The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Polycystic kidney disease
Open accessAbstract
Cystic kidneys are common causes of end-stage renal disease, both in children and in adults. Autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD) are cilia-related disorders and the two main forms of monogenic cystic kidney diseases. ADPKD is a common disease that mostly presents in adults, whereas ARPKD is a rarer and often more severe form of polycystic kidney disease (PKD) that usually presents perinatally or in early childhood. Cell biological and clinical research approaches have expanded our knowledge of the pathogenesis of ADPKD and ARPKD and revealed some mechanistic overlap between them. A reduced ‘dosage’ of PKD proteins is thought to disturb cell homeostasis and converging signalling pathways, such as Ca2+, cAMP, mechanistic target of rapamycin, WNT, vascular endothelial growth factor and Hippo signalling, and could explain the more severe clinical course in some patients with PKD. Genetic diagnosis might benefit families and improve the clinical management of patients, which might be enhanced even further with emerging therapeutic options. However, many important questions about the pathogenesis of PKD remain. In this Primer, we provide an overview of the current knowledge of PKD and its treatment.Autosomal dominant polycystic kidney disease (PKD) and autosomal recessive PKD are progressive cilia-related disorders that often lead to chronic kidney disease and end-stage renal disease. This Primer provides an overview of the current knowledge of PKD pathogenesis and its treatment.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells
Nauli, S. M., Alenghat, F. J., Luo, Y., Williams, E., Vassilev, P., Li, X., Elia, A. E. H., Lu, W., Brown, E. M., Quinn, S. J., et al. (2003) · Nature Genetics · doi:10.1038/ng1076 · Cited by 2,057
Autosomal dominant polycystic kidney disease
Torres, V. E., Harris, P. C., & Pirson, Y. (2007) · The Lancet · doi:10.1016/s0140-6736(07)60601-1 · Cited by 1,550
Self-citationHildebrandt, F., Benzing, T., & Katsanis, N. (2011) · New England Journal of Medicine · doi:10.1056/nejmra1010172 · Cited by 1,331
In vivo gene editing in dystrophic mouse muscle and muscle stem cells
Tabebordbar, M., Zhu, K., Cheng, J. K. W., Chew, W. L., Widrick, J. J., Yan, W. X., Maesner, C., Wu, E. Y., Xiao, R., Ran, F. A., et al. (2016) · Science · doi:10.1126/science.aad5177 · Cited by 1,046
Tolvaptan in Later-Stage Autosomal Dominant Polycystic Kidney Disease
Torres, V. E., Chapman, A. B., Devuyst, O., Gansevoort, R. T., Perrone, R. D., Koch, G., Ouyang, J., McQuade, R. D., Blais, J. D., Czerwiec, F. S., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1710030 · Cited by 639
Self-citationDefective glucose metabolism in polycystic kidney disease identifies a new therapeutic strategy
Rowe, I., Chiaravalli, M., Mannella, V., Ulisse, V., Quilici, G., Pema, M., Song, X. W., Xu, H., Mari, S., Qian, F., et al. (2013) · Nature Medicine · doi:10.1038/nm.3092 · Cited by 503
Porath, B., Gainullin, V. G., Cornec-Le Gall, E., Dillinger, E. K., Heyer, C. M., Hopp, K., Edwards, M. E., Madsen, C. D., Mauritz, S. R., Banks, C. J., et al. (2016) · The American Journal of Human Genetics · doi:10.1016/j.ajhg.2016.05.004 · Cited by 475
Self-citationLantinga-van Leeuwen, I. S., Leonhard, W. N., van der Wal, A., Breuning, M. H., de Heer, E., & Peters, D. J. M. (2007) · Human Molecular Genetics · doi:10.1093/hmg/ddm299 · Cited by 223
Self-citationMutations in PRKCSH cause isolated autosomal dominant polycystic liver disease
Li, A., Davila, S., Furu, L., Qian, Q., Tian, X., Kamath, P. S., King, B. F., Torres, V. E., & Somlo, S. (2003) · The American Journal of Human Genetics · doi:10.1086/368295 · Cited by 193
Self-citationAudrézet, M.-P., Cornec-Le Gall, E., Chen, J.-M., Redon, S., Quéré, I., Creff, J., Bénech, C., Maestri, S., Le Meur, Y., & Férec, C. (2012) · Human Mutation · doi:10.1002/humu.22103 · Cited by 183
Cited by
Chronic Kidney Disease Diagnosis and Management: A Review
Chen, T. K., Knicely, D. H., & Grams, M. E. (2019) · JAMA · doi:10.1001/jama.2019.14745 · Cited by 1,811
Targeting integrin pathways: mechanisms and advances in therapy
Pang, X., He, X., Qiu, Z., Zhang, H., Xie, R., Liu, Z., Gu, Y., Zhao, N., Xiang, Q., & Cui, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01259-6 · Cited by 1,275
Zhang, M., Ma, Y., Ye, X., Zhang, N., Pan, L., & Wang, B. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01464-x · Cited by 522
Bayır, H., Dixon, S. J., Tyurina, Y. Y., Kellum, J. A., & Kagan, V. E. (2023) · Nature Reviews Nephrology · doi:10.1038/s41581-023-00689-x · Cited by 331
Ciliopathies and the Kidney: A Review
McConnachie, D. J., Stow, J. L., & Mallett, A. J. (2021) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2020.08.012 · Cited by 257
Metadata
- Authors
- Bergmann, C., Guay-Woodford, L. M., Harris, P. C., Horie, S., Peters, D. J. M., & Torres, V. E.
- Venue
- Nature Reviews Disease Primers
- Published
- 2018-12-06
- Volume
- 4
- Issue
- 1
- Pages
- 50-50
- ISSN
- 2056-676X (ISSN-L)
- OpenAlex
- W3148049993
- Cited by
- 807
- References
- 13
- FWCI
- 6.67
- Type
- journal article
- Language
- en
- Open access
- green
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Polycystic kidney disease. https://app.cochat.ai/papers/10.1038/s41572-018-0047-y
- The paper
- Bergmann, C., Guay-Woodford, L. M., Harris, P. C., Horie, S., Peters, D. J. M., & Torres, V. E. (2018). Polycystic kidney disease. Nature Reviews Disease Primers. https://doi.org/10.1038/s41572-018-0047-y
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.