Kidney Week

Abstract: PO0784

Effect of Dapagliflozin on Soluble Urokinase-Type Plasminogen Activator Receptor in Type 2 Diabetes with Albuminuria

Session Information

• Diabetic Kidney Disease: Clinical
  November 04, 2021 | Location: On-Demand, Virtual Only
  Abstract Time: 10:00 AM - 12:00 PM

Category: Diabetic Kidney Disease

• 602 Diabetic Kidney Disease: Clinical

Authors

• Rotbain Curovic, Viktor, Steno Diabetes Center Copenhagen, Gentofte, Denmark

Viktor Rotbain Curovic, MD

• Eickhoff, Mie K., Steno Diabetes Center Copenhagen, Gentofte, Denmark

Mie K. Eickhoff,

• Houlind, Morten Baltzer, Clinical Research Centre, Amager Hvidovre University Hospital, Hvidovre, Denmark

Morten Baltzer Houlind,

• Frimodt-Moller, Marie, Steno Diabetes Center Copenhagen, Gentofte, Denmark

Marie Frimodt-Moller,

• Hansen, Tine, Steno Diabetes Center Copenhagen, Gentofte, Denmark

Tine Hansen,

• Eugen-Olsen, Jesper, Clinical Research Centre, Amager Hvidovre University Hospital, Hvidovre, Denmark

Jesper Eugen-Olsen,

• Rossing, Peter, Steno Diabetes Center Copenhagen, Gentofte, Denmark

Peter Rossing,

• Persson, Frederik, Steno Diabetes Center Copenhagen, Gentofte, Denmark

Frederik Persson,

Background

Given the documented protective effect of the sodium-glucose co-transporter 2 inhibitor, dapagliflozin on chronic kidney disease and the potency of soluble urokinase-type plasminogen activator receptor (suPAR) as a risk marker of the same, we investigated the effect of treatment with dapagliflozin on plasma suPAR in individuals with type 2 diabetes and albuminuria. Secondarily, we examined the association between the level of suPAR and the established early urinary proteomic classifier CKD273.

Methods

Post-hoc analysis of a double-blind, cross-over trial where persons with type 2 diabetes and albuminuria received treatment with dapagliflozin (10 mg/d) or placebo for 12 weeks in random order. The original primary outcome was change in the urinary proteomic classifier CKD273. suPAR level was assessed in plasma samples collected at all 3 visits. Effect of dapagliflozin on suPAR level was determined using unpaired t-test for comparison between baseline and end-of-treatment for the dapagliflozin and the placebo treatment period, and paired t-test for comparison between the two treatment periods. A secondary analysis investigated the association between baseline suPAR and CKD273 using Pearson correlation.

Results

Of the 36 persons who completed study, 11% were female, mean±SD age was 64±8 years, HbA_1c 73±15 mmol/mol (8.9±1.4%), eGFR 84±19 ml/min/1.73m², and median (IQR) urinary albumin creatinine ratio was 154 mg/g (94-329). Median (IQR) suPAR at baseline was 3.44 ng/ml (2.49;4.35) and CKD273 score was 0.59 (0.18;0.77). suPAR change after 12 weeks dapagliflozin was -0.13 ng/ml (95% CI -0.72;0.36, p=0.50) and placebo -0.19 ng/ml (-0.71;0.33, p=0.46), mean difference 0.06 ng/ml (95% CI -0.15;0.27, p=0.57). Pearson correlation R between baseline suPAR level and CKD273 score was 0.17 (95% CI -0.17;0.48, p=0.32).

Conclusion

This post-hoc analysis could not demonstrate an effect of 12 weeks of treatment with dapagliflozin on plasma suPAR level in individuals with type 2 diabetes and albuminuria. In addition, plasma suPAR was not correlated to the urinary proteomic CKD273 classifier.