Familial hyperkalemic hypertension: hyperkalemia not hypertension defines dominant KLHL3 disease and may permit earlier recognition and tailored therapy
Author:
Publisher
Springer Science and Business Media LLC
Subject
Nephrology
Link
https://link.springer.com/content/pdf/10.1007/s40620-021-01217-5.pdf
Reference9 articles.
1. Boyden LM et al (2012) Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities. Nature 482(7383):98–102. https://doi.org/10.1038/nature10814
2. H. Louis-Dit-Picard et al., "KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron," Nat Genet, vol. 44, no. 4, pp. 456–60, S1–3, Mar 11 2012. https://doi.org/10.1038/ng.2218
3. D. H. Ellison, "Pseudohypoaldosteronism Type II," in GeneReviews((R)), M. P. Adam et al. Eds. Seattle (WA), 1993
4. F. H. Wilson et al., "Human hypertension caused by mutations in WNK kinases," Science, vol. 293, no. 5532, pp. 1107–12., 2001. [Online]. Available: http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?db=m&form=6&dopt=r&uid=11498583, http://www.sciencemag.org/cgi/content/full/293/5532/1107, http://www.sciencemag.org/cgi/content/abstract/293/5532/1107.
5. Hadchouel J, Ellison DH, Gamba G (2016) Regulation of renal electrolyte transport by WNK and SPAK-OSR1 Kinases. Annu Rev Physiol 78:367–389. https://doi.org/10.1146/annurev-physiol-021115-105431
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