Author(s): Cheng, YC (Cheng, Yi-Chang); Kuo, WW (Kuo, Wei-Wen); Wu, CH (Wu, Chieh- Hsi); Shu, WT (Shu, Wen-Tong); Kuo, CH (Kuo, Chia-Hua); Hwang, JM (Hwang, Jin-Ming);
Hsu, HH (Hsu, Hsi-Hsien); Chen, LM (Chen, Li-Ming); Huang, CY (Huang, Chih-Yang); Lee, SD (Lee, Shin-Da)
Title: Iron status and cardiovascular risk factors in patients with haemodialysis versus patients with ischaemic heart disease
Source: NEPHROLOGY, 14 (1): 65-69 FEB 2009 Language: English
Document Type: Article
Author Keywords: cardiac markers; chronic renal failure; coronary artery disease;
proinflammatory; serum iron
KeyWords Plus: NECROSIS-FACTOR-ALPHA; C-REACTIVE-PROTEIN; HIGH-DENSITY- LIPOPROTEINS; GROWTH-FACTOR-AXIS; LACTATE-DEHYDROGENASE; MYOCARDIAL- INFARCTION; CHRONIC INFLAMMATION; RENAL-DISEASE; FACTOR-I; IGF-I
Abstract: The study aimed to investigate whether imbalanced iron status in patients with haemodialysis coexisted with abnormal lipid profile, higher inflammatory status and altered growth hormone-insulin-like growth factor (GH-IGF)-I axis and to compare these biochemical markers with patients with ischaemic heart disease.
Serum samples for biochemical and immunological analyses were collected from 74 normal subjects, 138 patients with ischaemic heart disease (IHD) and 115 patients on haemodialysis (HD).
Compared with normal subjects, lower serum iron, lower total iron-binding capacity (TIBC) and higher ferritin in HD patients coexisted with decreases in high-density lipoprotein cholesterol and total bilirubin as well as increases in lactate dehydrogenase (LDH), interleukin (IL)-6, C- reactive protein (CRP) and IL-10. Decreased IGF-I and increased GH were found in HD patients whereas unchanged GH-IGF axis were found in IHD patients. Compared with IHD, much higher ferritin, lower TIBC, lower bilirubin and higher LDH levels were found in HD patients.
Imbalanced iron status in patients on HD coexisted with abnormal lipid profiles, increased anaerobic activity and higher inflammatory status, which suggests that imbalanced iron status in HD patients may play a deleterious role in cardiovascular pathophysiology. Altered GH-IGF axis found in HD patients was more obvious than in IHD patients. This may imply that the GH- IGF axis system is modulated or adapted by HD.
Addresses: [Lee, Shin-Da] China Med Univ, Dept Phys Therapy, Inst Rehabil Sci, Taichung 40202, Taiwan; [Cheng, Yi-Chang] Taichung Vet Gen Hosp, Emergency Dept, Taichung, Taiwan; [Kuo, Wei-Wen; Wu, Chieh-Hsi] China Med Univ, Dept Biol Sci & Technol, Taichung 40202, Taiwan; [Shu, Wen-Tong; Chen, Li-Ming] Armed Force Taichung Gen Hosp, Dept
Internal Med, Taichung, Taiwan; [Hwang, Jin-Ming] Chung Shan Med Univ, Sch Appl Chem, Taichung, Taiwan; [Chen, Li-Ming] Cent Taiwan Univ Sci & Technol, Ctr Gen Educ, Taichung, Taiwan; [Huang, Chih-Yang] Grad Inst Chinese Med Sci, Taichung, Taiwan; [Huang, Chih- Yang] China Med Univ, Inst Med Sci, Taichung 40202, Taiwan; [Huang, Chih-Yang] Asia Univ, Dept Hlth & Nutr Biotechnol, Taichung, Taiwan; [Kuo, Chia-Hua] Taipei Phys Educ Coll, Lab Exercise Biochem, Taipei, Taiwan; [Hsu, Hsi-Hsien] Mackay Mem Hosp, Div Colorectal Surg, Taipei, Taiwan
Reprint Address: Lee, SD, China Med Univ, Dept Phys Therapy, Inst Rehabil Sci, 91 Hsueh Shih Rd, Taichung 40202, Taiwan.
