{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,9]],"date-time":"2025-09-09T22:02:35Z","timestamp":1757455355849,"version":"3.37.3"},"reference-count":25,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2016,5,11]],"date-time":"2016-05-11T00:00:00Z","timestamp":1462924800000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100003921","name":"Australian Government Department of Health","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100003921","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Internal Medicine Journal"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:p>Current guidelines recommend renin angiotensin system inhibitors (<jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content>) as key components of treatment of hypertension in patients with chronic kidney disease (<jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content>), because of their effect on reducing the future rate of loss of glomerular filtration rate (<jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content>). A common risk of <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content> in <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> is a haemodynamically mediated, and reversible, fall in <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> of varying severity and duration, any time after commencement of the Inhibitors. A benefit of the acute reduction in filtration rate with <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content> may be a reduction in the future rate of loss in <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content>: the greatest benefit likely to be in those patients with a greater rate of loss of <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> prior to, and a lesser acute loss of <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> after, introduction of <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content>; and in those patients with significant proteinuria. An acute loss of <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> of &gt;25% following the introduction of <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content> is an indication to cease the <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content>. An acute loss of <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> &lt; 25% requires consideration of the likely risks of the lower <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> and benefits of any future reduced rate of loss of <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content>. A fall in <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> in patients while on <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content> is usually associated with a remediable cause. When the cause for the fall in <jats:styled-content style=\"fixed-case\">GFR<\/jats:styled-content> is not revealed, and the fall is less than 25%, hopeful expectancy is recommended. Hyperkalaemia in patients with <jats:styled-content style=\"fixed-case\">CKD<\/jats:styled-content> on <jats:styled-content style=\"fixed-case\">RASI<\/jats:styled-content> is more common with more severe disease, potassium retaining diuretics and hypoaldosteronism. Treatment should be modified to maintain a plasma potassium &lt;6 mmol\/L.<\/jats:p>","DOI":"10.1111\/imj.13060","type":"journal-article","created":{"date-parts":[[2016,5,12]],"date-time":"2016-05-12T04:44:24Z","timestamp":1463028264000},"page":"626-630","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Use of renin angiotensin system inhibitors in patients with chronic kidney disease"],"prefix":"10.1111","volume":"46","author":[{"given":"W. R.","family":"Adam","sequence":"first","affiliation":[{"name":"Department of Rural Health, Melbourne Medical School University of Melbourne  Melbourne Victoria Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J. R.","family":"Wright","sequence":"additional","affiliation":[{"name":"Department of Rural Health, Melbourne Medical School University of Melbourne  Melbourne Victoria Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2016,5,11]]},"reference":[{"key":"e_1_2_9_2_1","unstructured":"V Mabbott M Robinson A Segrave 2011"},{"key":"e_1_2_9_3_1","unstructured":"PhoonR JohnsonD. Medical therapies to reduce chronic kidney disease progression and cardiovascular risk: anti\u2010hypertensive agents. Melbourne: Kidney Health Australia;2012. CARI Guidelines [cited 2016 Mar 27]. 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