[Objective] The usefulness of the eGFR rate of change (change between first and last eGFR, divided by time; hereafter "change rate") was investigated as a surrogate indicator for eGFR slope (slope), which is a predictor of end-stage renal failure (ESRD). [Methods] The subjects were 305 treatment-naïve patients with type 2 diabetes who visited a single hospital with a baseline eGFR ≥ 30 mL/min/1.73 m². The observation period was 13.4 years. The renal outcome was defined as ESRD (eGFR<15). Using a survival time analysis, the risk of developing ESRD was compared using the slope and change rate. [Results] The slope and change rate were correlated (r=0.812). According to the Cox proportional hazards model, the risk of developing ESRD was suppressed with an increase in slope (HR 0.65) and change rate (HR 0.69) (P <0.001, respectively). In the 62 subjects who were newly diagnosed with stage 3b chronic kidney disease during the observation period, both the slope (adjusted HR 13.5) and change rate (adjusted HR 16.3) independently contributed to the 5-year cumulative incidence of ESRD in the < −5 group. [Conclusion] The change rate was an equivalent risk factor to slope for the development of ESRD, and its usefulness as a surrogate indicator was suggested.

A 72-year-old woman was diagnosed with diabetes and initiated insulin therapy at 50 years of age. Despite multiple daily injection therapy, glycemic control remained suboptimal. At 68 years of age, continuous subcutaneous insulin infusion (CSII) was introduced, but HbA1c rose to 9.0 %, and insulin antibodies were detected (binding rate: 76.9 %). She developed fasting hypoglycemia and postprandial hyperglycemia despite changing insulin preparations. A Scatchard analysis showed antibodies with high binding capacity and low affinity at high-affinity sites, likely contributing to glycemic instability. The antibody characteristics remained unchanged with different insulin formulations, leading to discontinuation of CSII. After stopping CSII, both the antibody profile and glycemic variability gradually improved. These findings suggest that her unstable glycemic patterns were primarily due to insulin autoantibodies resembling those seen in insulin autoimmune syndrome, possibly induced during CSII therapy.

A 45-year-old woman with type 1 diabetes was treated with dapagliflozin and CSII. Diagnosed at 19 years of age, she began CSII at 34 years of age, and switched to a sensor-augmented pump at 40 years of age. Dapagliflozin was added at 44 years of age because she was overweight, but the HbA1c level remained high, leading to hospitalization for insulin adjustment. A fasting test was performed, while dapagliflozin was continued. Her blood glucose level remained stable (85-89 mg/dL over 8 h), but ketone bodies increased significantly; total ketones/3-hydroxybutyrate reached 1982/1569 μmol/L at 8 h. SGLT2 inhibitors may increase the risk of developing DKA in patients with type 1 diabetes. This suggests that prolonged fasting may induce DKA despite adequate basal insulin levels during SGLT2 inhibitor use.