Introduction and Objective: Type 1 diabetes (T1D) leads to vascular complications including chronic kidney disease (CKD) and major adverse cardiovascular events (MACE). Patients with T1D are at high risk for developing CKD, but contemporary data on the natural history of kidney function decline and the effect of therapies on slowing eGFR decline in T1D-related CKD are limited. We conducted a scoping review to describe the natural trajectory of kidney function and its effects in individuals with T1D in the United States (US). Methods: In our scoping review of observational studies and grey literature, we searched EMBASE (Ovid), CINAHL (EBSCO), MEDLINE (Ovid), SCOPUS (Elsevier), Global Health (Ovid), and the Food and Drug Administration from inception to April 25, 2025. The study population included adults (age ≥18 years) with T1D in the US. Our outcomes were change in eGFR and UACR, MACE (myocardial infarction, ischemic stroke, or cardiovascular death), and healthcare resource utilization (HCRU). We screened 6437 unique abstracts and selected 30 texts that matched our criteria. Results: In one cohort, 50% of individuals with T1D developed moderately increased albuminuria (UACR 30-299 mg/g) after 20 years and two cohort studies in T1D observed a progressive annual eGFR decline of 3 ml/min/1. 73 m2. Five cohort studies found higher proportions of individuals with T1D experienced MACE or kidney failure compared to those without T1D. Cross-sectional studies estimated total annual cost of HRCU at 17-27. 8 billion for those with T1D with annual per-patient costs ranging from 73, 534-112, 833 for kidney failure and 40, 889-86, 417 for components of MACE. Conclusion: Patients with T1D have a faster progression of kidney disease, higher rates of MACE, and higher healthcare costs compared to the general population. A clearer understanding of the natural trajectory of the loss of kidney function in patients with T1D would help providers and policy makers understand the long-term impact potential therapies to treat T1D-related CKD may have on reducing the risk of kidney failure, MACE, and HCRU. Disclosure F. Co: None. R. Whitlock: None. S. Leon: None. A. Katta: Employee; Current; Bayer AG. C. Aldworth: Employee; Current; Bayer AG. Employee; Ended; Novartis AG. J. Mares: Employee; Ended; Bayer AG. Employee; Current; AstraZeneca. Z. Zheng: Employee; Current; Bayer AG. M. Beller Ferri: Employee; Current; Bayer AG. Employee; Ended; Bristol-Myers Squibb Company. N. Askin: None. N. Tangri: Other - Grant/contracts, consulting fees, honoraria; Current; Bayer AG. Other - Grant/contracts, consulting fees, honoraria, committee; Current; AstraZeneca, Otsuka Pharmaceutical Co. , Ltd. , Eli Lilly and Company. Other - consulting fees, honoraria, committee; Current; Boehringer Ingelheim International GmbH. Consultant; Current; GSK, Prokidney. Other - honoraria; Current; Roche Canada. Other - consulting fees, honoraria; Current; Vera Theraupetics. Other - Leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid; Current; National Kidney Foundation. Funding The Seven Oaks Hospital Chronic Disease Innovation Centre received funding provided by Bayer U. S to conduct the research and final report. Applicable journal processing charges or open access are funded by Bayer U. S.
CO et al. (Fri,) studied this question.