Marcel H A Muskiet, David Z I Cherney
INTRODUCTION: Chronic kidney disease (CKD) affects ~30-40% of people living with type-1 diabetes (T1D) and remains a major driver of cardiovascular morbidity, kidney-failure, and premature mortality. Despite advances in diabetes-technologies, kidney-protective pharmacotherapy in T1D has remained largely unchanged since the introduction of renin-angiotensin-system (RAS)-inhibition >30 years ago. In contrast, CKD-treatment in type-2 diabetes (T2D) has been transformed by sodium-glucose co-transporter (SGLT)-inhibitors, glucagon-like peptide (GLP)-1-based therapies, and nonsteroidal mineralocorticoid receptor antagonists. Exclusion of people with T1D from these pivotal trials created a critical evidence-gap.
AREAS COVERED: We synthesizes mechanistic-/clinical evidence supporting a paradigm shift in kidney-protection for T1D. Literature searches of PubMed/MEDLINE, Embase, Web of Science, and ClinicalTrials.gov identified relevant English-language publications and ongoing studies through March 2026. We describe how the evolving T1D-phenotype, characterized by rising obesity and cardiometabolic dysfunction, strengthening the rationale for therapeutic translation. We critically evaluate current standards-of-care, unmet needs, and the renoprotective potential and safety of SGLT-inhibitors, GLP-1-based therapies, and finerenone in T1D, highlighting the pivotal FINE-ONE trial and albuminuria as a bridging biomarker for regulatory translation.
EXPERT OPINION: CKD-management in T1D is entering a long-overdue phase of therapeutic renewal. Ongoing trials, 'pillar'-strategies, validated surrogate endpoints, precision-medicine, and multidisciplinary care may finally enable meaningful modification of CKD-trajectories.