ArticleKidney international reports2024
Familial Variability of Disease Severity in Adult Patients With ADPKD.
Article in Kidney international reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Autosomal dominant polycystic kidney disease: an overview of recent genetic and clinical advances.Renal failure · 2025Review
- Evaluating gene variations in autosomal dominant polycystic kidney disease patients using whole exome sequencing and phenotype to genotype analysis.Renal failure · 2025Article
- Genetic and protein structure prediction analyses identify a rare pathogenic PKD1 variant causing autosomal dominant polycystic kidney disease.CEN case reports · 2025Article
- Phenotypic outcomes of PKD1 compared with non-PKD1 genetically confirmed autosomal dominant polycystic kidney disease.Journal of nephrology · 2025Observational
- Understanding Familial Variability in ADPKD: A Comprehensive Approach Integrating Genetics, Hormones, and Lifestyle for Tailored Management.Kidney international reports · 2025Article
- Response to "Understanding Familial Variability in ADPKD: a Comprehensive Approach Integrating Genetics, Hormones, and Lifestyle for Tailored Management".Kidney international reports · 2025Article
- Biomarkers of Kidney Disease Progression in ADPKD.Kidney international reports · 2024Review
- Single-Base Substitution Causing Dual-Exon Skipping Event inJournal of clinical medicine · 2024Article
- Progression to kidney failure in ADPKD: the PROPKD score underestimates the risk assessed by the Mayo imaging classification.Frontiers in medicine · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic nephropathy and has striking familial variability of disease severity. Methods: To better comprehend familial phenotypic variability, we analyzed clinical and pedigree data on 92 unrelated ADPKD kindreds with ≥2 affected individuals ( Results: Marked intrafamilial variability was observed in at least 13% of the 92 families, with a higher proportion of families carrying Conclusion: Using objective measures, we quantified marked intrafamilial variability in ADPKD disease phenotype in at least 13% of families. Our findings indicate that intrafamilial phenotypic variability remains incompletely understood and necessitates a more thorough identification of relevant clinical and genotypic factors.
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Registered trials
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