小管肾小球反馈在梗阻性黄疸急性肾功能损害中的作用。

P Wunderlich, M Hermle, J M Davis, M Mihatsch, F Brunner, G Thiel
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引用次数: 3

摘要

急性肾功能损害常伴有肝功能障碍,尤其是胆管梗阻,可能非常严重。最近的研究表明,在肝功能障碍时发生的循环非电解质因子激活的小管肾小球反馈(TGF)可能导致肾血管强烈收缩,被认为是功能性肾功能损害的核心。本研究对两例梗阻性黄疸(OJ)合并肾功能损害患者和胆管结扎引起OJ大鼠的血清进行透析或用已知可阻断电解质介导的TGF的速尿处理。当将这些血清灌注到大鼠肾细胞的Henle袢中时,可导致止流压显著下降28%,止流压是肾小球毛细血管压力的间接测量指标,因此暗示小动脉血管收缩。这些发现与循环的非电解质因素刺激TGF在梗阻性黄疸病例中出现的假设是一致的,这些因素可能导致肾脏损害。
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The role of tubuloglomerular feedback in acute impairment of renal function in obstructive jaundice.

Acute renal functional impairment not infrequently accompanies liver dysfunction and, particularly with bile duct obstruction, may be extremely severe. Recent studies suggest that tubuloglomerular feedback (TGF) activated by circulating non-electrolyte factors which occur during liver dysfunction may contribute to the intense renal vasoconstriction thought to be central to the functional renal impairment. In this study, serum from two patients with obstructive jaundice (OJ) and renal impairment, and from rats with OJ due to bile duct ligation were either dialysed or treated with furosemide, known to block electrolyte-mediated TGF. These sera, when perfused into loops of Henle in rat nephrons, induced a significant fall of 28% in stop-flow pressure, an indirect measure of glomerular capillary pressure thus implying arteriolar vasoconstriction. These findings are consistent with the hypothesis that circulating, non-electrolyte factors, which stimulate TGF, occur in cases of obstructive jaundice and that these may contribute to the renal impairment.

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