ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: PUB115

Effect of SGLT2 Inhibitor Therapy on Urinary Podocyte Markers in Diabetic Kidney Disease

Session Information

Category: Diabetic Kidney Disease

  • 702 Diabetic Kidney Disease: Clinical

Authors

  • Li, Chuanlei, Departments of Medicine & Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong
  • Szeto, Cheuk-Chun, Departments of Medicine & Therapeutics, Prince of Wales Hospital, Hong Kong, Hong Kong
Background

Sodium glucose cotransporter 2 inhibitor (SGLT2i) is a standard treatment for kidney and cardiovascular protection in diabetic kidney disease (DKD). Previous studies suggested that urinary level of podocyte-associated molecules may predict the progression of DKD. We determined the effect of SGLT2i on the urinary podocyte-associated molecules levels in patients with DKD.

Methods

We studied 24 DKD patients who were started on SGLT2i treatment and 25 patients who were not treated (control group). Urinary levels of podocyte-associated molecules, their corresponding mRNA levels in urinary sediment, estimated glomerular filtration rate (eGFR), and urine albumin-creatinine ratio (UACR) were measured at baseline and then again at 3 months.

Results

Urinary levels of podocin, podocalyxin, nephrin and synaptopodin did not change from baseline to 3 months in the SGLT2i treatment group. However, in the control group, urinary podocin, podocalyxin, and synaptopodin levels increased from (4.63 ± 4.84 to 18.49 ± 22.22 ng/μmol-Cr, 489.75 ± 480.62 to 1399.53 ± 1265.27 ng/mmol-Cr, and 38.61 ± 42.56 to 78.50 ± 85.61 ng/μmol-Cr, p = 0.0006, 0.0002, and 0.03, respetively) over 3 months, while unriary nephrin level did not change significantly. Urinary sediment podocin, podocalyxin, nephrin and synaptopodin mRNA levels did not change from baseline to 3 months in control and SGLT2i treatment groups. There were no significant correlations between urinary podocyte-associated marker levels and eGFR and UACR at baseline, and there was no significant correlation between urinary sediment mRNA levels of nephrin, podocin, podocalyxin, synaptopodin and eGFR or UACR at baseline. After 3-month treatment, podocalyxin mRNA level had a significant inverse correlation with eGFR (r = -0.392, p = 0.009) but not UACR. In the control group, the change in podocalyxin (r = -0.389, p = 0.017) and nephrin (r = -0.471, p = 0.010) mRNA level had significant inverse correlations with the change in eGFR and UACR, respectively.

Conclusion

SGLT2i has a small but significant effect on preventing the progressive rise in urinary podocyte-associated molecule levels but not sediment mRNA level. Our result suggests that SGLT2i therapy may affect podocyte function in DKD.