ReviewWiley interdisciplinary reviews. Developmental biology
Kidney: polycystic kidney disease.
Review in Wiley interdisciplinary reviews. Developmental biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06601829 (Congenital Hepatic Fibrosis and Autosomal Recessive Polycystic Kidney Disease in Children at Sohag University Hospital), which is not on this map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Congenital Hepatic Fibrosis and Autosomal Recessive Polycystic Kidney Disease in Children at Sohag University Hospital
Who cites it
47 citing papers in PubMed, 85 citations in OpenAlex.
- A new conceptual framework for PKD1 in ADPKD; integrating DNA structures and inflammation.BMC nephrology · 2026Review
- Glycolytic alterations as biomarkers in polycystic kidney disease: A study using a PKD1 knockout model in NRK-52E rat kidney epithelial cells.Physiological reports · 2026Article
- Evaluating gene variations in autosomal dominant polycystic kidney disease patients using whole exome sequencing and phenotype to genotype analysis.Renal failure · 2025Article
- Review
- Metabolomic profiling of renal cyst fluid in advanced ADPKD: insights from dialysis and transplantation cohorts.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- A Snake Toxin Derivative for Treatment of Hyponatremia and Polycystic Kidney Diseases.Journal of the American Society of Nephrology : JASN · 2025Article
- CRISPR-Cas9 system in autosomal dominant polycystic kidney disease: a comprehensive review.Childhood kidney diseases · 2025Review
- G-quadruplex stabilization provokes DNA breaks in human PKD1, revealing a second hit mechanism for ADPKD.Nature communications · 2025Article
- Low-dose tolvaptan to control disease progression in Chinese patients with autosomal dominant polycystic kidney disease: a retrospective cohort study.Translational andrology and urology · 2024Article
- Dynamic Kidney Organoid Microphysiological Analysis Platform.bioRxiv : the preprint server for biology · 2024Article
- EZH2 inhibition or genetic ablation suppresses cyst growth in autosomal dominant polycystic kidney disease.Journal of translational medicine · 2024Article
- Computational exploration of protein structure dynamics and RNA structural consequences of3 Biotech · 2024Article
- Prevalence and outcomes of polycystic kidney disease in African populations: A systematic review.World journal of nephrology · 2024Article
- TheBiomedicines · 2024Review
- [C/EBPβ mediates expressions of downstream inflammatory factors of the tumor necrosis factor-Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- HumanmicroPublication biology · 2024Article
- Case report: Rare genetic liver disease - a case of congenital hepatic fibrosis in adults with autosomal dominant polycystic kidney disease.Frontiers in medicine · 2024Article
- Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023Article
- A kidney resident macrophage subset is a candidate biomarker for renal cystic disease in preclinical models.Disease models & mechanisms · 2023Article
- A common intronic single nucleotide variant modifies PKD1 expression level.Clinical genetics · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Polycystic kidney disease (PKD) is a life-threatening genetic disorder characterized by the presence of fluid-filled cysts primarily in the kidneys. PKD can be inherited as autosomal recessive (ARPKD) or autosomal dominant (ADPKD) traits. Mutations in either the PKD1 or PKD2 genes, which encode polycystin 1 and polycystin 2, are the underlying cause of ADPKD. Progressive cyst formation and renal enlargement lead to renal insufficiency in these patients, which need to be managed by lifelong dialysis or renal transplantation. While characteristic features of PKD are abnormalities in epithelial cell proliferation, fluid secretion, extracellular matrix and differentiation, the molecular mechanisms underlying these events are not understood. Here we review the progress that has been made in defining the function of the polycystins, and how disruption of these functions may be involved in cystogenesis.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.