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Volume 57, Issue 10, Pages 1323-1327 (October 2008)


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Lipoprotein (a) as a risk factor for silent cerebral infarction in hemodialysis patients

Naoya Fukunagaac, Futoshi AnanbCorresponding Author Informationemail address, Koji Kanedaa, Tomoko Nawatac, Tetsunori Saikawad, Hironobu Yoshimatsuc

Received 16 October 2007; accepted 31 January 2008.

Abstract 

In patients with chronic renal failure undergoing hemodialysis (HD), silent cerebral infarctions (SCIs) are associated with high mortality. Levels of lipoprotein (a) (Lp[a]) increase with renal dysfunction and may be a novel predictor for cerebrovascular events. We tested the hypothesis that increased Lp(a) levels correlate with the occurrence of SCI in HD patients. Using cranial magnetic resonance imaging findings, we divided 62 Japanese patients undergoing HD into with-SCI group (61 ± 7 years, mean ± SD, n = 34) and without-SCI group (60 ± 6 years, n = 28). We compared the sex, body mass index, metabolic profiles, Lp(a) levels, and smoking habits between the 2 groups. The following observations were noted: (1) The number of patients with diabetes or hypertension did not differ between the 2 groups. (2) The levels of Lp(a) were higher in the with-SCI group in comparison with the without-SCI group (P < .0001). (3) The proportion of smokers was higher in the with-SCI group than in the without-SCI group (P < .05). (4) Plasma levels of high-density lipoprotein cholesterol were lower, whereas uric acid was higher, in the with-SCI group than in the without-SCI group (P < .001 and P < .05, respectively). (5) Multiple logistic regression analysis identified Lp(a) levels as being significantly associated with the presence of SCI (odds ratio, 1.23; 95% confidence interval, 1.09-1.38; P < .0001). This study indicates that patients with chronic renal failure, who are maintained on HD, exhibit an increased prevalence of SCI and that Lp(a) is significantly associated with the presence of SCI in HD patients.

a Department of Nephrology, Oita Red Cross Hospital, Oita 870-0033, Japan

b Department of Cardiology, Oita Red Cross Hospital, Oita 870-0033, Japan

c First Department of Internal Medicine, School of Medicine, Oita University, Oita 879-5511, Japan

d Department of Cardiovascular Science, School of Medicine, Oita University, Oita 879-5511, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 97 532 6181; fax: +81 97 533 1207.

PII: S0026-0495(08)00066-8

doi:10.1016/j.metabol.2008.01.033


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