{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T06:44:20Z","timestamp":1775025860822,"version":"3.50.1"},"reference-count":41,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T00:00:00Z","timestamp":1775001600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Residual kidney risk persists in hypertensive patients despite guideline-directed blood pressure (BP) management. Whether systemic inflammation is preferentially associated with the development of distinct early chronic kidney disease (CKD) phenotypes remains uncertain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This retrospective cohort study included 5,904 hypertensive patients with preserved baseline kidney function. The primary exposure was the C-reactive protein-to-lymphocyte ratio (CLR). Outcomes assessed were incident proteinuric CKD, isolated estimated glomerular filtration rate (eGFR) decline, and any incident CKD. Phenotype-specific associations were evaluated using multivariable cause-specific Cox models. We additionally assessed the additive interaction between CLR and BP control, and evaluated the incremental predictive value of CLR beyond traditional risk factors.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>During a median follow-up of 34.1 months, 598 participants developed proteinuric CKD, 89 developed isolated eGFR decline, and 728 developed any incident CKD. Higher CLR was independently associated with proteinuric CKD (per 1-SD: HR 1.14, 95% CI 1.05\u20131.24; highest vs lowest quartile: HR 1.46, 95% CI 1.15\u20131.85) and any incident CKD (per 1-SD: HR 1.13, 95% CI 1.05\u20131.22), but not with isolated eGFR decline (per 1-SD: HR 1.05, 95% CI 0.85\u20131.29). A significant additive interaction emerged between high CLR and uncontrolled BP (RERI 0.30), synergistically amplifying renal risk. Adding CLR to traditional risk models significantly improved risk reclassification (NRI 0.083, P\u00a0=\u00a00.008).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>In hypertensive patients, elevated CLR preferentially predicts new-onset proteinuria over isolated eGFR decline. As an accessible biomarker for renal risk stratification, CLR can identify patients requiring vigilant proteinuria surveillance and comprehensive management, particularly those with uncontrolled BP.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fendo.2026.1769059","type":"journal-article","created":{"date-parts":[[2026,4,1]],"date-time":"2026-04-01T04:49:30Z","timestamp":1775018970000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Phenotype-specific association of C-reactive protein-to-lymphocyte ratio with incident proteinuric CKD versus isolated eGFR decline: a real-world retrospective cohort study"],"prefix":"10.3389","volume":"17","author":[{"given":"Wenbo","family":"Yang","sequence":"first","affiliation":[{"name":"Graduate School, Xinjiang Medical University","place":["Urumqi, Xinjiang, 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