Dyslipidemia and nephrotic syndrome: recent advances.
Abstract
Patients with nephrotic syndrome (NS) have one of the most pronounced secondary changes in lipoprotein metabolism known, and the magnitude of the changes correlates with the severity of the disease. These changes are of a quantitative as well as a qualitative nature. All apolipoprotein B (apo B)-containing lipoproteins, such as very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and lipoprotein(a) [Lp(a)], are elevated in nephrotic syndrome. High-density lipoproteins (HDL) are reported to be unchanged or reduced. In addition to these quantitative changes, the lipoprotein composition is markedly changed, with a higher ratio of cholesterol to triglycerides in the apo B-containing lipoproteins and an increase in the proportion of cholesterol, cholesterol ester, and phospholipids compared with proteins. Also apolipoproteins show major changes, with an increase in apolipoprotein A-I, A-IV, B, C, and E. Particularly the changes in apo C-II, which is an activator of the enzyme lipoprotein lipase (LPL), and apo C-III, an inhibitor of LPL, with an increase of the C-III to C-II ratio, might contribute to the impaired lipoprotein catabolism in NS. The mechanisms for these changes in lipoprotein metabolism are discussed in this review as far as they are known. Furthermore, the tremendous elevations of Lp(a) in nephrotic syndrome and its primary and secondary causes are reviewed. Primary causes became recently apparent by a significantly higher frequency of low-molecular-weight apo(a) phenotypes in patients compared with controls. The secondary causes were shown by an increase of Lp(a) in all apo(a) isoform groups. Because Lp(a) is an LDL-like particle that is usually included in the measured or calculated LDL cholesterol fraction, the influence of the extremely high Lp(a) levels in NS on the measurement of LDL cholesterol is discussed.
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Nephrotic syndrome causes increased production of apoB-containing lipoproteins, including VLDL, by the liver.
“Nephrotic syndrome causes increased production of apoB-containing lipoproteins, including VLDL, by the liver (103).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [103]
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- Authors
- Kronenberg, F.
- Affiliations
- Innsbruck Medical University (AT)
- Corresponding author
- Kronenberg, Florian
- ORCID
- Kronenberg, Florian
- Venue
- Journal of Renal Nutrition
- Publisher
- Elsevier BV
- Published
- 2005-04
- Volume
- 15
- Issue
- 2
- Pages
- 195-203
- ISSN
- 1051-2276 (ISSN-L)
- OpenAlex
- W2031919772
- Cited by
- 85
- References
- 60
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 5 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 2 · 2015: 10 · 2014: 11 · 2013: 8 · 2012: 5
- FWCI
- 0.51
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Renal Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- nephrotic syndrome, dyslipidemia, lipoprotein metabolism, apolipoprotein B, apolipoprotein C-II, apolipoprotein C-III, lipoprotein lipase, lipoprotein(a), LDL cholesterol measurement, apolipoprotein A-I, apolipoprotein A-IV, apolipoprotein E, apolipoprotein C, hypercholesterolemia
- MeSH terms
- Animals, Apolipoproteins A, Apolipoproteins E, Humans, Hyperlipidemias, Cholesterol, HDL, Cholesterol, LDL, Nephrotic Syndrome, Polymorphism, Genetic, Triglycerides, Lipoprotein(a)
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