{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T20:30:32Z","timestamp":1786480232665,"version":"build-2736575974"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2025,1,16]],"date-time":"2025-01-16T00:00:00Z","timestamp":1736985600000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["Kidney360"],"published-print":{"date-parts":[[2025,4]]},"abstract":"<jats:sec>\n                    <jats:title>Key Points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Multiple assays are available to measure calciprotein particles (CPP), but a direct comparison of their association with clinical outcomes is lacking.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Higher levels of high-density CPP and secondary CPP were independently associated with all-cause mortality in a CKD cohort.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Higher levels of low-density CPP, primary CPP, and secondary CPP were each independently associated with progression of CKD.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Mineral metabolism abnormalities are an almost universal feature of CKD and are believed to contribute to the development of many adverse events. Calciprotein particles (CPP) form spontaneously in biological fluids from calcium and phosphate together with the glycoprotein fetuin-A. While CPP formation is a part of normal mineral homeostasis, levels are chronically elevated in CKD. Several assays have been developed to measure serum CPP, each linking high CPP levels to adverse clinical outcomes in CKD. However, direct comparisons among these assays are lacking. The aim of this exploratory study was to compare these assays to assess their association with CKD progression and mortality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We measured baseline CPP levels using various methods on stored serum samples from 189 participants in a prospective observational cohort study of patients with CKD stage 3\/4. Three assays were used to measure CPP: (\n                      <jats:italic toggle=\"yes\">1<\/jats:italic>\n                      ) ELISA (fetuin-A CPP), (\n                      <jats:italic toggle=\"yes\">2<\/jats:italic>\n                      ) low-density CPP (L-CPP) and high-density CPP by gel filtration, and (\n                      <jats:italic toggle=\"yes\">3<\/jats:italic>\n                      ) primary CPP and secondary CPP (CPP-II) by flow cytometry. We examined the association of each CPP measure with all-cause mortality and CKD progression using unadjusted and covariate-adjusted Cox proportional hazard regression models.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In fully adjusted models, high-density CPP (hazard ratio [HR], 1.53; 95% confidence interval [CI], 1.05 to 2.23;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.028) and CPP-II (HR, 3.11; 95% CI, 1.97 to 4.98;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.001) were significantly associated with an increased risk of all-cause mortality. In addition, L-CPP (HR, 1.91; 95% CI, 1.43 to 2.62;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.001), primary CPP (HR, 1.31; 95% CI, 1.04 to 1.65;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.023), and CPP-II (HR, 1.66; 95% CI, 1.20 to 2.29;\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.002) were significantly associated with CKD progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In a cohort of patients with CKD stages 3 and 4, serum CPP-II levels demonstrated the strongest association with all-cause mortality, while L-CPP levels showed the strongest association with CKD progression.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.34067\/kid.0000000700","type":"journal-article","created":{"date-parts":[[2025,1,16]],"date-time":"2025-01-16T12:00:27Z","timestamp":1737028827000},"page":"550-560","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":4,"title":["Simultaneous Measurement of Calciprotein Particles with Different Assays and Clinical Outcomes in CKD"],"prefix":"10.34067","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9348-4638","authenticated-orcid":false,"given":"Mark K.","family":"Tiong","sequence":"first","affiliation":[{"name":"Department of Nephrology, The Royal Melbourne Hospital, Parkville, Victoria, Australia"},{"name":"Department of Medicine (RMH), University of Melbourne, Parkville, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5004-5539","authenticated-orcid":false,"given":"Stephen G.","family":"Holt","sequence":"additional","affiliation":[{"name":"SEHA Kidney Care, Abu Dhabi Health Services Company, Abu Dhabi, United Arab Emirates"},{"name":"Khalifa University, Abu Dhabi, United Arab Emirates"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4926-3189","authenticated-orcid":false,"given":"Martin L.","family":"Ford","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, King's College Hospital NHS Foundation Trust, London, United Kingdom"},{"name":"Faculty of Life Sciences and Medicine, Kings College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edward R.","family":"Smith","sequence":"additional","affiliation":[{"name":"SEHA Kidney Care, Abu Dhabi Health Services Company, Abu Dhabi, United Arab Emirates"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,1,16]]},"reference":[{"issue":"12","key":"B1-20250609","doi-asserted-by":"crossref","first-page":"1370","DOI":"10.1038\/ki.2011.47","article-title":"Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease","volume":"79","author":"Isakova","year":"2011","journal-title":"Kidney Int."},{"issue":"2","key":"B2-20250609","doi-asserted-by":"crossref","first-page":"235","DOI":"10.1053\/j.ajkd.2019.07.022","article-title":"Longitudinal evolution of markers of mineral metabolism in patients with CKD: the chronic renal insufficiency cohort (CRIC) study","volume":"75","author":"Isakova","year":"2020","journal-title":"Am J Kidney Dis."},{"issue":"1","key":"B3-20250609","doi-asserted-by":"crossref","first-page":"7","DOI":"10.1016\/j.kisu.2021.11.003","article-title":"Epidemiology of chronic kidney disease: an update 2022","volume":"12","author":"Kovesdy","year":"2022","journal-title":"Kidney Int Suppl (2011)."},{"issue":"14","key":"B4-20250609","doi-asserted-by":"crossref","first-page":"1823","DOI":"10.1016\/j.jacc.2019.08.1017","article-title":"Chronic kidney disease and coronary artery disease: JACC state-of-the-art review","volume":"74","author":"Sarnak","year":"2019","journal-title":"J Am Coll Cardiol."},{"issue":"12","key":"B5-20250609","doi-asserted-by":"crossref","first-page":"3986","DOI":"10.1016\/j.bpj.2010.10.030","article-title":"Fetuin-A is a mineral carrier protein: small angle neutron scattering provides new insight on Fetuin-A controlled calcification inhibition","volume":"99","author":"Heiss","year":"2010","journal-title":"Biophys J."},{"issue":"34","key":"B6-20250609","doi-asserted-by":"crossref","first-page":"20789","DOI":"10.1074\/jbc.271.34.20789","article-title":"The serum protein alpha2-HS glycoprotein\/fetuin inhibits apatite formation in vitro and in mineralizing calvaria cells. A possible role in mineralization and calcium homeostasis","volume":"271","author":"Schinke","year":"1996","journal-title":"J Biol Chem."},{"issue":"15","key":"B7-20250609","doi-asserted-by":"crossref","first-page":"13333","DOI":"10.1074\/jbc.M210868200","article-title":"Structural basis of calcification inhibition by alpha 2-HS glycoprotein\/fetuin-A. 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