Journal of diabetes investigation · 2026
Dapagliflozin does not impair microvascular hemorheology in type 2 diabetes mellitus: A multicenter randomized controlled trial (D-PATH study).
СтатьяМногоцентровое исследованиеРандомизированное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Nakatani Yuki, Banba Nobuyuki, Ono Shoya, Turumi Tomoki, Hoshiai Megumi, Sugiyama Takushi, Tomoe Takashi, Tamiya Hajime, Otani Naoyuki, Sugimura Hiroyuki, Ikemiyagi Hidekazu, Ohya Yusuke, Yokokawa Koji, Ueda Shinichiro, Aso Yoshimasa, Maejima Yasuhiro, Yasu Takanori
Аннотация
AIMS: Sodium-glucose cotransporter 2 inhibitors reduce cardiovascular and renal events beyond glucose lowering, but their hematocrit-raising effects raise concerns about increased blood viscosity and microvascular impairment. We investigated whether dapagliflozin adversely affects microvascular hemorheology in patients with type 2 diabetes.
MATERIALS AND METHODS: In this multicenter, open-label, randomized controlled trial, 82 adults with type 2 diabetes received dapagliflozin (5 mg/day) or conventional therapy for 16 weeks. The primary endpoint was the change in whole blood passage time (WBPT), measured using a microchannel flow analyzer that simulates precapillary arterioles (7 × 7 μm), with a prespecified noninferiority margin of 6.0 s (15%). Secondary outcomes included apparent microvascular viscosity, adhesive leukocyte count, and oxidative stress markers. Serum erythropoietin (EPO) was evaluated in an ancillary analysis.
RESULTS: WBPT changed minimally in the dapagliflozin group (+1.4 s; 95% CI, 0.0-2.9) and slightly decreased in the control group (-0.6 s; 95% CI, -1.9 to 0.6), yielding a between-group difference of 2.0 s (95% CI, -0.2 to 3.9), with the upper bound below the prespecified noninferiority margin. Microvascular viscosity, hematocrit-standardized viscosity, leukocyte adhesion, and oxidative stress markers remained stable in both groups. Dapagliflozin increased hematocrit and EPO, particularly in participants with lower baseline hematocrit, whereas those with hematocrit >45% showed minimal change.
CONCLUSIONS: Dapagliflozin did not impair microvascular hemorheology despite modest increases in hematocrit and EPO. These findings support the microvascular safety of dapagliflozin and reinforce its role in cardio-renal risk management in type 2 diabetes.
MATERIALS AND METHODS: In this multicenter, open-label, randomized controlled trial, 82 adults with type 2 diabetes received dapagliflozin (5 mg/day) or conventional therapy for 16 weeks. The primary endpoint was the change in whole blood passage time (WBPT), measured using a microchannel flow analyzer that simulates precapillary arterioles (7 × 7 μm), with a prespecified noninferiority margin of 6.0 s (15%). Secondary outcomes included apparent microvascular viscosity, adhesive leukocyte count, and oxidative stress markers. Serum erythropoietin (EPO) was evaluated in an ancillary analysis.
RESULTS: WBPT changed minimally in the dapagliflozin group (+1.4 s; 95% CI, 0.0-2.9) and slightly decreased in the control group (-0.6 s; 95% CI, -1.9 to 0.6), yielding a between-group difference of 2.0 s (95% CI, -0.2 to 3.9), with the upper bound below the prespecified noninferiority margin. Microvascular viscosity, hematocrit-standardized viscosity, leukocyte adhesion, and oxidative stress markers remained stable in both groups. Dapagliflozin increased hematocrit and EPO, particularly in participants with lower baseline hematocrit, whereas those with hematocrit >45% showed minimal change.
CONCLUSIONS: Dapagliflozin did not impair microvascular hemorheology despite modest increases in hematocrit and EPO. These findings support the microvascular safety of dapagliflozin and reinforce its role in cardio-renal risk management in type 2 diabetes.