Gadano A, Moreau R, Heller J, Chagneau C, Vachiéry F, Trombino C, Elman A, Denié C, Valla D, Lebrec D
Laboratoire d'Hémodynamique Splanchnique et de Biologie Vasculaire, INSERM and Service d'Hépatologie, Hôpital Beaujon, Clichy, France.
Gut. 1999 Jul;45(1):117-21. doi: 10.1136/gut.45.1.117.
Worsening cirrhosis may lead to increased renal O2 metabolism caused by activation of neurohumoral antinatriuretic substances.
To evaluate the relation between the severity of liver disease, sodium excretion, and neurohumoral antinatriuretic substances on the one hand and renal O2 metabolism on the other in patients with cirrhosis.
Renal O2 consumption and haemodynamics as well as plasma concentrations of noradrenaline, renin, and aldosterone were measured. Investigations were performed in 14 patients with Pugh's grade A, 43 with grade B, and 29 with grade C liver disease.
Renal O2 consumption significantly increased with the severity of cirrhosis (grade A, 8.9 (1.6); grade B, 15.5 (1.3); grade C, 18.0 (1.5) ml/min/m2). Plasma concentrations of noradrenaline, renin, and aldosterone significantly increased while mean arterial presssure and systemic vascular resistance significantly decreased with the severity of the disease. A significant inverse correlation was found between renal O2 consumption and sodium excretion. A significant direct correlation was found between plasma levels of noradrenaline and aldosterone on the one hand and renal O2 consumption on the other. Renal blood flow and the glomerular filtration rate did not differ significantly between patients with grade C and grade A or B disease.
This study shows for the first time that, in patients with cirrhosis, worsening of the disease is associated with an increase in renal O2 consumption. The results suggest that increased renal O2 consumption is due to renal tubular sodium retention caused by increased levels of neurohumoral antinatriuretic substances. This neurohumoral activation is related to cirrhosis induced vasodilation.
肝硬化病情恶化可能导致神经体液性利钠物质激活,从而使肾脏氧代谢增加。
评估肝硬化患者肝病严重程度、钠排泄、神经体液性利钠物质与肾脏氧代谢之间的关系。
测量肾脏氧消耗、血流动力学以及去甲肾上腺素、肾素和醛固酮的血浆浓度。对14例肝功能Pugh A级、43例B级和29例C级的患者进行了研究。
肾脏氧消耗随肝硬化严重程度显著增加(A级,8.9(1.6);B级,15.5(1.3);C级,18.0(1.5)ml/min/m²)。随着疾病严重程度增加,去甲肾上腺素、肾素和醛固酮的血浆浓度显著升高,而平均动脉压和全身血管阻力显著降低。发现肾脏氧消耗与钠排泄之间存在显著负相关。发现去甲肾上腺素和醛固酮的血浆水平与肾脏氧消耗之间存在显著正相关。C级患者与A级或B级患者之间的肾血流量和肾小球滤过率无显著差异。
本研究首次表明,在肝硬化患者中,疾病恶化与肾脏氧消耗增加有关。结果表明,肾脏氧消耗增加是由于神经体液性利钠物质水平升高导致肾小管钠潴留。这种神经体液激活与肝硬化诱导的血管舒张有关。