<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18</volume><submitter>Zubidat D</submitter><pubmed_abstract>ADPKD is caused by pathogenic variants in &lt;i>PKD1&lt;/i> or &lt;i>PKD2&lt;/i>, encoding polycystin-1 and -2 proteins. Polycystins are expressed in osteoblasts and chondrocytes in animal models, and loss of function is associated with low bone mineral density (BMD) and volume. However, it is unclear whether these variants impact bone strength in ADPKD patients. Here, we examined BMD in ADPKD after kidney transplantation (KTx). This retrospective observational study retrieved data from adult patients who received a KTx over the past 15 years. Patients with available dual-energy X-ray absorptiometry (DXA) of the hip and/or lumbar spine (LS) post-transplant were included. ADPKD patients (n = 340) were matched 1:1 by age (±2 years) at KTx and sex with non-diabetic non-ADPKD patients (n = 340). Patients </pubmed_abstract><journal>Bone reports</journal><pagination>101655</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9842864</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Bone health in autosomal dominant polycystic kidney disease (ADPKD) patients after kidney transplantation.</pubmed_title><pmcid>PMC9842864</pmcid><pubmed_authors>Madsen CD</pubmed_authors><pubmed_authors>Zoghby ZM</pubmed_authors><pubmed_authors>Hanna C</pubmed_authors><pubmed_authors>Senum SR</pubmed_authors><pubmed_authors>Kaidbay DN</pubmed_authors><pubmed_authors>Broski SM</pubmed_authors><pubmed_authors>Issa NS</pubmed_authors><pubmed_authors>Smith BH</pubmed_authors><pubmed_authors>Mkhaimer YG</pubmed_authors><pubmed_authors>Harris PC</pubmed_authors><pubmed_authors>Zubidat D</pubmed_authors><pubmed_authors>Chedid M</pubmed_authors><pubmed_authors>Torres VE</pubmed_authors><pubmed_authors>Sfeir JG</pubmed_authors><pubmed_authors>Neal RM</pubmed_authors><pubmed_authors>Nardelli L</pubmed_authors><pubmed_authors>Gregory AV</pubmed_authors><pubmed_authors>Randhawa AK</pubmed_authors><pubmed_authors>Kline TL</pubmed_authors><pubmed_authors>Chebib FT</pubmed_authors></additional><is_claimable>false</is_claimable><name>Bone health in autosomal dominant polycystic kidney disease (ADPKD) patients after kidney transplantation.</name><description>ADPKD is caused by pathogenic variants in &lt;i>PKD1&lt;/i> or &lt;i>PKD2&lt;/i>, encoding polycystin-1 and -2 proteins. Polycystins are expressed in osteoblasts and chondrocytes in animal models, and loss of function is associated with low bone mineral density (BMD) and volume. However, it is unclear whether these variants impact bone strength in ADPKD patients. Here, we examined BMD in ADPKD after kidney transplantation (KTx). This retrospective observational study retrieved data from adult patients who received a KTx over the past 15 years. Patients with available dual-energy X-ray absorptiometry (DXA) of the hip and/or lumbar spine (LS) post-transplant were included. ADPKD patients (n = 340) were matched 1:1 by age (±2 years) at KTx and sex with non-diabetic non-ADPKD patients (n = 340). Patients </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jun</publication><modification>2025-04-04T08:29:09.41Z</modification><creation>2025-04-04T08:29:09.41Z</creation></dates><accession>S-EPMC9842864</accession><cross_references><pubmed>36659900</pubmed><doi>10.1016/j.bonr.2023.101655</doi></cross_references></HashMap>