<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Torres VE</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NCRR NIH HHS</funding><pagination>577-85</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3580956</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>81(6)</volume><pubmed_abstract>HALT PKD consists of two ongoing randomized trials with the largest cohort of systematically studied patients with autosomal dominant polycystic kidney disease to date. Study A will compare combined treatment with an angiotensin-converting inhibitor and receptor blocker to inhibitor alone and standard compared with low blood pressure targets in 558 early-stage disease patients with an eGFR over 60 ml/min per 1.73 m(2). Study B will compare inhibitor-blocker treatment to the inhibitor alone in 486 late-stage patients with eGFR 25-60 ml/min per 1.73 m(2). We used correlation and multiple regression cross-sectional analyses to determine associations of baseline parameters with total kidney, liver, or liver cyst volumes measured by MRI in Study A and eGFR in both studies. Lower eGFR and higher</pubmed_abstract><journal>Kidney international</journal><pubmed_title>Analysis of baseline parameters in the HALT polycystic kidney disease trials.</pubmed_title><pmcid>PMC3580956</pmcid><funding_grant_id>M01 RR000051</funding_grant_id><funding_grant_id>DK62411</funding_grant_id><funding_grant_id>DK62410</funding_grant_id><funding_grant_id>RR025008</funding_grant_id><funding_grant_id>UL1 TR000454</funding_grant_id><funding_grant_id>U01 DK062410</funding_grant_id><funding_grant_id>U01 DK062411</funding_grant_id><funding_grant_id>RR23940</funding_grant_id><funding_grant_id>RR00585</funding_grant_id><funding_grant_id>UL1 RR025008</funding_grant_id><funding_grant_id>M01 RR000039</funding_grant_id><funding_grant_id>U01 DK062408</funding_grant_id><funding_grant_id>UL1 RR025780</funding_grant_id><funding_grant_id>RR000054</funding_grant_id><funding_grant_id>UL1 RR024150</funding_grant_id><funding_grant_id>M01 RR000054</funding_grant_id><funding_grant_id>RR000051</funding_grant_id><funding_grant_id>RR025752</funding_grant_id><funding_grant_id>DK62402</funding_grant_id><funding_grant_id>DK62401</funding_grant_id><funding_grant_id>U01 DK082230</funding_grant_id><funding_grant_id>RR000039</funding_grant_id><funding_grant_id>RR024989</funding_grant_id><funding_grant_id>DK62408</funding_grant_id><funding_grant_id>U01 DK062401</funding_grant_id><funding_grant_id>U01 DK062402</funding_grant_id><funding_grant_id>UL1 RR024989</funding_grant_id><funding_grant_id>UL1 RR025752</funding_grant_id><funding_grant_id>RR024150</funding_grant_id><funding_grant_id>M01 RR000585</funding_grant_id><funding_grant_id>M01 RR023940</funding_grant_id><funding_grant_id>RR025780</funding_grant_id><pubmed_authors>Chapman AB</pubmed_authors><pubmed_authors>Bost JE</pubmed_authors><pubmed_authors>Masoumi A</pubmed_authors><pubmed_authors>HALT PKD Study Group</pubmed_authors><pubmed_authors>Remer E</pubmed_authors><pubmed_authors>Bae KT</pubmed_authors><pubmed_authors>Winklhofer FT</pubmed_authors><pubmed_authors>Baker D</pubmed_authors><pubmed_authors>Kelleher C</pubmed_authors><pubmed_authors>Miskulin DC</pubmed_authors><pubmed_authors>Otto K</pubmed_authors><pubmed_authors>Torres VE</pubmed_authors><pubmed_authors>Thompson PA</pubmed_authors><pubmed_authors>Maxwell B</pubmed_authors><pubmed_authors>Halin NJ</pubmed_authors><pubmed_authors>Patel N</pubmed_authors><pubmed_authors>Abebe KZ</pubmed_authors><pubmed_authors>Hitchcock S</pubmed_authors><pubmed_authors>Braun WE</pubmed_authors><pubmed_authors>Steinman TI</pubmed_authors><pubmed_authors>Perkins L</pubmed_authors><pubmed_authors>Spirko R</pubmed_authors><pubmed_authors>Pedrosa I</pubmed_authors><pubmed_authors>Perrone RD</pubmed_authors><pubmed_authors>Flynn G</pubmed_authors><pubmed_authors>Martin DR</pubmed_authors><pubmed_authors>Woltman R</pubmed_authors><pubmed_authors>Watkins D</pubmed_authors><pubmed_authors>Fishman M</pubmed_authors><pubmed_authors>Ondler H</pubmed_authors><pubmed_authors>Jolley A</pubmed_authors><pubmed_authors>Erfort A</pubmed_authors><pubmed_authors>Glockner J</pubmed_authors><pubmed_authors>Smith P</pubmed_authors><pubmed_authors>Lanza P</pubmed_authors><pubmed_authors>Meyers CM</pubmed_authors><pubmed_authors>Wetzel LH</pubmed_authors><pubmed_authors>Oskoui FR</pubmed_authors><pubmed_authors>Morgan P</pubmed_authors><pubmed_authors>Simon G</pubmed_authors><pubmed_authors>Hogan MC</pubmed_authors><pubmed_authors>Miller JP</pubmed_authors><pubmed_authors>Driggs J</pubmed_authors><pubmed_authors>Schrier RW</pubmed_authors></additional><is_claimable>false</is_claimable><name>Analysis of baseline parameters in the HALT polycystic kidney disease trials.</name><description>HALT PKD consists of two ongoing randomized trials with the largest cohort of systematically studied patients with autosomal dominant polycystic kidney disease to date. Study A will compare combined treatment with an angiotensin-converting inhibitor and receptor blocker to inhibitor alone and standard compared with low blood pressure targets in 558 early-stage disease patients with an eGFR over 60 ml/min per 1.73 m(2). Study B will compare inhibitor-blocker treatment to the inhibitor alone in 486 late-stage patients with eGFR 25-60 ml/min per 1.73 m(2). We used correlation and multiple regression cross-sectional analyses to determine associations of baseline parameters with total kidney, liver, or liver cyst volumes measured by MRI in Study A and eGFR in both studies. Lower eGFR and higher</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Mar</publication><modification>2025-04-18T17:02:55.533Z</modification><creation>2019-03-26T23:05:23Z</creation></dates><accession>S-EPMC3580956</accession><cross_references><pubmed>22205355</pubmed><doi>10.1038/ki.2011.411</doi></cross_references></HashMap>