Abnormal sodium-lithium countertransport kinetics in immunoglobulin A nephropathy patients and their families: Association with hypertension

被引:5
作者
Ho, KL [1 ]
Rutherford, PA [1 ]
Thomas, TH [1 ]
Wilkinson, R [1 ]
机构
[1] UNIV NEWCASTLE UPON TYNE,FREEMAN HOSP,DEPT MED NEPHROL,NEWCASTLE TYNE,TYNE & WEAR,ENGLAND
关键词
sodium; lithium; erythrocyte; immunoglobulin A nephropathy; hypertension;
D O I
10.1016/S0272-6386(96)90355-8
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
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis worldwide. There is an increased prevalence of hypertension, which is an important risk factor for progressive renal impairment, in patients with IgAN. Changes in sodium-lithium countertransport (Na/Li CT) kinetics, particularly high Vmax/Km, have been shown in familial essential hypertension. In this study a high Vmax/Km was observed in IgA probands with hypertension and/or progressive renal impairment. Mean blood pressure was higher in the first-degree relatives of hypertensive patients with IgAN compared with the relatives of normotensive IgAN probands. These hypertensive relatives had an increased Vmax/Km ratio and a low Km of Na/Li CT. There is a strong correlation of Vmax/Km (r = 0.82) between the IgA probands and their first-degree relatives, suggesting strong familial factors contributing to this Na/Li CT kinetic parameter. An increased Vmax/Km ratio of Na/Li CT seems to be a better marker for familial hypertension than Km alone and may be useful in identifying those patients who are at greater risk of developing hypertension. (C) 1996 by the National Kidney Foundation, Inc.
引用
收藏
页码:334 / 340
页数:7
相关论文
共 30 条
[1]   REDUCTION OF BLOOD-PRESSURE RETARDS THE PROGRESSION OF CHRONIC RENAL-FAILURE IN MAN [J].
ALVESTRAND, A ;
GUTIERREZ, A ;
BUCHT, H ;
BERGSTROM, J .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 1988, 3 (05) :624-631
[2]   METHODS FOR EXPRESSING THE CHARACTERISTICS OF TRANSMEMBRANE ION-TRANSPORT SYSTEMS [J].
ARONSON, JK .
CLINICAL SCIENCE, 1990, 78 (03) :247-254
[3]  
AUTULY V, 1991, J HYPERTENS, V9, pS220
[4]   CHRONIC GLOMERULONEPHRITIS - NON-IMMUNOLOGIC MECHANISMS OF PROGRESSIVE GLOMERULAR DAMAGE [J].
BALDWIN, DS ;
COHEN, JJ ;
HARRINGTON, JT ;
KASSIRER, JP ;
CLIVE, D ;
MADIAS, NE ;
STROM, J ;
ZELMAN, S ;
MADAIO, M .
KIDNEY INTERNATIONAL, 1982, 21 (01) :109-120
[5]   INCREASED SODIUM-LITHIUM COUNTERTRANSPORT ACTIVITY IN RED-CELLS OF IGA NEPHROPATHY PATIENTS [J].
BOERO, R ;
ESPOSTI, ED ;
FABBRI, A ;
GUARENA, C ;
FORNERIS, G ;
QUARELLO, F ;
FUSAROLI, M ;
PICCOLI, G .
KIDNEY INTERNATIONAL, 1991, 40 (06) :1118-1122
[6]  
Boerwinkle E, 1984, Prog Clin Biol Res, V165, P479
[7]   INCREASED SODIUM-LITHIUM COUNTERTRANSPORT IN RED-CELLS OF PATIENTS WITH ESSENTIAL-HYPERTENSION [J].
CANESSA, M ;
ADRAGNA, N ;
SOLOMON, HS ;
CONNOLLY, TM ;
TOSTESON, DC .
NEW ENGLAND JOURNAL OF MEDICINE, 1980, 302 (14) :772-776
[8]   ELEVATED SODIUM-LITHIUM COUNTERTRANSPORT - A FAMILIAL MARKER OF HYPERLIPEMIA AND HYPERTENSION [J].
CARR, SJ ;
THOMAS, TH ;
LAKER, MF ;
WILKINSON, R .
JOURNAL OF HYPERTENSION, 1990, 8 (02) :139-146
[9]  
CLARKSON AR, 1987, SEMIN NEPHROL, V7, P377
[10]   INCREASED SODIUM-LITHIUM COUNTERTRANSPORT IN COLLEGE-STUDENTS WITH ELEVATED BLOOD-PRESSURE [J].
COOPER, R ;
LEGRADY, D ;
NANAS, S ;
TREVISAN, M ;
MANSOUR, M ;
HISTAND, P ;
OSTROW, D ;
STAMLER, J .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1983, 249 (08) :1030-1034