ReviewPediatric nephrology (Berlin, Germany)2013
From bone abnormalities to mineral metabolism dysregulation in autosomal dominant polycystic kidney disease.
Review in Pediatric nephrology (Berlin, Germany), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Heterogeneous regulation of fibroblast growth factor 23 in acute kidney injury, chronic kidney disease, and polycystic kidney disease: mechanisms, diagnostic utility, and clinical implications.Frontiers in molecular biosciences · 2026Review
- Article
- Cardiovascular Complications in ADPKD.Kidney international reports · 2025Review
- Autosomal Dominant Polycystic Kidney Disease: Extrarenal Involvement.International journal of molecular sciences · 2024Review
- Mutational burden of XPNPEP3 leads to defects in mitochondrial complex I and cilia in NPHPL1.iScience · 2023Article
- Interactions between FGF23 and Genotype in Autosomal Dominant Polycystic Kidney Disease.Kidney360 · 2020Article
- Expanding the role of vasopressin antagonism in polycystic kidney diseases: From adults to children?Pediatric nephrology (Berlin, Germany) · 2018Review
- Fibroblast Growth Factor 23 and Kidney Disease Progression in Autosomal Dominant Polycystic Kidney Disease.Clinical journal of the American Society of Nephrology : CJASN · 2017Observational
- Is Autosomal Dominant Polycystic Kidney Disease Becoming a Pediatric Disorder?Frontiers in pediatrics · 2017Review
- Hyperaldosteronism and cardiovascular risk in patients with autosomal dominant polycystic kidney disease.Medicine · 2016Article
- Article
- Osteoblast-specific deletion of Pkd2 leads to low-turnover osteopenia and reduced bone marrow adiposity.PloS one · 2014Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of kidney failure. It is a systemic disorder, not only affecting the kidneys, but also associated with cyst formation in other organs such as the liver, spleen, pancreas, and seminal vesicles. Other extra-renal symptoms may consist of intracranial arterial aneurysms, cardiac valvular defects, abdominal and inguinal hernias and colonic diverticulosis. Very little is known regarding bone involvement in ADPKD; however, recent evidence has revealed the potential role of fibroblast growth factor 23 (FGF23). FGF23 is an endocrine fibroblast growth factor acting in the kidney as a phosphaturic hormone and a suppressor of active vitamin D with key effects on the bone/kidney/parathyroid axis, and has been shown to increase in patients with ADPKD, even with normal renal function. The aim of this review is to provide an overview of bone and mineral abnormalities found in experimental models and in patients with ADPKD, and to discuss the possible role of FGF23 in this disease.
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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.