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American Journal of Clinical Nutrition, Vol. 77, No. 4, 993, April 2003
© 2003 American Society for Clinical Nutrition


Letter to the Editor

Pregnancy-related decrease in total plasma homocysteine

Lars Brattström

Department of Neurology, Kalmar Hospital, SE-391 85 Kalmar, Sweden. E-mail: lars.brattstrom{at}ltkalmar.se

Dear Sir:

Murphy et al (1) confirmed previous observations that total plasma homocysteine concentrations decrease markedly during pregnancy (2). They did not find support for the suggestions that the decrease is due to folic acid supplementation, hemodilution, or a decrease in albumin (2). Instead, they suggested an endocrine-based mechanism.

An alternative mechanism for the pregnancy-related decrease in total plasma homocysteine concentration is the change in renal hemodynamics during pregnancy. It is well known that the glomerular filtration rate (GFR) and renal plasma flow increase markedly in pregnancy (3, 4). In the third trimester, the GFR of low-molecular-mass substances is known to increase by >= 40% (4). The mechanism for this change is unknown but may be endocrine-based.

Renal function is of great importance for the plasma total homocysteine concentration. We know that plasma total homocysteine increases when the GFR decreases but also that the plasma total homocysteine concentration tends to decrease when the GFR increases (hyperfiltration) (5, 6). Although the exact mechanism for the renal handling of homocysteine is unknown, the pregnancy-related increase in renal hemodynamics (endocrine-based or not) may well have importance for the pregnancy-related decrease in plasma total homocysteine, which must be considered in future studies on this subject.

REFERENCES

  1. Murphy MM, Scott JM, McPartlin JM, Fernandez-Ballart JD. The pregnancy-related decrease in fasting plasma homocysteine is not explained by folic acid supplementation, hemodilution, or a decrease in albumin in a longitudinal study. Am J Clin Nutr 2002;76:614–9.[Abstract/Free Full Text]
  2. Andersson A, Hultberg B, Brattstrom L, Isaksson A. Decreased serum homocysteine in pregnancy. Eur J Clin Chem Clin Biochem 1992;30:377–9.[Medline]
  3. Lindheimer MD, Davison JM, Katz AI. The kidney and hypertension in pregnancy: twenty exciting years. Semin Nephrol 2001;21:173–89.[Medline]
  4. Strevens H, Wide-Swensson D, Torffvit O, Grubb A. Serum cystatin C for assessment of glomerular filtration rate in pregnant and non-pregnant women. Indications of altered filtration process in pregnancy. Scand J Clin Lab Invest 2002;62:141–7.[Medline]
  5. Wollesen F, Brattstrom L, Refsum H, Ueland PM, Berglund L, Berne C. Plasma total homocysteine and cysteine in relation to glomerular filtration rate in diabetes mellitus. Kidney Int 1999;55:1028–35.[Medline]
  6. Kielstein JT, Boger RH, Bode-Boger SM, et al. Marked increase of asymmetric dimethylarginine in patients with incipient primary chronic renal disease. J Am Soc Nephrol 2002;13:170–6.[Abstract/Free Full Text]




This Article
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