ReviewCurrent hypertension reviews2013
The genetics of vascular complications in autosomal dominant polycystic kidney disease (ADPKD).
Review in Current hypertension reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 39 citations in OpenAlex.
- Modeling Complex Developmental Disease: The Case of Polycystic Kidney Disease.Journal of developmental biology · 2026Review
- Article
- Autosomal Dominant Polycystic Kidney Disease: Extrarenal Involvement.International journal of molecular sciences · 2024Review
- MR Brain Screening in ADPKD Patients : To Screen or not to Screen?Clinical neuroradiology · 2022Article
- Association of autosomal dominant polycystic kidney disease, asymptomatic multiple giant coronary arteries aneurysms and abdominal aortic aneurysm: a case report.Oxford medical case reports · 2020Article
- Disease Modeling To Understand the Pathomechanisms of Human Genetic Kidney Disorders.Clinical journal of the American Society of Nephrology : CJASN · 2020Review
- TRPP2 dysfunction decreases ATP-evoked calcium, induces cell aggregation and stimulates proliferation in T lymphocytes.BMC nephrology · 2019Article
- Autosomal dominant polycystic kidney disease: Disrupted pathways and potential therapeutic interventions.Journal of cellular physiology · 2019Review
- Subarachnoid Hemorrhage in Hospitalized Renal Transplant Recipients with Autosomal Dominant Polycystic Kidney Disease: A Nationwide Analysis.Journal of clinical medicine · 2019Article
- Deletion of Pkd1 in renal stromal cells causes defects in the renal stromal compartment and progressive cystogenesis in the kidney.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Identification of MMP1 as a novel risk factor for intracranial aneurysms in ADPKD using iPSC models.Scientific reports · 2016Article
- Vascular complications in autosomal dominant polycystic kidney disease.Nature reviews. Nephrology · 2015Review
- Novel therapeutic approaches to autosomal dominant polycystic kidney disease.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Mesenchymal Stromal Cells Improve Renovascular Function in Polycystic Kidney Disease.Cell transplantation · 2015Article
- A young patient with a family history of hypertension.Clinical journal of the American Society of Nephrology : CJASN · 2014Article
- Pkd1 regulates lymphatic vascular morphogenesis during development.Cell reports · 2014Article
- Risk of intracranial hemorrhage associated with autosomal dominant polycystic kidney disease in patients with end stage renal disease.BMC nephrology · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The most important extra-renal manifestation of autosomal dominant polycystic kidney disease (ADPKD) in terms of debilitating injury and premature death is the development of intracranial aneurysms (IAs) and other vascular complications, resulting in subarachnoid hemorrhage (SAH). IAs are found at a rate approximately five times higher in ADPKD patients than in the general population and in patients with a family history of SAH/IAs the frequency is elevated further three to five times, indicating the importance of genetic factors in its etiology. Expression of the ADPKD gene products, polycystin-1 (PKD1) and polycystin-2 (PKD2), in vascular smooth muscle and the endothelium, and evidence that reduced levels of these proteins leads to IA development in mouse models, suggests a direct role of these proteins in the vascular disease. PKD1 and PKD2 patients seem equally likely to develop IAs, while patients with mutations to the 5' half of PKD1 may more likely have vascular complications. Genome wide association and candidate studies of multiplex families with IAs without ADPKD have identified a number of genes/proteins that may be risk factors for the development of IAs. These candidate proteins largely have roles in the maintenance and remodeling of the arterial wall of small brain arteries. The development of the genetic methodologies of massively parallel sequencing mean it is now possible to test these and other candidates in ADPKD families with multiplex and singleton IA cases. Identifying strong modifiers of this phenotype will be important for prioritizing patients for presymptomatic screening and interventions.
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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.