LETTER
Lipoprotein(a) Levels in the Nephrotic Syndrome
Wendy Y. Craig, PhD, and
Robert F. Richie, MD
15 January 1994 | Volume 120 Issue 2 | Pages 165-166
TO THE EDITOR:
We read with interest the article by Wanner and colleagues [1] reporting that plasma lipoprotein(a) (Lp[a]) levels are elevated in patients with the nephrotic syndrome. The authors speculated that decreased oncotic pressure might stimulate hepatic protein secretion, and as apolipoprotein(a) (apo[a]) is synthesized by the liver, this might result in elevated plasma levels. Also, if the kidney has a role in Lp(a) catabolism, deterioration of function might lead to increased plasma Lp(a) levels. We suggest further possibilities related to the physical characteristics of Lp(a) itself.
Lipoprotein(a) is a large particle, similar in composition to low-density lipoprotein, except that the unique protein component, apo(a), is attached by covalent linkage to apolipoprotein B (apo B). Apolipoprotein(a) isoforms range in molecular weight from 238 to 643 kDa [2]; the molecular weight of apo B is 512 to 550 kDa. Further, apo(a) is heavily sialated [3], a factor that leads to significant negative charge.
The nephrotic syndrome is associated with heavy proteinuria, which can result from defects in glomerular charge-selective or size-selective barriers or both [4]. In general, an inverse relation exists between protein molecular size and clearance rate, which might lead to selective increases (or decreases) in serum levels of a particular protein. For example, whereas serum levels of albumin (66.5 kDa) are invariably decreased in patients with the nephrotic syndrome, levels of 
2 macroglobulin (725 kDa), pentameric IgM (971 kDa), and ferritin (450 kDa) are increased [4, 5]. The Lp(a) molecule is also large, and plasma Lp(a) levels might therefore be increased because of a size selectivity effect.
|
Author and Article Information
|
|---|
Foundation for Blood Research; Scarborough, ME
1. Wanner C, Rader D, Bartens W, Kramer J, Brewer HB, Schollmeyer P, et al. Elevated plasma lipoprotein(a) in patients with the nephrotic syndrome. Ann Intern Med. 1993; 119:263-9.
2. Craig WY, Poulin SE, Ledue TB, Kamboh MI. Apolipoprotein(a): a comparison of isoforms identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis or by sodium dodecyl sulfate-agarose gel electrophoresis. Electrophoresis. 1993; 14:1038-41.
3. Ehnholm C, Garoff H, Renkonen O, Simons K. Protein and carbohydrate composition of Lp(a) lipoprotein from human plasma. Biochemistry. 1972; 11:3229-32.
4. Glassock RJ, Adler SG, Ward HJ, Cohen AH. Primary glomerular diseases. In: Brenner BM and Rector FC Jr, eds. The Kidney. Third edition. Philadelphia: W.B. Saunders; 1986:955-9.
5. Tietz NW, ed. Clinical Guide to Laboratory Tests. Philadelphia: W.B. Saunders; 1990:71, 381.
About Letters
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.
Top
Author & Article Info
References
Article
