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Lipoprotein(a) Levels in the Nephrotic Syndrome
- Christoph Wanner, MD; and
- Werner Bartens, MD
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IN RESPONSE:
Hyperlipoproteinemia of the nephrotic syndrome is multifactorial. It is generally agreed that hepatic synthesis of lipoproteins is increased (overproduction), whereas removal of lipoproteins, chylomicrons, very-low-density lipoprotein, and intermediate density lipoprotein is reduced (delayed catabolism). The precise mechanisms of increased lipogenesis and decreased lipid catabolism and their relations to urinary protein loss, hypoalbuminemia, and reduced serum oncotic pressure remain controversial. Overproduction and delayed catabolism affect almost all classes of lipoproteins, altering their concentration, composition, and metabolic rate [1].
Drs. Craig and Ritchie suggest another potential factor, the physical properties of Lp(a), which may contribute to the elevated Lp(a) levels in the plasma of patients with the nephrotic syndrome. We agree that, despite altered glomerular permselectivity, the size of this large macromolecule should not allow substantial filtration through the glomerular basement membrane. However, Oida and colleagues [2] observed that Lp(a) or its fragments are secreted in the urine of patients with renal disease and that urinary excretion decreased as the glomerular filtration rate decreased. Passage of macromolecules through the fenestrated glomerular endothelium and access to the glomerular mesangium are possible. In patients with pre-existing renal disease, trapping of Lp(a) molecules in the mesangium, interaction of apo(a) with extracellular matrix proteins, and subsequent “clearance” of Lp(a) are likely [3].
Serum albumin concentration is a function of albumin synthesis and catabolism rates and of urinary albumin loss in patients with the nephrotic syndrome. It may therefore be difficult to infer a causal relation between serum albumin concentration and blood Lp(a) concentration by showing a correlation between the two, although reduction in proteinuria alone may reduce blood lipid and lipoprotein concentration in patients with the nephrotic syndrome [4].
Despite the probability that deranged lipid catabolism results in part from the urinary loss of a substance (or of a group of substances), hyperlipidemia is not likely to result from the urinary loss of any of the putative liporegulatory substances isolated from the urine of patients or animals with the nephrotic syndrome.
Christoph Wanner, MD
Werner Bartens, MD
University Hospital of Freiburg; Freiburg 79106; Germany
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
