Higher levels of HDL cholesterol are associated with a decreased likelihood of albuminuria in patients with long-standing standing type 1 diabetes

被引:40
作者
Molitch, ME
Rupp, D
Carnethon, M
机构
[1] Northwestern Univ, Div Endocrinol Metab & Mol Med, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA
[2] Northwestern Univ, Dept Prevent Med, Feinberg Sch Med, Chicago, IL 60611 USA
关键词
D O I
10.2337/diacare.29.01.06.dc05-1583
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
OBJECTIVE - The objective of this study was to determine whether high levels of HDL cholesterol are associated with a lower prevalence of albuminuria. RESEARCH DESIGN AND METHODS - We analyzed the lipid profiles of patients with type I diabetes of >= 20 years duration in 42 patients With albuminuria (28 microalbuminuria and 14 macroalbuminuria) and 65 patients without increased albumin excretion before any interventions with either statins or ACE inhibitors. RESULTS - Several characteristics were similar in the two groups: sex, age, duration of diabetes, total cholesterol, LDL cholesterol, and triglycerides. By univariate analysis, significant differences (P < 0.01) were found in HDL cholesterol (albuminuria 1.42 mg/dl, no albuminuria 1.71 mg/dl, P < 0.01), HbA(1c) (AlC) (albuminuria 8.5%, no albuminuria 7.5%), and proportions with no, background, and proliferative retinopathy (albuminuria 2.4, 16.7, and 81%; no albuminuria 24.6, 52.3, and 23.1%, respectively). When adjusted for age and sex, a 0.26-mmol/l (10-mg/dl) increase in HDL cholesterol is associated with an odds ratio (OR) of 0.70 (95% CI 0.54-0.90) for having albuminuria. In a multivariate model that adjusted for age, sex, diabetes duration, and AlC, for every 0.54-mmol/l (21-mg/dl) increase in HDL cholesterol, patients are approximately half (OR 0.51 [95% CI 0.30-0.86]) as likely to have albuminuria, even after controlling or AlC. CONCLUSIONS - Higher HDL cholesterol levels may be protective against the development of albuminuria in patients with type I diabetes. Whether this is due to the HDL cholesterol levels or whether they serve as a marker for some other mechanism remains to be determined.
引用
收藏
页码:78 / 82
页数:5
相关论文
共 44 条
[31]  
Molitch ME, 1997, SEMIN NEPHROL, V17, P101
[32]  
*NAT CTR HLTH STAT, 2000, LDL CHOL 1999 2000 D
[33]   Nephropathy in type I diabetes: A manifestation of insulin resistance and multiple genetic susceptibilities? Further evidence from the Pittsburgh Epidemiology of Diabetes Complication Study [J].
Orchard, TJ ;
Chang, YF ;
Ferrell, RE ;
Petro, N ;
Ellis, DE .
KIDNEY INTERNATIONAL, 2002, 62 (03) :963-970
[34]   Renoprotection in diabetes: genetic and non-genetic risk factors and treatment [J].
Parving, HH .
DIABETOLOGIA, 1998, 41 (07) :745-759
[35]   FAMILIAL CLUSTERING OF DIABETIC KIDNEY-DISEASE - EVIDENCE FOR GENETIC SUSCEPTIBILITY TO DIABETIC NEPHROPATHY [J].
SEAQUIST, ER ;
GOETZ, FC ;
RICH, S ;
BARBOSA, J .
NEW ENGLAND JOURNAL OF MEDICINE, 1989, 320 (18) :1161-1165
[36]   THE EFFECT OF INTENSIVE TREATMENT OF DIABETES ON THE DEVELOPMENT AND PROGRESSION OF LONG-TERM COMPLICATIONS IN INSULIN-DEPENDENT DIABETES-MELLITUS [J].
SHAMOON, H ;
DUFFY, H ;
FLEISCHER, N ;
ENGEL, S ;
SAENGER, P ;
STRELZYN, M ;
LITWAK, M ;
WYLIEROSETT, J ;
FARKASH, A ;
GEIGER, D ;
ENGEL, H ;
FLEISCHMAN, J ;
POMPI, D ;
GINSBERG, N ;
GLOVER, M ;
BRISMAN, M ;
WALKER, E ;
THOMASHUNIS, A ;
GONZALEZ, J ;
GENUTH, S ;
BROWN, E ;
DAHMS, W ;
PUGSLEY, P ;
MAYER, L ;
KERR, D ;
LANDAU, B ;
SINGERMAN, L ;
RICE, T ;
NOVAK, M ;
SMITHBREWER, S ;
MCCONNELL, J ;
DROTAR, D ;
WOODS, D ;
KATIRGI, B ;
LITVENE, M ;
BROWN, C ;
LUSK, M ;
CAMPBELL, R ;
LACKAYE, M ;
RICHARDSON, M ;
LEVY, B ;
CHANG, S ;
HEINHEINEMANN, M ;
BARRON, S ;
ASTOR, L ;
LEBECK, D ;
BRILLON, D ;
DIAMOND, B ;
VASILASDWOSKIN, A ;
LAURENZI, B .
NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (14) :977-986
[37]   Increased small dense LDL and intermediate-density lipoprotein with albuminuria in type 1 diabetes [J].
Sibley, SD ;
Hokanson, JE ;
Steffes, MW ;
Purnell, JQ ;
Marcovina, SM ;
Cleary, PA ;
Brunzell, JD .
DIABETES CARE, 1999, 22 (07) :1165-1170
[38]   Differences in HDL-cholesterol:apoA-I plus apoA-II ratio and apoE phenotype with albuminuric status in Type I diabetic patients [J].
Soedamah-Muthu, SS ;
Colhoun, HM ;
Taskinen, MR ;
Idzior-Walus, B ;
Fuller, JH .
DIABETOLOGIA, 2000, 43 (11) :1353-1359
[39]  
Steffes MW, 2003, JAMA-J AM MED ASSOC, V290, P2159, DOI 10.1001/jama.290.16.2159
[40]  
TREVISAN R, 1995, J LAB CLIN MED, V126, P342