The 825C/T polymorphism of the G-protein subunit β3 does not influence blood pressure and renal function in kidney transplant recipients

被引:9
作者
Wüthrich, RP [1 ]
Cicvara, S [1 ]
Booy, C [1 ]
Widmer, U [1 ]
Binswanger, U [1 ]
机构
[1] Univ Zurich Hosp, Dept Med, Div Nephrol, CH-8091 Zurich, Switzerland
关键词
blood pressure; 825C/T polymorphism; G-protein subunit beta 3; renal function; renal transplant; T allele;
D O I
10.1093/ndt/15.10.1663
中图分类号
R3 [基础医学]; R4 [临床医学];
学科分类号
1001 ; 1002 ; 100602 ;
摘要
Background. Recently, a polymorphism at position 825 (C-->T) of the cDNA that encodes the beta 3 subunit of heterotrimeric G proteins (G beta 3) was found to be associated with essential hypertension. The T allele leads to the formation of a truncated splice variant (G beta 3-s) with enhanced activity, promoting hypertension. We examined whether the T allele had an influence on blood pressure (BP) and early renal function after renal transplantation. Methods. We determined the G beta 3 genotype and T allele frequencies in renal transplant patients and examined associations with BP, BP medications, and renal function in the first year after transplantation. Results, In renal transplant recipients (n = 216) the frequency of the T allele was marginally increased (0.34 vs 0.29) compared with normal healthy blood donors (n = 163. Age, sex and body mass index were similar in patients with the CC, CT and TT genotype. BP, number of BP medications, and serum creatinine levels were also similar for the three genotypes within the first year after transplantation. Significantly more patients with the TT genotype (48%) had glomerulonephritis as the underlying renal disease, compared with the CT (29%) and CC (27%) genotypes. Conclusions. The T allele of G beta 3 does not have a negative impact on BP and early renal function in recipients of a renal allograft. The T allele might play a role in the pathogenesis of chronic glomerulonephritides.
引用
收藏
页码:1663 / 1666
页数:4
相关论文
共 15 条
  • [1] Beige J, 1999, J AM SOC NEPHROL, V10, P1717
  • [2] G-protein β3 subunit C825T variant and ambulatory blood pressure in essential hypertension
    Beige, J
    Hohenbleicher, H
    Distler, A
    Sharma, AM
    [J]. HYPERTENSION, 1999, 33 (04) : 1049 - 1051
  • [3] G-protein β3 subunit gene (GNB3) variant in causation of essential hypertension
    Benjafield, AV
    Jeyasingam, CL
    Nyholt, DR
    Griffiths, LR
    Morris, BJ
    [J]. HYPERTENSION, 1998, 32 (06) : 1094 - 1097
  • [4] Increased frequency of G-protein β3-subunit 825 T allele in dialyzed patients with type 2 diabetes
    Blüthner, M
    Schmidt, S
    Siffert, W
    Knigge, H
    Nawroth, P
    Ritz, E
    [J]. KIDNEY INTERNATIONAL, 1999, 55 (04) : 1247 - 1250
  • [5] The 825C/T polymorphism of the G-protein subunit β3 is not related to hypertension
    Brand, E
    Herrmann, SM
    Nicaud, V
    Ruidavets, JB
    Evans, A
    Arveiler, D
    Luc, G
    Plouin, PF
    Tiret, L
    Cambien, F
    [J]. HYPERTENSION, 1999, 33 (05) : 1175 - 1178
  • [6] The C825T polymorphism in the human G-protein β3 subunit gene is not associated with diabetic nephropathy its Type I diabetes mellitus
    Fogarty, DG
    Zychma, MJ
    Scott, LJ
    Warram, JH
    Krolewski, AS
    [J]. DIABETOLOGIA, 1998, 41 (11) : 1304 - 1308
  • [7] G protein β3 subunit variant and essential hypertension in Japanese
    Kato, N
    Sugiyama, T
    Morita, H
    Kurihara, H
    Yamori, Y
    Yazaki, Y
    [J]. HYPERTENSION, 1998, 32 (05) : 935 - 938
  • [8] LUKE RG, 1991, J AM SOC NEPHROL, V2, pS37
  • [9] MECHANISM OF CYCLOSPORINE-INDUCED HYPERTENSION
    LUKE, RG
    [J]. AMERICAN JOURNAL OF HYPERTENSION, 1991, 4 (05) : 468 - 471
  • [10] HYPERTENSIVE SODIUM-PROTON EXCHANGER PHENOTYPE PERSISTS IN IMMORTALIZED LYMPHOBLASTS FROM ESSENTIAL HYPERTENSIVE PATIENTS - A CELL-CULTURE MODEL FOR HUMAN HYPERTENSION
    ROSSKOPF, D
    FROMTER, E
    SIFFERT, W
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (05) : 2553 - 2559