The Differences in CKM Risk Factors Between Patients With Type 1 and Type 2 Diabetes and Potential Challenges to Therapy in These Groups

Objective: To compare cardio-kidney-metabolic (CKM) risk profiles between individuals with type 1 diabetes (T1DM) and type 2 diabetes (T2DM), and to identify diabetes-specific therapeutic challenges affecting CKM risk management.Design and method: This observational analysis evaluated CKM characteristics in adults with T1DM and T2DM, including body mass index, blood pressure, albuminuria, lipid and glycaemic control, age distribution, and completeness of renal surveillance. Blood pressure categories and albuminuria strata were examined to assess suitability for CKM-directed therapies. Availability of BP measurements and urinary albumin-to-creatinine ratio data was assessed to identify gaps in monitoring. Results: CKM profiles differed substantially between diabetes types. Nearly half of T1DM patients (50.6%) had BMI <25 kg/m2, limiting eligibility for weight-loss–directed therapies such as GLP-1 receptor agonists or dual GLP/GIP agonists. Blood pressure control was markedly better in T1DM, with 85.9% achieving systolic BP <130 mmHg compared with 66.1% of T2DM, complicating safe titration of renin–angiotensin system inhibitors (RAS-i) due to risks of hypotension and acute kidney injury. Albuminuria was less prevalent in T1DM (A2/A3: 9.9%) than in T2DM (21.1%), suggesting that early CKM interventions in T1DM may need to precede overt renal involvement. Metabolic target attainment also differed: fewer T1DM patients achieved LDL-cholesterol <1.8 mmol/L or HbA1c <7%. T1DM showed higher rates of missing UACR values, reflecting challenges in routine renal surveillance. T1DM patients were substantially younger (median age 24 years) than those with T2DM (median age 59 years), complicating adherence, monitoring, and long-term treatment continuity. Blood pressure distributions reinforced these differences, with most T1DM individuals in low or normal BP categories, while hypertension was more prevalent in T2DM. Absence of sitting and standing BP measurements precluded assessment of autonomic neuropathy or postural hypotension. Conclusions: CKM risk profiles and therapeutic feasibility differ markedly between T1DM and T2DM. T1DM patients are less suited to GLP/GIP therapies, less amenable to RAS-i titration, and are not recommended SGLT2 inhibitors due to euglycaemic diabetic ketoacidosis risk. T2DM patients demonstrate greater suitability for RAS-i, SGLT2 inhibitors, and finerenone, provided structured monitoring is in place. These findings highlight the need for diabetes-specific CKM strategies and enhanced surveillance systems.