{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T15:52:10Z","timestamp":1791388330245,"version":"4.3.3"},"reference-count":45,"publisher":"American Medical Association (AMA)","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Netw Open"],"abstract":"\n Importance<\/jats:title>\n Real-time continuous glucose monitoring (rtCGM) improves short-term glycemic control in diabetes. However, scant evidence exists regarding rtCGM\u2019s longer-term benefits for glycemia or kidney health.<\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To evaluate whether rtCGM initiation and sustained use is associated with improved glycemic control and kidney markers in high-risk adults with type 2 diabetes (T2D).<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n \n This comparative effectiveness research study compared glycemic control and kidney markers among high-risk adults with T2D initiating and sustaining use of rtCGM (rtCGM arm) vs no initiation (controls) using inverse probability\u2013weighted marginal structural models to estimate per-protocol outcomes of an emulated target trial. Target trial eligibility criteria were as follows: age of 19 years or older, T2D, no prior CGM use, and poor glycemic control (hemoglobin A\n 1c<\/jats:sub>\n [HbA\n 1c<\/jats:sub>\n ] &amp;gt;8%) or emergency department or inpatient treatment for hypoglycemia. Baseline was defined by the rtCGM initiation date and applied to temporally matched CGM-naive controls who met the eligibility criteria, sampled monthly from risk sets from January 1, 2015, to June 30, 2023. Data were censored at nonadherence to the target trial protocol (eg, rtCGM arm discontinued use or controls initiated CGM), coverage gaps, death, or after 36 months of follow-up. Data analysis was performed July 2025 to March 2026.\n <\/jats:p>\n <\/jats:sec>\n \n Exposure<\/jats:title>\n rtCGM use.<\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n \n Cumulative differences for HbA\n 1c<\/jats:sub>\n , urinary albumin-creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR).\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n The study included 25\u202f648 individuals (2771 in the rtCGM arm and 22\u202f877 in the control arm) who were target trial eligible (mean [SD] age, 61.5 [13.1] years; 13\u202f885 [54.7%] male). The mean (SD) baseline HbA\n 1c<\/jats:sub>\n level was 9.5% (1.5%). After 36 months of follow-up, the rtCGM arm had an approximately 0.8\u2013percentage point lower HbA\n 1c<\/jats:sub>\n level than controls (7.83% [95% CI, 7.55%-8.11%] vs 8.58% [95% CI, 8.49%-8.66%],\n P<\/jats:italic>\n \u2009&amp;lt;\u2009.001). There was substantial attrition during follow-up; 1228 (44.3%) in the rtCGM arm were censored due to discontinuation and 4284 (18.7%) in the control group were censored due to CGM initiation. There were no significant differences in UACR between arms initially; however, by the end of 36 months, rtCGM initiators had a UACR of 125.3 mg\/g (95% CI, \u2212196.6 to \u221254.0 mg\/g;\n P<\/jats:italic>\n \u2009=\u2009.001) lower than that of controls. There were no differences in eGFR during follow-up.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n In this comparative effectiveness study using a target trial emulation, sustained, longer-term use of rtCGM was associated with durable improvements in glycemic control and later regression of UACR. By addressing glycemic deterioration, rtCGM may extend the time before pharmacologic escalation is required and potentially delay diabetic kidney disease progression.<\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamanetworkopen.2026.37698","type":"journal-article","created":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T15:00:38Z","timestamp":1791385238000},"page":"e2637698","source":"Crossref","is-referenced-by-count":0,"title":["Continuous Glucose Monitoring and Long-Term Glycemic and Kidney Outcomes"],"prefix":"10.1001","volume":"9","author":[{"given":"Andrew J.","family":"Karter","sequence":"first","affiliation":[{"name":"Division of Research, Kaiser Permanente, Pleasanton, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melissa M.","family":"Parker","sequence":"additional","affiliation":[{"name":"Division of Research, Kaiser Permanente, Pleasanton, 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