The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences
Abstract
Chronic renal failure (CRF) results in profound lipid disorders, which stem largely from dysregulation of high-density lipoprotein (HDL) and triglyceride-rich lipoprotein metabolism. Specifically, maturation of HDL is impaired and its composition is altered in CRF. In addition, clearance of triglyceride-rich lipoproteins and their atherogenic remnants is impaired, their composition is altered, and their plasma concentrations are elevated in CRF. Impaired maturation of HDL in CRF is primarily due to downregulation of lecithin-cholesterol acyltransferase (LCAT) and, to a lesser extent, increased plasma cholesteryl ester transfer protein (CETP). Triglyceride enrichment of HDL in CRF is primarily due to hepatic lipase deficiency and elevated CETP activity. The CRF-induced hypertriglyceridemia, abnormal composition, and impaired clearance of triglyceride-rich lipoproteins and their remnants are primarily due to downregulation of lipoprotein lipase, hepatic lipase, and the very-low-density lipoprotein receptor, as well as, upregulation of hepatic acyl-CoA cholesterol acyltransferase (ACAT). In addition, impaired HDL metabolism contributes to the disturbances of triglyceride-rich lipoprotein metabolism. These abnormalities are compounded by downregulation of apolipoproteins apoA-I, apoA-II, and apoC-II in CRF. Together, these abnormalities may contribute to the risk of arteriosclerotic cardiovascular disease and may adversely affect progression of renal disease and energy metabolism in CRF.
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Cites
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Cited by
Rosuvastatin and Cardiovascular Events in Patients Undergoing Hemodialysis
Fellström, B. C., Jardine, A. G., Schmieder, R. E., Holdaas, H., Bannister, K., Beutler, J., Chae, D.-W., Chevaile, A., Cobbe, S. M., Grönhagen-Riska, C., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810177 · Cited by 2,036
Dyslipidaemia in nephrotic syndrome: mechanisms and treatment
Agrawal, S., Zaritsky, J. J., Fornoni, A., & Smoyer, W. E. (2018) · Nature Reviews Nephrology · doi:10.1038/nrneph.2017.155 · Cited by 325
Serum Amyloid A in Uremic HDL Promotes Inflammation
Weichhart, T., Kopecky, C., Kubicek, M., Haidinger, M., Döller, D., Katholnig, K., Suarna, C., Eller, P., Tölle, M., Gerner, C., et al. (2012) · Journal of the American Society of Nephrology · doi:10.1681/asn.2011070668 · Cited by 201
Drury, P. L., Ting, R., Zannino, D., Ehnholm, C., Flack, J., Whiting, M., Fassett, R., Ansquer, J.-C., Dixon, P., Davis, T. M. E., et al. (2011) · Diabetologia · doi:10.1007/s00125-010-1854-1 · Cited by 195
Effects of Fibrates in Kidney Disease
Jun, M., Zhu, B., Tonelli, M., Jardine, M. J., Patel, A., Neal, B., Liyanage, T., Keech, A., Cass, A., & Perkovic, V. (2012) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2012.07.049 · Cited by 189
Metadata
- Authors
- Vaziri, N. D.
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2006-02
- Volume
- 290
- Issue
- 2
- Pages
- F262-F272
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2101967622
- Cited by
- 538
- References
- 81
- FWCI
- 14.65
- Type
- journal article
- Language
- en
- Open access
- closed
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