 occurred in females. Analysis of kidney size and function showed the mosaic cases had milder disease than a control PKD1 population, but only a few had clearly asymmetric disease. Thus, in a typical ADPKD population, readily detectable mosaicism by next generation sequencing accounts for about 1% of cases, and about 10% of genetically unresolved cases with an uncertain family history. Hence, identification of mosaicism is important to fully characterize ADPKD populations and provides informed prognostic information.
KW - ADPKD
KW - PKD1
KW - diagnostics
KW - genotype/phenotype correlations
KW - mosaicism
KW - mutations
KW - prognostics
UR - http://www.scopus.com/inward/record.url?scp=85076864885&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85076864885&partnerID=8YFLogxK
U2 - 10.1016/j.kint.2019.08.038
DO - 10.1016/j.kint.2019.08.038
M3 - Article
C2 - 31874800
AN - SCOPUS:85076864885
SN - 0085-2538
VL - 97
SP - 370
EP - 382
JO - Kidney international
JF - Kidney international
IS - 2
ER -