{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T17:28:35Z","timestamp":1790616515545,"version":"4.1.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":2831,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003554","name":"Lundbeck Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100003554","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Hvidovre Hospital Foundation for Liver Disease"},{"name":"Ferring Pharmaceuticals Inc."},{"DOI":"10.13039\/501100001734","name":"University of Copenhagen","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100001734","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2007,12]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>\n                                 <jats:bold>Patients with advanced cirrhosis and ascites are characterized by circulatory dysfunction with splanchnic vasodilatation and renal vasoconstriction, which often lead to ascites. The vasoconstrictor terlipressin improves renal function in hepatorenal syndrome (HRS). The aim of this study was to evaluate if terlipressin also improves renal function in patients with ascites without HRS. Twenty-three patients with cirrhosis participated; 15 with nonrefractory ascites were randomized to either terlipressin (N group, n = 11) or a placebo (P group, n = 4), and 8 had refractory ascites and received terlipressin (R group). The glomerular filtration rate (GFR), sodium clearance (<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Na), lithium clearance (<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Li), osmolal clearance (<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Osm), and urine sodium concentration (<\/jats:bold>\n                                 <jats:bold>\n                                    U\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Na) were assessed before and after the injection of 2 mg of terlipressin or the placebo. GFR increased in the N group (69 \u00b1 19 versus 92 \u00b1 25 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.005) and in the R group (31 \u00b1 19 versus 41 \u00b1 31 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05) after terlipressin. In the N group, terlipressin induced an increase in<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Na (0.89 \u00b1 0.21 versus 1.52 \u00b1 1.45 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05),<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Li (17.3 \u00b1 8.9 versus 21.5 \u00b1 11.6 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05), and<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Osm (2.10 \u00b1 0.81 versus 3.06 \u00b1 2.0 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05). In the R group, terlipressin induced an increase in<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Na (0.11 \u00b1 0.18 versus 0.35 \u00b1 0.40 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05) and<\/jats:bold>\n                                 <jats:bold>\n                                    C\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Li (5.5 \u00b1 4.2 versus 9.5 \u00b1 8.55 mL\/min,<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05).<\/jats:bold>\n                                 <jats:bold>\n                                    U\n                                 <\/jats:bold>\n                                 <jats:bold>\n                                    Na increased in both groups after terlipressin (<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.005). Plasma norepinephrine (<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05) and renin (<\/jats:bold>\n                                 <jats:bold>\n                                    P\n                                 <\/jats:bold>\n                                 <jats:bold>&lt; 0.05) decreased after terlipressin. All parameters remained unchanged after the placebo.<\/jats:bold>\n                                 <jats:bold>\n                                    Conclusion:\n                                 <\/jats:bold>\n                                 <jats:bold>The vasopressin 1 receptor agonist terlipressin improves renal function and induces natriuresis in patients with cirrhosis and ascites without HRS. Vasoconstrictors may represent a novel future treatment modality for these patients. (Hepatology 2007.)<\/jats:bold>\n                              <\/jats:p>\n          <\/jats:sec>","DOI":"10.1002\/hep.21901","type":"journal-article","created":{"date-parts":[[2007,11,20]],"date-time":"2007-11-20T23:17:55Z","timestamp":1195600675000},"page":"1863-1871","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":123,"title":["Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome"],"prefix":"10.1097","volume":"46","author":[{"given":"Aleksander","family":"Krag","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u03c6ren","family":"M\u03c6ller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens H.","family":"Henriksen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niels-Henrik","family":"Holstein-Rathlou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fin Stolze","family":"Larsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Flemming","family":"Bendtsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-25-20241201","doi-asserted-by":"crossref","first-page":"468","DOI":"10.1007\/BF01320309","article-title":"Survival and prognostic indicators in compensated and decompensated cirrhosis.","volume":"31","author":"DAmico","year":"1986","journal-title":"Dig Dis Sci"},{"key":"R2-25-20241201","doi-asserted-by":"crossref","first-page":"122","DOI":"10.1002\/hep.1840070124","article-title":"Compensated cirrhosis: natural history and prognostic factors.","volume":"7","author":"Gines","year":"1987","journal-title":"Hepatology"},{"key":"R3-25-20241201","first-page":"164","article-title":", for the International Ascites Club. 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