E-mail Address: [email protected] Funding Acknowledgement:
Funding Agency Grant Number
National Science Council, Taiwan NSC 95-2314-B-039-040 NSC 95-2314-B-039-043-MY3
The study is partially supported by grants NSC 95-2314-B-039-040 and NSC 95-2314-B-039- 043-MY3 from the National Science Council, Taiwan.
Cited References: BAYESGENIS A, 2000, CIRC RES, V86, P125.
BLEUMINK GS, 2004, AM J CARDIOL, V94, P384, DOI 10.1016/j.amjcard.2004.04.044.
BOENISCH O, 2002, J NEPHROL, V15, P547.
CALABRESI L, 2003, CIRC RES, V92, P330, DOI 10.1161/01.RES.0000054201.60308.1A.
CENGI N, 2005, TRANSPLANT P, V37, P2915, DOI 10.1016/j.transproceed.2005.07.058.
CHAN CT, 2004, SEMIN DIALYSIS, V17, P99.
DANESH J, 2004, NEW ENGL J MED, V350, P1387.
DEVALK B, 1999, ARCH INTERN MED, V159, P1542.
DOWELL RT, 1994, METHOD FIND EXP CLIN, V16, P109.
FOLEY RN, 1995, J AM SOC NEPHROL, V5, P2024.
FOLEY RN, 1998, AM J KIDNEY DIS S3, V32, S112.
FRUCHART JC, 1998, BIOCHIMIE, V80, P167.
GOLDSTEIN SL, 2003, J PEDIATR, V143, P653, DOI 10.1067/S0022-3476(03)00534-1.
GONZALEZ AI, 2003, METABOLISM, V52, P116, DOI 10.1053/meta.2003.50018.
GREABU M, 2001, ACTA POL PHARM, V58, P225.
HAIDARI M, 2001, CLIN CHEM, V47, P1666.
HE J, 2004, CIRCULATION, V110, P405, DOI 10.1161/01.CIR.0000136583.52681.0D.
HOJO Y, 1998, NIPPON RINSHO, V56, P2500.
HUIJGEN HJ, 1997, EUR J CLIN CHEM CLIN, V35, P569.
JENSEN PB, 1999, CLIN NEPHROL, V52, P103.
KOUKKUNEN H, 2001, ANN MED, V33, P37.
KUO WW, 2006, APOPTOSIS, V11, P1075, DOI 10.1007/s10495-006-7028-4.
LEE SD, 2006, CLIN CHIM ACTA, V367, P62, DOI 10.1016/j.cca.2005.11.015.
LEE SD, 2006, CLIN CHIM ACTA, V370, P50, DOI 10.1016/j.cca.2006.01.012.
MAGNUSSON MK, 1994, CIRCULATION, V89, P102.
MAYER M, 2000, CLIN CHEM, V46, P1723.
MCGEARY RP, 2003, MINI-REV MED CHEM, V3, P253.
ONESTI G, 1975, CIRC RES, V36, P145.
OPGAARD OS, 2005, GROWTH HORM IGF RES, V15, P89, DOI 10.1016/j.ghir.2005.02.002.
RAMIREZ G, 1994, J CLIN ENDOCR METAB, V78, P63.
REN J, 1999, J MOL CELL CARDIOL, V31, P2049.
RIDKER PM, 2000, CIRCULATION, V101, P2149.
RIFAI N, 2001, CARD TOXICOL, V1, P153.
SHAH SV, 2003, AM J KIDNEY DIS S1, V41, S80, DOI 10.1053/ajkd.2003.50091.
TENTOLOURIS C, 2004, INT J CARDIOL, V94, P301, DOI 10.1016/j.ijcard.2003.08.002.
VALENTI L, 2007, AM J NEPHROL, V27, P101, DOI 10.1159/000099635.
VAZIRI N, 1990, INT J ARTIF ORGANS, V13, P223.
YANG ZQ, 2000, CIRCULATION, V101, P1019.
ZOCCALI C, 2003, KIDNEY INT S, S105.
Cited Reference Count: 39 Times Cited: 0
Publisher: WILEY-BLACKWELL PUBLISHING, INC
Publisher Address: COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA ISSN: 1320-5358
DOI: 10.1111/j.1440-1797.2008.01004.x 29-char Source Abbrev.: NEPHROLOGY ISO Source Abbrev.: Nephrology
Source Item Page Count: 5
Subject Category: Urology & Nephrology ISI Document Delivery No.: 424GE