{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T17:54:31Z","timestamp":1778262871044,"version":"3.51.4"},"reference-count":50,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2009,9,3]],"date-time":"2009-09-03T00:00:00Z","timestamp":1251936000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Ann Clin Biochem"],"published-print":{"date-parts":[[2009,11]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Random urine protein-to-creatinine (PCR) and albumin-to-creatinine (ACR) ratios have been proposed as alternatives to 24 h urine measurements to simplify sample collection and overcome errors. The aim of this study was to examine the ability of PCR and ACR to predict urinary 24 h protein and albumin loss, respectively, in patients with kidney disease, and determine the most appropriate time of collection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Eighty-three patients were recruited from a renal outpatient clinic. In a 24 h period, each collected an early-morning urine (EMU), second and third voids, and the remaining urine passed that day. PCR and ACR were determined in random urines and compared with the 24 h loss of protein and albumin, respectively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      For all patients, median (range) 24 h urine protein and albumin losses were 220 (30\u201315600) and 60 (&lt;8\u201310,557) mg, respectively. Ratios derived from each of three random urines correlated well with 24 h protein or albumin loss (Spearman's r\n                      <jats:sub>s<\/jats:sub>\n                      &gt; 0.87, P &lt; 0.0001). Receiver operator characteristic (ROC) curve analysis showed PCR accurately predicted both an abnormal 24 h urine protein \u2265150 mg\/24 h (areas under curves [AUC] 0.90\u20130.92) and significant proteinuria above 300 mg\/24 h (AUC between 0.97 and 1.00). ACR accurately predicted both an abnormal 24 h urine albumin \u226530 mg\/24 h (AUC 0.98 to 0.99) and frank albuminuria at \u2265300 mg\/24 h or \u2265700 mg\/24 h (AUC between 0.99 and 1.00). EMU and random urines performed equally well in predicting proteinuria and albuminuria from PCR and ACR, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>By careful choice of cut-offs, both PCR and ACR can be used in patients with kidney disease to rule in or rule out abnormal 24 h losses of protein and albumin. EMU and, importantly, random samples can be used as surrogates for 24 h urine collections.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1258\/acb.2009.009001","type":"journal-article","created":{"date-parts":[[2009,9,3]],"date-time":"2009-09-03T21:49:58Z","timestamp":1252014598000},"page":"468-476","source":"Crossref","is-referenced-by-count":49,"title":["Protein and albumin-to-creatinine ratios in random urines accurately predict 24 h protein and albumin loss in patients with kidney disease"],"prefix":"10.1177","volume":"46","author":[{"given":"Mark","family":"Guy","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, Salford Royal NHS Foundation Trust, Hope Hospital, Salford"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanna K","family":"Borzomato","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, Salford Royal NHS Foundation Trust, Hope Hospital, Salford"},{"name":"Present address: Department of Clinical Biochemistry, Royal Albert Edward Infirmary, Wigan, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ronald G","family":"Newall","sequence":"additional","affiliation":[{"name":"Highover Park, Amersham, Bucks"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Philip A","family":"Kalra","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, Salford Royal NHS Foundation Trust, Salford"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christopher P","family":"Price","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, University of Oxford, Oxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2009,9,3]]},"reference":[{"key":"bibr-ACB-09-001C1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199811123392007"},{"key":"bibr-ACB-09-001C2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1997.2"},{"key":"bibr-ACB-09-001C3","doi-asserted-by":"publisher","DOI":"10.1053\/ajkd.2001.20732"},{"key":"bibr-ACB-09-001C4","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00874.x"},{"key":"bibr-ACB-09-001C5","doi-asserted-by":"publisher","DOI":"10.1007\/s11886-002-0106-5"},{"key":"bibr-ACB-09-001C6","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM198402093100605"},{"key":"bibr-ACB-09-001C7","doi-asserted-by":"publisher","DOI":"10.1161\/01.CIR.0000031732.78052.81"},{"key":"bibr-ACB-09-001C8","doi-asserted-by":"publisher","DOI":"10.1038\/sj.jhh.1001316"},{"key":"bibr-ACB-09-001C9","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-139-2-200307150-00013"},{"key":"bibr-ACB-09-001C10","doi-asserted-by":"publisher","DOI":"10.1111\/j.1523-1755.2005.00365.x"},{"key":"bibr-ACB-09-001C11","unstructured":"Joint Speciality Committee for Renal Disease. 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