{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T23:27:24Z","timestamp":1792020444408,"version":"4.4.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and objectives<\/jats:title>\n                    <jats:p>Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent hereditary renal disease, characterized by cyst formation in the kidneys leading to end stage kidney failure. It is clinically acknowledged that ADPKD patients have impaired urine concentrating capacity, but the mechanism behind this observation is unknown.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design, setting, participants, &amp; measurements<\/jats:title>\n                    <jats:p>\n                      Fifteen ADPKD patients (estimated GFR \u226560 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      ) and 15 age- and sex-matched healthy controls underwent a standard prolonged water deprivation test in which urine and plasma osmolality, vasopressin, and copeptin were measured. The effect of a synthetic vasopressin analog (desmopressin) injected at the moment of maximal urine concentrating capacity was also studied.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      After 14 hours of water deprivation, ADPKD patients tended to have higher plasma osmolality (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.07) and significantly higher vasopressin and copeptin levels (both\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.05), whereas urine osmolality was similar in ADPKD patients and controls (710 versus 742 mOsmol\/kg;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.61). Maximal urine concentrating capacity was lower in ADPKD patients (758 versus 915 mOsmol\/kg in controls;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.001). At maximal urine concentrating capacity, plasma osmolality, vasopressin, and copeptin levels were significantly higher in ADPKD patients. The median increase in urine osmolality after desmopressin administration in ADPKD patients was less than in healthy controls.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Already early in their disease, ADPKD patients have impaired maximal urine concentrating capacity brought out upon dehydration, with no evidence of impaired hypothalamic response. To maintain fluid balance, vasopressin concentration increases, which is hypothesized to play a role in ADPKD disease progression.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2215\/cjn.11311111","type":"journal-article","created":{"date-parts":[[2012,4,20]],"date-time":"2012-04-20T20:36:40Z","timestamp":1334954200000},"page":"906-913","source":"Crossref","is-referenced-by-count":100,"title":["Vasopressin, Copeptin, and Renal Concentrating Capacity in Patients with Autosomal Dominant Polycystic Kidney Disease without Renal Impairment"],"prefix":"10.2215","volume":"7","author":[{"given":"Debbie","family":"Zittema","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wendy E.","family":"Boertien","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andr\u00e9 P.","family":"van 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