{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T02:02:28Z","timestamp":1793325748354,"version":"4.5.0"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2019,7]]},"abstract":"\n Significance Statement<\/jats:title>\n Soluble urokinase plasminogen activator receptor (suPAR), a marker of inflammation, is also an independent marker for incidence and progression of renal diseases. Mechanistically, it has been shown to activate podocytes in glomerular diseases. In this study, the authors provide the first description linking suPAR levels with disease progression for a major genetic renal disease that mainly affects the extraglomerular compartment, autosomal dominant polycystic kidney disease (ADPKD). They found an association between suPAR levels and height-adjusted total kidney volume, independent of age, sex, race, hypertension, and eGFR. In addition, patients with suPAR levels >2.82 ng\/ml had a 3.38-fold increase in risk of incident ESRD. These findings suggest that suPAR levels may be useful for early identification of patients with ADPKD at high risk of disease progression.<\/jats:p>\n <\/jats:sec>\n \n Background<\/jats:title>\n Levels of soluble urokinase plasminogen activator receptor (suPAR), an inflammation marker, are strongly predictive of incident kidney disease. Patients with autosomal dominant polycystic kidney disease (ADPKD) experience progressive decline in renal function, but rates of decline and outcomes vary greatly. Whether suPAR levels are predictive of declining kidney function in patients with ADPKD is unknown.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n We assessed suPAR levels in 649 patients with ADPKD who underwent scheduled follow-up for at least 3 years, with repeated measurements of height-adjusted total kidney volume and creatinine-derived eGFR. We used linear mixed models for repeated measures and Cox proportional hazards to characterize associations between baseline suPAR levels and follow-up eGFR or incident ESRD.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The median suPAR level was 2.47 ng\/ml and median height-adjusted total kidney volume was 778, whereas mean eGFR was 84 ml\/min per 1.73 m\n 2<\/jats:sup>\n . suPAR levels were associated with height-adjusted total kidney volume (\n \u03b2<\/jats:italic>\n =0.02; 95% confidence interval, 0.01 to 0.03), independent of age, sex, race, hypertension, and eGFR. Patients in the lowest suPAR tertile (<2.18 ng\/ml) had a 6.8% decline in eGFR at 3 years and 22% developed CKD stage 3, whereas those in the highest tertile (suPAR>2.83 ng\/ml) had a 19.4% decline in eGFR at 3 years and 68% developed CKD stage 3. suPAR levels >2.82 ng\/ml had a 3.38-fold increase in the risk of incident ESRD.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n suPAR levels were associated with progressive decline in renal function and incident ESRD in patients with ADPKD, and may aid early identification of patients at high risk of disease progression.<\/jats:p>\n <\/jats:sec>","DOI":"10.1681\/asn.2018121227","type":"journal-article","created":{"date-parts":[[2019,6,6]],"date-time":"2019-06-06T16:05:31Z","timestamp":1559837131000},"page":"1305-1313","source":"Crossref","is-referenced-by-count":30,"title":["Soluble Urokinase Plasminogen Activator Receptor and Decline in Kidney Function in Autosomal Dominant Polycystic Kidney Disease"],"prefix":"10.1681","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0180-349X","authenticated-orcid":false,"given":"Salim S.","family":"Hayek","sequence":"first","affiliation":[{"name":"Division of Cardiology, Department of Medicine, University of Michigan, Ann Arbor Michigan;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas P.","family":"Landsittel","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, University of Pittsburgh, Pittsburgh, Pennsylvania;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Changli","family":"Wei","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rush University Medical Center, Chicago, Illinois;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Zeier","sequence":"additional","affiliation":[{"name":"Division of Nephrology, University of Heidelberg, Heidelberg, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan S.L.","family":"Yu","sequence":"additional","affiliation":[{"name":"Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vicente E.","family":"Torres","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Mayo Clinic, Rochester, Minnesota; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharin","family":"Roth","sequence":"additional","affiliation":[{"name":"Otsuka Pharmaceutical Development & Commercialization, Inc., Rockville, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina S.","family":"Pao","sequence":"additional","affiliation":[{"name":"Otsuka Pharmaceutical Development & Commercialization, Inc., Rockville, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jochen","family":"Reiser","sequence":"additional","affiliation":[{"name":"Department of Medicine, Rush University Medical Center, Chicago, Illinois;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2019,6,6]]},"reference":[{"key":"B1-20230819","doi-asserted-by":"crossref","first-page":"1993","DOI":"10.1016\/S0140-6736(15)60907-2","article-title":"Autosomal dominant polycystic kidney disease: The changing face of clinical management.","volume":"385","author":"Ong","year":"2015","journal-title":"Lancet"},{"key":"B3-20230819","doi-asserted-by":"crossref","first-page":"7","DOI":"10.2215\/CJN.04140510","article-title":"Inflammation, oxidative stress, and insulin resistance in polycystic kidney disease.","volume":"6","author":"Menon","year":"2011","journal-title":"Clin J Am Soc 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