URINARY-EXCRETION OF URODILATIN IN PATIENTS WITH CIRRHOSIS

Cirrhotic patients with ascites show increased plasma levels of natriu retic peptides from cardiac origin (i.e., atrial natriuretic peptide [ ANP] and brain natriuretic peptide [BNP]). Urodilatin is a unique memb er of the natriuretic peptide family because it is exclusively synthes ized 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 so dium retention, urodilatin excretion and plasma levels of ANP were mea sured in 21 healthy subjects, 13 cirrhotic patients without ascites an d 23 cirrhotic patients with ascites. Urine urodilatin was measured wi th a highly specific radioimmunoassay using a polyclonal antibody agai nst human urodilatin. Patients with ascites had marked sodium retentio n (UNa 7 +/- 2 mEq/d) as compared to patients without ascites and heal thy 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 pmo l/g, 95 +/- 10 pmol/g, and 89 +/- 9 pmol/ g of creatinine, respectivel y; not significant). In addition, immunoreactive urodilatin from cirrh otic patients with ascites and healthy subjects showed a similar chrom atographic pattern. By contrast, plasma ANP levels were increased sign ificantly 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 natriureti c peptides are regulated independently.