Saló J, Jiménez W, Kuhn M, Ginès A, Ginès P, Fernández-Esparrach G, Angeli P, Clària J, Bataller R, Arroyo V, Forssmann W G, Rodés J
Liver Unit, Department of Medicine, Hospital Clínic i Provincial, University of Barcelona, Spain.
Hepatology. 1996 Dec;24(6):1428-32. doi: 10.1002/hep.510240621.
Cirrhotic patients with ascites show increased plasma levels of natriuretic peptides from cardiac origin (i.e., atrial natriuretic peptide [ANP] and brain natriuretic peptide [BNP]). Urodilatin is a unique member of the natriuretic peptide family because it is exclusively synthesized in the kidney acting on a paracrine fashion in the regulation of sodium excretion. To investigate the renal production of urodilatin in cirrhosis and its relationship with other natriuretic peptides and sodium retention, urodilatin excretion and plasma levels of ANP were measured in 21 healthy subjects, 13 cirrhotic patients without ascites and 23 cirrhotic patients with ascites. Urine urodilatin was measured with a highly specific radioimmunoassay using a polyclonal antibody against human urodilatin. Patients with ascites had marked sodium retention (UNa 7 +/- 2 mEq/d) as compared to patients without ascites and healthy subjects (29 +/- 3 mEq/d and 34 +/- 5 mEq/d, respectively, P < .001). Patients with cirrhosis and ascites had urine urodilatin excretion similar to patients without ascites and healthy subjects (82 +/- 8 pmol/g, 95 +/- 10 pmol/g, and 89 +/- 9 pmol/ g of creatinine, respectively; not significant). In addition, immunoreactive urodilatin from cirrhotic patients with ascites and healthy subjects showed a similar chromatographic pattern. By contrast, plasma ANP levels were increased significantly in patients with ascites (29 +/- 3 fmol/mL) as compared with patients without ascites or healthy subjects (14 +/- 3 fmol/mL and 6 +/- 1 fmol/mL, respectively; P < .01). In conclusion, urine urodilatin excretion is normal in patients with cirrhosis even in the presence of marked sodium retention. The coexistence of increased ANP levels and normal urodilatin excretion suggests that in cirrhosis both natriuretic peptides are regulated independently.
肝硬化腹水患者心脏来源的利钠肽（即心房利钠肽[ANP]和脑利钠肽[BNP]）血浆水平升高。尿钠素是利钠肽家族的独特成员，因为它仅在肾脏合成，以旁分泌方式调节钠排泄。为了研究肝硬化患者尿钠素的肾脏生成及其与其他利钠肽和钠潴留的关系，对21名健康受试者、13名无腹水的肝硬化患者和23名有腹水的肝硬化患者测量了尿钠素排泄及ANP血浆水平。使用抗人尿钠素的多克隆抗体通过高度特异性放射免疫测定法测量尿钠素。与无腹水患者和健康受试者相比（分别为29±3 mEq/d和34±5 mEq/d），有腹水患者有明显的钠潴留（尿钠7±2 mEq/d）（P<.001）。肝硬化腹水患者的尿钠素排泄与无腹水患者和健康受试者相似（分别为每克肌酐82±8 pmol/g、95±10 pmol/g和89±9 pmol/g；无显著差异）。此外，有腹水的肝硬化患者和健康受试者的免疫反应性尿钠素显示出相似的色谱图。相比之下，与无腹水患者或健康受试者相比（分别为14±3 fmol/mL和6±1 fmol/mL），有腹水患者的血浆ANP水平显著升高（29±3 fmol/mL）（P<.01）。总之，即使存在明显的钠潴留，肝硬化患者的尿钠素排泄仍正常。ANP水平升高与尿钠素排泄正常并存表明，在肝硬化中，两种利钠肽是独立调节的。
