Association of 14-day continuous glucose monitoring-derived postprandial hyperglycemic area with 6-month change in urinary albumin-to-creatinine ratio in patients with newly diagnosed type 2 diabetes mellitus.

BACKGROUND: Early kidney involvement may already be present at the diagnosis of type 2 diabetes mellitus (T2DM), whereas glycated hemoglobin A1c (HbA1c) and fasting plasma glucose do not fully characterize postprandial exposure. We evaluated the association of continuous glucose monitoring (CGM)-derived postprandial hyperglycemic area (PPHA) with 6-month change in urinary albumin-to-creatinine ratio (UACR) in adults with newly diagnosed T2DM. METHODS: This single-center retrospective study consecutively screened 381 adults with newly diagnosed diabetes who underwent professional CGM from January 1, 2020, to December 31, 2024. After predefined exclusions, 297 participants with valid 14-day CGM and baseline and 6-month UACR measurements were analyzed. PPHA was the daily mean threshold-excess area above 10.0 mmol/L during 0-4 h after each main meal, calculated from valid monitoring days beginning on the first complete day after all components of the initial treatment regimen had been started. The primary outcome was ΔlnUACR [ln(6-month UACR + 1)-ln(baseline UACR + 1)]; exploratory UACR worsening was secondary. Multivariable regression, restricted cubic spline analyses, treatment-interaction analyses, and sensitivity analyses were performed. RESULTS: UACR worsening occurred in 88 participants (29.6%). ΔlnUACR and the frequency of UACR worsening showed an increasing descriptive pattern across PPHA quartiles, with significant overall between-group differences (both P < 0.001). After adjustment for age, sex, body mass index, systolic blood pressure, HbA1c, fasting plasma glucose, estimated glomerular filtration rate, and baseline lnUACR, each 5 mmol·h·L-¹·d-¹ increase in PPHA was associated with a 0.08 higher ΔlnUACR (95% confidence interval [CI], 0.05-0.12; P < 0.001) and higher odds of UACR worsening (odds ratio [OR], 1.73; 95% CI, 1.27-2.36; P < 0.001). The association was approximately linear (P for nonlinearity=0.932), remained directionally consistent after simultaneous adjustment for recorded chronic comorbidities, and showed no statistically significant interaction with initial metformin, insulin, sodium-glucose cotransporter 2 inhibitor, or glucagon-like peptide-1 receptor agonist therapy (all interaction P>0.05). CONCLUSIONS: Higher CGM-derived PPHA was associated with greater 6-month change in UACR after adjustment for fasting plasma glucose and HbA1c. PPHA may complement conventional glycemic measures in early kidney-risk assessment; external validation is required.