ASSOCIATION BETWEEN WHITE BLOOD CELL COUNT AND LEVELS OF SERUM HOMOCYSTEINE IN END-STAGE RENAL FAILURE PATIENTS TREATING WITH HEMODIALYSIS
Abstract
Background: In hemodialysis patients, plasma levels of total homocysteine are influenced bynutritional status in patients with chronic kidney disease .To investigate the association betweenserum homocysteine (Hcy) level as a marker of nutritional status and WBC counts as a marker ofinflammation, a cross-sectional study was conducted on patients with end-stage renal disease(ESRD), who were undergoing maintenance hemodialysis treatment. Methods: Serumhomocysteine (total) and WBC count were measured. Other biochemical analysis including serumpredialysis creatinine (Creat), post and predialysis blood urea nitrogen (BUN), albumin (Alb),serum C-reactive protein (CRP) and serum ferritin were measured, also intact serum PTH (iPTH)and plasma HCO3 was measured too. For the efficacy of hemodialysis the urea reduction rate(URR) was calculated from pre- and post-blood urea nitrogen (BUN) data. The body mass index(BMI) was also calculated. For correlations the partial correlation test was used. Results: Totalpatients were 36(f=15 m=21), consisting of 25non-diabetic HD patients and 11diabetic HDpatients. The mean patient's age was 47±17years. In all patients a significant inverse correlationof serum homocysteine with WBC count and a significant positive correlation of serumHomocysteine with BMI and a near significant positive correlation of WBC count with serumCRP were found. Conclusion: In hemodialysis patients an inverse correlation between WBCcount as a marker of inflammation with serum Hcy level as a marker of nutritional status, furthersupport the hypothesis of the malnutrition-inflammation cachexia syndromeKeywords: White blood cell, Serum homocysteineReferences
Stein JH, McBride PE. Hyperhomocysteinemia and
atherosclerotic vascular disease: pathophysiology, screening
and treatment. Arch Intern Med 1998; 158: 1301-6.
Boysen G, Brander T, Christensen H, Gideon R, Truelsen T.
Homocysteine and risk of recurrent stroke. Stroke 2003; 34:
-61.
Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A
quantitative assessment of plasma homocysteine as a risk factor
for vascular disease. Probable benefits of increasing folic acid
intakes. JAMA 1995; 274: 1049-57.
Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of
cardiovascular disease in chronic renal disease. Am J Kidney
Dis 1998; 32 (suppl 3): S112-9.
Parfrey PS. Cardiac and cerebrovascular disease in chronic
uremia. Am J Kidney Dis 1993; 21: 77-80.
Jakubowski H. Metabolism of homocysteine thiolactone in
human cell cultures. Possible mechanism for pathological
consequences of elevated homocysteine levels. J Biol Chem
; 272:1935-42.
Mehta JL, Saldeen TG, Rand K. Interactive role of infection,
inflammation and traditional risk factors in atherosclerosis and
coronary artery disease. J Am Coll Cardiol 1998;31:1217-25.
Brown DW, Giles WH, Croft JB. White blood cell count: an
independent predictor of coronary heart disease mortality
among a national cohort. J Clin Epidemiol 2001;54:316-22.
Ksiazek A, Sokolowska G, Marczewski K, Solski J.Leukopenia
with different regenerated haemodialysis mbranes. Int Urol
Nephrol 1984;16(1):61-7.
Wegmuller E, Montandon A, Nydegger U, Descoeudres
C.Biocompatibility of different hemodialysis membranes:
activation of complement and leukopenia. Int J Artif Organs.
;9(2):85-92.
Suliman ME, Stenvinkel P, Qureshi AR, Barany P, Heimburger
O, Anderstam B et al. Hyperhomocysteinemia in relation to
plasma free amino acids, biomarkers of inflammation and
mortality in patients with chronic kidney disease starting
dialysis therapy. Am J Kidney Dis 2004;44(3):455-65.
Mallamaci F, Zoccali C, Tripepi G ,Fermo I,Benedetto FA,
Cataliotti A, et al. Hyperhomocysteinemia predicts
cardiovascular outcomes in hemodialysis patients. Kidney Int
; 61: 609–614.
Kalantar-Zadeh K, Block G, Humphreys MH, McAllister CJ,
Kopple JD. A low, rather than a high, total plasma homocysteine
is an indicator of poor outcome in hemodialysis patients. J Am
Soc Nephrol 2004;15(2):442-53.
Suliman ME, Stenvinkel P, Barany P, Heimburger O,
Anderstam B, Lindholm B. Hyperhomocysteinemia and its
relationship to cardiovascular disease in ESRD: Influence of
hypoalbuminemia, malnutrition, inflammation, and diabetes
mellitus. Am J Kidney Dis 2003;41: S89–S95.
Suliman ME, Lindholm B, Barany P, Bergstrom J:
Hyperhomocysteinemia in chronic renal failure patients:
Relation to nutritional status and cardiovascular disease. Clin
Chem Lab Med 2001;39: 734–738
Kalantar-Zadeh K, Block G, Humphreys MH, Kopple JD.
Reverse epidemiology of cardiovascular risk factors in
maintenance dialysis patients. Kidney Int 2003;63:793–808.
Fleischmann EH, Bower JD, Salahudeen AK: Risk factor
paradox in hemodialysis: Better nutrition as a partial
explanation. ASAIO J 2001;47:74–81.
Nishizawa Y, Shoji T, Ishimura E, Inaba M, Morii H: Paradox
of risk factors for cardiovascular mortality in uremia: Is a higher
cholesterol level better for atherosclerosis in uremia? Am J
Kidney Dis 2001;38: S4–S7.
Zeng X, Dai J, Remick DG, Wang X. Homocysteine mediated
expression and secretion of monocyte chemoattractant protein-1
and interleukin-8 in human monocytes. Circ Res 2003;93:311-
Boag JT. Basic Truths in Optimal Hemodialysis, Dialysis &
Transplantation 1994;23(11)636.
http://www.halls.md/body-mass-index/av.htm
Carru C, Deiana L, Sotgia S, Usai MF, Zinellu A. Relationships
between white blood cell count and levels of serum
homocysteine and cysteine in healthy subjects. Haematologica.
;90(1):136-7.
Heinecke JW, Rosen H, Suzuki LA, Chait A. The role of sulfurcontaining amino acids in superoxide production and
modification of low density lipoprotein by arterial smooth
muscle cells. J Biol Chem 1987;262:10098-103.
Sakuta H, Suzuki T, Yasuda H, Ito T.White blood cell count is
associated with plasma total homocysteine in Japanese men.
Scand J Clin Lab Invest. 2005;65(6):447-52.
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