RENAL ELIMINATION OF BETA-2-MICROGLOBULIN AND MYOGLOBIN IN PATIENTS WITH NORMAL AND IMPAIRED RENAL-FUNCTION

被引:9
作者
FLOEGE, J
WILKS, MF
SOOSE, M
KOTZERKE, J
SHALDON, S
KOCH, KM
机构
[1] UNIV HOSP NIMES,DEPT NEPHROL,NIMES,FRANCE
[2] HANOVER MED SCH,DEPT NUCL MED,W-3000 HANOVER 61,GERMANY
来源
NEPHRON | 1990年 / 55卷 / 04期
关键词
Low-molecular-weight proteins; Myoglobin; β[!sub]2[!/sub]-Microglobulin;
D O I
10.1159/000186000
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Since the demonstration that β2-microglobulin (β2M) is an amyloidogenic protein in man, the excretion of this low-molecular-weight protein under conditions with normal and reduced function has received increased interest. The renal arteriovenous extraction of β2M, polyfructosan (an inulin analogue), and a second low-molecular-weight protein, myoglobin, was measured in vivo in 16 human kidneys with normal renal function/gross morphology and in 22 kidneys with reduced function. In kidneys with normal function, the extraction of β2M significantly exceeded that of polyfructosan (0.198 ± 0.037 vs 0.182 ± 0.05; p = 0.04), while that of myoglobin (0.177 ± 0.068) was not different from that of polyfructosan. In kidneys with reduced function, the extraction of polyfructosan or myoglobin was not significantly altered. In contrast, the β2M extraction decreased to 0.110 ± 0.060 (p<0.01 vs. extraction of polyfructosan or myoglobin). This decrease was significantly correlated with the decrease of the endogenous creatinine clearance or the total or unilateral 131I-hippuran clearance. These results indicate that in normal renal function the glomerular filtration of β2M may be supplemented by a peritubular mode of removal. The mechanisms(s) underlying the selective decrease of β2M extraction in kidneys with reduced function remain speculative. However, this decrease will lead to a further augmentation of the retention of β2M in renal failure.
引用
收藏
页码:361 / 367
页数:7
相关论文
共 37 条
[1]   RENAL EXTRACTION OF GLUCAGON IN RATS WITH NORMAL AND REDUCED RENAL-FUNCTION [J].
BASTL, C ;
FINKELSTEIN, FO ;
SHERWIN, R ;
HENDLER, R ;
FELIG, P ;
HAYSLETT, JP .
AMERICAN JOURNAL OF PHYSIOLOGY, 1977, 233 (01) :F67-F71
[2]  
BAUMANN K, 1965, PFLUG ARCH GES PHYS, V282, P238
[3]   A RAPID, SENSITIVE METHOD FOR DETECTION OF ALKALINE-PHOSPHATASE CONJUGATED ANTI-ANTIBODY ON WESTERN BLOTS [J].
BLAKE, MS ;
JOHNSTON, KH ;
RUSSELLJONES, GJ ;
GOTSCHLICH, EC .
ANALYTICAL BIOCHEMISTRY, 1984, 136 (01) :175-179
[4]  
CORNELL R, 1971, LAB INVEST, V25, P42
[5]   PATHOGENESIS AND CHARACTERIZATION OF HYPERGLUCAGONEMIA IN UREMIC RAT [J].
EMMANOUEL, DS ;
JASPAN, JB ;
KUKU, SF ;
KATZ, AI .
JOURNAL OF CLINICAL INVESTIGATION, 1976, 58 (05) :1266-1272
[6]   PROLACTIN METABOLISM IN THE RAT - ROLE OF THE KIDNEY IN DEGRADATION OF THE HORMONE [J].
EMMANOUEL, DS ;
FANG, VS ;
KATZ, AI .
AMERICAN JOURNAL OF PHYSIOLOGY, 1981, 240 (05) :F437-F445
[7]  
FLOEGE J, UNPUB TURNOVER 131I
[8]  
FLOEGE J, 1989, NEPHRON, V51, P320
[9]   A METHOD TO DETECT THE INVITRO MODIFICATION OF SERUM BETA-2-MICROGLOBULIN IN HEALTH AND DISEASE [J].
FORBES, MA ;
COX, AM ;
COOPER, EH .
CLINICA CHIMICA ACTA, 1988, 177 (01) :89-99
[10]  
FREDRIKSSON A, 1975, SCAND J CLIN LAB INV, V35, P591