NDT Advance Access originally published online on November 19, 2007
Nephrology Dialysis Transplantation 2008 23(4):1462; doi:10.1093/ndt/gfm820
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
An understanding of trace metal physiology as an aid to interpretation of clearance studies by artificial organs
E-mail: HNDT512{at}bellsouth.netSir,
I would like to congratulate Dr Churchwell et al. for their efforts to improve our understanding of trace metal clearance by the Optiflux F-160 and CA-HP 170 artificial kidneys [1]. Their work adds significant data to this subject; however, allow me to add a cautionary note that an understanding of the physiology of these elements is essential to a true analysis of the meaning of their findings. Due to space limitations, I will confine my remarks to selenium which has been an area of interest of our group over the last 30 years [2–3], especially in renal failure [4–9]. While the transport mechanisms for selenium are similar to sulfur, once in the blood, selenium is thought to be usually initially bound electrostatically to albumin, before it becomes incorporated into globular protein [2,7]. Normally, the major excretion routes are either through the kidneys as trimethylselonium or through the lungs as dimethylselenide. In haemodialysis patients, we have found that the 
-2 globulin fraction is a major carrier and is often drawn into the clot [4], thus yielding lower serum values than plasma or whole blood, which investigators often mistakenly use interchangeably. Except for what I assume to be a typographical error where Dr Churchwell notes, ‘Plasma serum levels of trace elements likely differ...’ on page 2975, I find that she has admirably dealt with the discussion of her plasma samples. Unfortunately, she has not accounted for the different levels of binding proteins. Typically, patients in the intensive care unit are catabolic. If she re-examines her data, she would likely find that many of her study patients have low serum albumin and protein values, which would consequently result in a higher fraction of unbound selenium available for clearance through the kidneys at the time of her study. Since she notes that at least one of her patients was receiving MTE-5, that supplementation with less binding protein available would be at great risk for falsely elevating her loss into the dialysate. Selenium loss into the dialysate has not been observed with low-flux kidneys [9], and since protein loss is unmeasurable in unprocessed high-flux kidneys [10], one might hypothesize that the clearance found by Dr Churchwell is falsely elevated as a result of the supplementation of free unbound elements in the absence of a protein carrier.
Conflict of interest statement. None declared.
Hypertension, Nephrology, Dialysis and Transplantation, Auburn University, Bldg 21, 121 N. 20th Street, Opelika, AL 36801, USA
References
- Churchwell MD, Pasko DA, Btaiche IF, et al. Trace element removal during in vitro and in vivo continuous haemodialysis. Nephrol Dial Transplant (2007) 22:2970–2977.
[Abstract/Free Full Text] - Diskin CJ, Tomasso CL, Alper JC, et al. Long-term selenium exposure. Arch Intern Med (1979) 139:824–826.
[Abstract/Free Full Text] - Diskin CJ. Caution with selenium replacement. Lancet (1979) 2:1249.[Web of Science][Medline]
- Diskin CJ. Plasma selenium levels in renal failure. Nephron (1986) 44:155–156.[Web of Science][Medline]
- Berlyne GM, Diskin C, Gonick H, et al. Trace elements in dialysis patients. ASAIO Trans (1986) 32:662–670.[Medline]
- Milly K, Wit L, Diskin C, et al. Selenium in renal failure patients. Nephron (1992) 61:139–144.[Web of Science][Medline]
- Diskin CJ. Does trace metal metabolism contribute to dialysis patient morbidity? Semin Dial. 12:18–20.
- Diskin CJ. Selenium binding proteins, renal failure, graft rejection and intimal hyperplasia: which are causes and which are effects? Am J Transplant (2005) 5:2592.[CrossRef][Web of Science][Medline]
- Diskin CJ. Multiple mechanisms for abnormal selenium levels and vascular disease in renal failure. Am J Kidney Dis (2006) 47:924. author reply: 924–925.[Web of Science][Medline]
- Kaplan AA, Halley SE, Lapkin RA, et al. Dialysate protein losses with bleach processed polysulfone dialyzers. Kidney Int (1995) 47:573–578.[Web of Science][Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||