{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T01:32:30Z","timestamp":1791855150224,"version":"4.3.4"},"reference-count":17,"publisher":"S. Karger AG","issue":"4","license":[{"start":{"date-parts":[[2011,2,16]],"date-time":"2011-02-16T00:00:00Z","timestamp":1297814400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2011,2,16]],"date-time":"2011-02-16T00:00:00Z","timestamp":1297814400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nephron Clin Pract"],"abstract":"<i>Introduction:<\/i> Chronic kidney disease (CKD) is a progressive disease leading to loss of glomerular filtration rate (\u0394GFR, measured in ml\/min\/1.73 m<sup>2<\/sup>\/year). \u0394GFR is usually assumed to be constant, but the hyperfiltration theory suggests that it accelerates in severe uraemia. A retrospective analysis of estimated GFR (eGFR) calculated from the Modification of Diet in Renal Disease equation was performed to evaluate whether \u0394GFR is constant or accelerating. <i>Methods:<\/i> 1,441 patients attending a nephrology clinic over a 21-year period, with an initial eGFR <60 ml\/min\/1.73 m<sup>2<\/sup> and an observation period \u22672 years, were included. eGFR was calculated from all creatinine measurements. 420 patients developed end-stage renal disease (ESRD). First- and second-order polynomial regression analysis of eGFR against time was performed for each patient individually. Patients had accelerating uraemia progression if the second-order term coefficient was negative. <i>Results:<\/i> The initial eGFR was 30.8 \u00b115.1 ml\/min\/1.73 m<sup>2<\/sup>. The second-order coefficient was median \u20130.15 ml\/min\/1.73 m<sup>2<\/sup>\/year<sup>2<\/sup> (interquartile range \u20130.92, +0.34). Significantly more patients had an accelerating loss (62%, p < 0.001). Acceleration was mainly seen when eGFR was <30 ml\/min. \u0394GFR was mean 1.47 \u00b1 4.5 ml\/min\/1.73 m<sup>2<\/sup>\/year (male 1.67, female 1.22). ESRD patients lost 5.4 \u00b1 5.4 ml\/min\/year\/1.73 m<sup>2<\/sup> during the last year before ESRD. Accelerating loss was seen for all diagnoses except polycystic disease. Diagnoses with higher \u0394GFR were polycystic renal disease (3.3 ml\/min\/1.73 m<sup>2<\/sup>\/year), hypertensive nephropathy (2.1 ml\/min\/1.73 m<sup>2<\/sup>\/year) and diabetic nephropathy (2.6 ml\/min\/ 1.73 m<sup>2<\/sup>\/year). There was no evidence of improvement in overall uraemia progression during the period of observation. <i>Conclusions:<\/i> Uraemia progression in CKD stages 3\u20135 is not linear, but shows an accelerating trend. This suggests that hyperfiltration mechanisms play a role in CKD progression. ESRD cannot thus be predicted from previous \u0394GFR alone.<\/jats:p>","DOI":"10.1159\/000323391","type":"journal-article","created":{"date-parts":[[2011,2,18]],"date-time":"2011-02-18T15:56:52Z","timestamp":1298044612000},"page":"c367-c374","source":"Crossref","is-referenced-by-count":10,"title":["Uraemia Progression in Chronic Kidney Disease Stages 3\u20135 Is Not Constant"],"prefix":"10.1159","volume":"118","author":[{"given":"James Goya","family":"Heaf","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leif Spange","family":"Mortensen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2011,2,16]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","DOI":"10.1016%2F0140-6736%2891%2992977-A"},{"key":"ref2","doi-asserted-by":"publisher","DOI":"10.1056%2FNEJMoa053107"},{"key":"ref3","doi-asserted-by":"publisher","DOI":"10.1056%2FNEJM199403313301301"},{"key":"ref4","doi-asserted-by":"publisher","DOI":"10.1016%2Fj.amjcard.2004.10.008"},{"key":"ref5","doi-asserted-by":"publisher","DOI":"10.1056%2FNEJM199604113341502"},{"key":"ref6","doi-asserted-by":"publisher","DOI":"10.1111%2Fj.1523-1755.2005.09712.x"},{"key":"ref7","doi-asserted-by":"publisher","DOI":"10.1084%2Fjem.123.5.829"},{"key":"ref8","doi-asserted-by":"publisher","DOI":"10.1093%2Fndt%2Fgfg549"},{"key":"ref9","doi-asserted-by":"publisher","DOI":"10.1097%2FMNH.0b013e328335f9f4"},{"key":"ref10","doi-asserted-by":"publisher","DOI":"10.1093%2Fndt%2Fgfp391"},{"key":"ref11","doi-asserted-by":"publisher","DOI":"10.1056%2FNEJMoa021778"},{"key":"ref12","doi-asserted-by":"publisher","DOI":"10.1093%2Fndt%2F14.10.2392"},{"key":"ref13","doi-asserted-by":"publisher","DOI":"10.1001%2Fjama.288.19.2421"},{"key":"ref14","doi-asserted-by":"publisher","DOI":"10.1093%2Fndt%2F13.6.1430"},{"key":"ref15","doi-asserted-by":"publisher","DOI":"10.1093%2Fndt%2F14.8.1889"},{"key":"ref16","doi-asserted-by":"publisher","DOI":"10.1681%2FASN.2008111205"},{"key":"ref17","doi-asserted-by":"publisher","DOI":"10.1097%2F01.ASN.0000146688.74084.A3"}],"container-title":["Nephron Clinical Practice"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/323391","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/323391","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T19:21:03Z","timestamp":1745436063000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000323391"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2011,2,16]]},"references-count":17,"journal-issue":{"issue":"4","published-online":{"date-parts":[[2011,7,1]]},"published-print":{"date-parts":[[2011,7,29]]}},"URL":"https:\/\/doi.org\/10.1159\/000323391","archive":["Portico"],"relation":{},"ISSN":["1660-2110"],"issn-type":[{"value":"1660-2110","type":"electronic"}],"subject":[],"published":{"date-parts":[[2011,2,16]]}}}