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Participants with consistently hyperuricemia, hypouricemia, or normouricemia (7\u00a0mg\/dL\u2009\u2265\u2009SUA\u2009&gt;\u20093\u00a0mg\/dL) throughout follow-up were categorized as consistent hyperuricemia (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200936), consistent hypouricemia (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20098) and normouricemia (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009759), respectively. Others were classified as transient hyperuricemia (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009282) and transient hypouricemia (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200957). Annualized eGFR decline was compared using ANOVA, and incident CKD stage 3 events were evaluated using \u03c7\u00b2 or Fisher\u2019s exact tests. Multivariable analyses were performed to examine the association between baseline SUA and subsequent renal outcomes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Hyperuricemia was positively associated with obesity, liver dysfunction, dyslipidemia, and higher baseline eGFR compared with normouricemia, whereas hypouricemia showed negative associations with obesity and liver dysfunction. Transient hyperuricemia was significantly associated with obesity, liver dysfunction, and dyslipidemia relative to consistent normouricemia, while transient hypouricemia was negatively associated with obesity and liver dysfunction. Transient hyperuricemia exhibited significantly faster annual eGFR decline than normouricemia, while transient hypouricemia showed no significant difference. Baseline SUA\u2009\u2265\u20097\u00a0mg\/dL was associated with higher baseline eGFR but predicted a significantly faster subsequent eGFR decline. In multivariable linear regression, baseline SUA level was independently associated with eGFR change, whereas baseline SUA status did not independently predict incident CKD stage 3.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Transient hyperuricemia, rather than transient hypouricemia, is associated with accelerated eGFR decline in healthy individuals. Baseline SUA provides prognostic information regarding renal function trajectory, but does not independently predict CKD stage 3, suggesting that SUA should be interpreted as a clinically useful marker of renal vulnerability rather than a proven causal factor.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12882-026-04875-4","type":"journal-article","created":{"date-parts":[[2026,3,6]],"date-time":"2026-03-06T09:39:45Z","timestamp":1772789985000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Differential associations of transient hyperuricemia and transient hypouricemia with annual changes in estimated glomerular filtration rate in healthy participants: an observational study"],"prefix":"10.1186","volume":"27","author":[{"given":"Naoyuki","family":"Otani","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katsuyuki","family":"Tomita","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tomoaki","family":"Takata","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masanari","family":"Kuwabara","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sunao","family":"Kojima","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satoshi","family":"Miyazaki","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuro","family":"Ohta","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ichiro","family":"Hisatome","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,3,6]]},"reference":[{"key":"4875_CR1","doi-asserted-by":"publisher","first-page":"621","DOI":"10.1007\/s10157-009-0199-x","volume":"13","author":"E Imai","year":"2009","unstructured":"Imai E, Horio M, Watanabe T, et al. 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All study procedures adhered to the principles of the Declaration of Helsinki and applicable institutional guidelines. Informed consent was obtained in the form of opt-out. Patient privacy was protected in accordance with the Declaration of Helsinki.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"Naoyuki Otani reports receiving research funding from Sato Pharmaceutical Co., Ltd. Ichiro Hisatome reports receiving honoraria from Fuji Pharma Co., Ltd. and Mochida Pharmaceutical Co., Ltd., and research funding from both companies. Masanari Kuwabara reports receiving research grants from the Japan Society for the Promotion of Science (JSPS KAKENHI; 20K17168 and 23K07493). All other authors declare no conflicts of interest related to the content of this manuscript.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Disclosure statement"}},{"value":"The authors declare no competing interests.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"236"}}