IS INCREASED ERYTHROCYTE SODIUM-LITHIUM COUNTERTRANSPORT A USEFUL MARKER FOR DIABETIC NEPHROPATHY

被引:39
作者
ELVING, LD
WETZELS, JFM
DEPONT, JJHHM
BERDEN, JHM
机构
[1] UNIV HOSP NIJMEGEN, DEPT MED, DIV NEPHROL, NIJMEGEN, NETHERLANDS
[2] CATHOLIC UNIV NIJMEGEN, DEPT BIOCHIM & GENET MICROBIENNE, NIJMEGEN, NETHERLANDS
关键词
D O I
10.1038/ki.1992.132
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
Genetic predisposition to essential hypertension has been proposed as a risk factor for the development of diabetic nephropathy in type 1 (insulin-dependent) diabetes mellitus. An increased sodium-lithium countertransport activity (NaLiCT) has been suggested as a genetic marker for essential hypertension. We therefore evaluated NaLiCT in diabetic patients with (N = 39) or without (N = 23) diabetic nephropathy (DNP), patients with nondiabetic renal diseases (N = 42) and in healthy controls (N = 24). The NaLiCT was elevated in both diabetic patient groups compared to healthy controls (median 244; range 134 to 390-mu-mol . liter cells-1 . hr-1), but was not different in patients with DNP (median 314; range 162 to 676), without DNP (median 325; range 189 to 627) and patients with non-diabetic renal disease (median 300; range 142 to 655). The genetic predisposition to DNP is illustrated by the fact that diabetic sibs of probands with DNP showed a higher occurrence of DNP than diabetic sibs of patients without DNP. We analyzed whether familial DNP clustered with an increased NaLiCT. The NaLiCT in sibs concordant for the presence of DNP (N = 10; median 307; range 217 to 428-mu-mol . liter cells-1 . hr-1) was not significantly different from that in sibs concordant for absence of DNP (N = 15; median 279; range 189 to 442). We conclude that erythrocyte sodium-lithium countertransport activity cannot be used as a marker to identify patients at risk for the development of diabetic nephropathy.
引用
收藏
页码:862 / 871
页数:10
相关论文
共 66 条
[1]   EFFECT OF EXERCISE ON CATION-TRANSPORT IN HUMAN RED-CELLS [J].
ADRAGNA, NC ;
CHANG, JL ;
MOREY, MC ;
WILLIAMS, RS .
HYPERTENSION, 1985, 7 (01) :132-139
[2]   ELEVATED INTRACELLULAR CA-2+ AFFECTS LII-NAO COUNTERTRANSPORT IN HUMAN RED-BLOOD-CELLS [J].
AGAM, G ;
HATZAV, P ;
ABEKASIS, S ;
LOVEN, A ;
LIVNE, A .
BIOCHIMICA ET BIOPHYSICA ACTA, 1987, 904 (02) :207-215
[3]  
ANDERSEN AR, 1983, DIABETOLOGIA, V25, P496
[4]   LEAD INCREASES RED-CELL SODIUM-LITHIUM COUNTERTRANSPORT [J].
BATUMAN, V ;
DREISBACH, A ;
CHUN, E ;
NAUMOFF, M .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1989, 14 (03) :200-203
[5]  
BERDEN J H M, 1990, Diabetologia, V33, pA12
[6]   EXOGENOUS FACTORS INFLUENCING THE HUMAN-ERYTHROCYTE SODIUM LITHIUM COUNTERTRANSPORT SYSTEM [J].
BEUCKELMANN, D ;
ERDMANN, E .
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, 1984, 14 (05) :392-397
[7]   RENAL DYSFUNCTION AS A POSSIBLE CAUSE OF ESSENTIAL-HYPERTENSION IN PREDISPOSED SUBJECTS [J].
BIANCHI, G ;
CUSI, D ;
BARLASSINA, C ;
LUPI, GP ;
FERRARI, P ;
PICOTTI, GB ;
GATTI, M ;
POLLI, E .
KIDNEY INTERNATIONAL, 1983, 23 (06) :870-875
[8]   EXAGGERATED RENAL VASODILATOR RESPONSE TO CALCIUM ENTRY BLOCKADE IN 1ST-DEGREE RELATIVES OF ESSENTIAL HYPERTENSIVE SUBJECTS [J].
BLACKSHEAR, JL ;
GARNIC, D ;
WILLIAMS, GH ;
HARRINGTON, DP ;
HOLLENBERG, NK .
HYPERTENSION, 1987, 9 (04) :384-389
[9]   RENAL-TRANSPLANTATION AND RED-BLOOD-CELL SODIUM-TRANSPORT - ROLE OF PREDNISONE TREATMENT [J].
BOSCH, RJ ;
HERNANDO, N ;
PLAZA, JJ ;
CASADO, S ;
LOPEZNOVOA, JM .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 1991, 6 (04) :286-291
[10]   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