The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation
Open accessAbstract
Urate is a cause of gout, kidney stones, and acute kidney injury from tumor lysis syndrome, but its relationship to kidney disease, cardiovascular disease, and diabetes remains controversial. A scientific workshop organized by the National Kidney Foundation was held in September 2016 to review current evidence. Cell culture studies and animal models suggest that elevated serum urate concentrations can contribute to kidney disease, hypertension, and metabolic syndrome. Epidemiologic evidence also supports elevated serum urate concentrations as a risk factor for the development of kidney disease, hypertension, and diabetes, but differences in methodologies and inpacts on serum urate concentrations by even subtle changes in kidney function render conclusions uncertain. Mendelian randomization studies generally do not support a causal role of serum urate in kidney disease, hypertension, or diabetes, although interpretation is complicated by nonhomogeneous populations, a failure to consider environmental interactions, and a lack of understanding of how the genetic polymorphisms affect biological mechanisms related to urate. Although several small clinical trials suggest benefits of urate-lowering therapies on kidney function, blood pressure, and insulin resistance, others have been negative, with many trials having design limitations and insufficient power. Thus, whether uric acid has a causal role in kidney and cardiovascular diseases requires further study.
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Cites
Yu, M.-A., Sánchez-Lozada, L. G., Johnson, R. J., & Kang, D.-H. (2010) · Journal of Hypertension · doi:10.1097/hjh.0b013e328337da1d · Cited by 626
Self-citationMatsuo, H., Takada, T., Ichida, K., Nakamura, T., Nakayama, A., Ikebuchi, Y., Ito, K., Kusanagi, Y., Chiba, T., Tadokoro, S., et al. (2009) · Science Translational Medicine · doi:10.1126/scitranslmed.3000237 · Cited by 437
Palmer, T. M., Nordestgaard, B. G., Benn, M., Tybjaerg-Hansen, A., Davey Smith, G., Lawlor, D. A., & Timpson, N. J. (2013) · BMJ · doi:10.1136/bmj.f4262 · Cited by 282
Multiple organic anion transporters contribute to net renal excretion of uric acid
Eraly, S. A., Vallon, V., Rieg, T., Gangoiti, J. A., Wikoff, W. R., Siuzdak, G., Barshop, B. A., & Nigam, S. K. (2008) · Physiological Genomics · doi:10.1152/physiolgenomics.00207.2007 · Cited by 235
Cited by
SGLT2 inhibition and renal urate excretion: role of luminal glucose, GLUT9, and URAT1
Novikov, A., Fu, Y., Huang, W., Freeman, B., Patel, R., van Ginkel, C., Koepsell, H., Busslinger, M., Onishi, A., Nespoux, J., et al. (2019) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00462.2018 · Cited by 186
Metadata
- Authors
- Johnson, R. J., Bakris, G. L., Borghi, C., Chonchol, M. B., Feldman, D., Lanaspa, M. A., Merriman, T. R., Moe, O. W., Mount, D. B., Sanchez Lozada, L. G., Stahl, E., Weiner, D. E., & Chertow, G. M.
- Venue
- American Journal of Kidney Diseases
- Publisher
- Elsevier BV
- Published
- 2018-06
- Volume
- 71
- Issue
- 6
- Pages
- 851-865
- ISSN
- 0272-6386 (ISSN-L)
- OpenAlex
- W2789006309
- Cited by
- 644
- References
- 4
- FWCI
- 32.43
- Type
- journal article
- Language
- en
- Open access
- green
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- Johnson, R. J., Bakris, G. L., Borghi, C., Chonchol, M. B., Feldman, D., Lanaspa, M. A., Merriman, T. R., Moe, O. W., Mount, D. B., Sanchez Lozada, L. G., Stahl, E., Weiner, D. E., & Chertow, G. M. (2018). Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation. American Journal of Kidney Diseases. https://doi.org/10.1053/j.ajkd.2017.12.009
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