Predominant Liver Cystic Disease in a New Heterozygotic PKHD1 Variant: A Case Report.
Journal
The American journal of case reports
ISSN: 1941-5923
Titre abrégé: Am J Case Rep
Pays: United States
ID NLM: 101489566
Informations de publication
Date de publication:
24 Jan 2023
24 Jan 2023
Historique:
entrez:
24
1
2023
pubmed:
25
1
2023
medline:
26
1
2023
Statut:
epublish
Résumé
BACKGROUND The polycystic kidney and hepatic disease 1 (PKHD1) gene codes for fibrocystin-polyductin, a protein that takes part in cell-signaling for cell differentiation, especially in kidney tubules and bile ducts. A homozygous or compound heterozygous defect in this gene can cause autosomal recessive polycystic kidney disease (ARPKD). Polycystic liver disease (PCLD) can also be caused by single heterozygous variants in the PKHD1 gene. ARPKD presents with renal insufficiency and cystic dilatation of bile ducts, although disease is not expected with a single heterozygous mutation. PCLD presents with multiple cysts in the liver and dilated bile ducts as well, but with less of an impact on the kidneys than with ARPKD. Our purpose in publishing this report is to introduce an as-yet unknown variant to the body of genetic defects associated with ARPKD and PCLD, as well as to argue for the likely pathogenicity of the variant according to the prevailing criteria used for classifying gene variants. CASE REPORT We present a patient with a de novo PKHD1 variant currently classified as a variant of unknown significance manifesting with bilaterally enlarged cystic kidneys and echogenic cystic structures in the hepatic portal system, indicative of cystic disease. CONCLUSIONS Given this patient's liver and kidney presentation that does not fully align with either ARPKD or PCLD, the authors believe that the single heterozygous variant in this patient's PKHD1 gene is worthy of reporting. This new single heterozygous variant in PKHD1 gene causing cystic kidney and cystic hepatic disease in the patient should be considered 'likely pathogenic' according to the criteria set by the American College of Medical Genetics.
Identifiants
pubmed: 36691356
pii: 938507
doi: 10.12659/AJCR.938507
pmc: PMC9883601
doi:
Substances chimiques
Transcription Factors
0
PKHD1 protein, human
0
Receptors, Cell Surface
0
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e938507Références
Nat Biomed Eng. 2022 Apr;6(4):463-475
pubmed: 35478224
Hum Mol Genet. 2007 Aug 15;16(16):1940-50
pubmed: 17575307
Hum Mutat. 2011 May;32(5):557-63
pubmed: 21520333
J Mol Med (Berl). 1998 Apr;76(5):303-9
pubmed: 9587064
Proc Natl Acad Sci U S A. 2009 Nov 10;106(45):18954-9
pubmed: 19855008
J Clin Invest. 2017 May 1;127(5):1772-1785
pubmed: 28375157
Curr Opin Pediatr. 2015 Apr;27(2):186-92
pubmed: 25689455
Am J Hum Genet. 2002 May;70(5):1305-17
pubmed: 11898128
Genet Med. 2015 May;17(5):405-24
pubmed: 25741868
PLoS One. 2014 Apr 07;9(4):e92661
pubmed: 24710345
Nat Genet. 2011 Jun 19;43(7):639-47
pubmed: 21685914
Mol Genet Metab. 2010 Feb;99(2):160-73
pubmed: 19914852
Bioinformatics. 2019 Jun 1;35(11):1978-1980
pubmed: 30376034
J Hum Genet. 2016 Sep;61(9):811-21
pubmed: 27225849
Nucleic Acids Res. 2018 Jan 4;46(D1):D1062-D1067
pubmed: 29165669