Abstract: FR-PO0524
Urinary Kallistatin as a Novel Biomarker and Independent Predictor of Cardiorenal outcomes in Patients with Type 2 Diabetes and CKD
Session Information
- CKM: Clinical - Trials, Epidemiology, and Biomarkers
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Cardiovascular-Kidney-Metabolic Health
- 602 Cardiovascular-Kidney-Metabolic Health: Clinical
Authors
- Tang, Sydney, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Yiu, Wai Han, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Lam, Derek Kong, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Tang, Arthur Ho Cheung, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Lie, Davina Ngoi Wah, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Chan, Gary Chi Wang, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Tan, Kathryn, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
- Lai, Kar Neng, The University of Hong Kong Li Ka Shing Faculty of Medicine, Hong Kong, Hong Kong
Background
Vascular complication is prevalent in diabetes. Kallistatin, an endogenous vasodilator with anti- angiogenesis, inflammation, fibrosis, oxidative stress and apoptosis effect is a key innate immunity marker for diabetes in experimental models.
Methods
To investigate the association between baseline serum/urinary kallistatin levels and subsequent cardiorenal outcomes including longitudinal change in kidney function among patients with diabetes and CKD, we included a retrospective cohort of 336 adult patients from combined prospective cohorts recruited for DKD clinical trials in Hong Kong since 2015. Serum and urine kallistatin levels were measured by ELISA. The primary outcome was a cardiorenal composite of MACE (myocardial infarction, coronary revascularization, stroke and hospitalized heart failure) and MAKE (initiation of kidney replacement therapy, doubling of serum creatinine, kidney failure and all-cause mortality).
Results
During a median of 2.9 years’ follow-up, higher baseline urinary kallistatin-to-creatinine ratio (KCR) (upper 25%, equivalent cut-off: 1717.1 ng/mmol) was associated with a higher incidence (per 1000 person-years) of cardiorenal (175.5 vs 55), MAKE (165.1 vs 47.6) and all-cause mortality (61.7 vs 6.9) (Figure). Each doubling of baseline urinary KCR increased the hazards of cardiorenal outcome (adjHR: 1.326, 95%CI: 1.058 to 1.661, p=0.014), MAKE (adjHR: 1.347, 95%CI: 1.070 to 1.696, p=0.011) and all-cause mortality (adjHR: 2.029, 95%CI: 1.276 to 3.226, p=0.003) after adjusting for age, gender, levels of urine ACR and eGFR, HbA1c, SBP, and LDL. Higher baseline urinary KCR was also associated with faster kidney function decline.
Conclusion
Urinary kallistatin excretion independently predicts cardiorenal outcomes in type 2 diabetes and CKD, which could be developed into a novel prognostic marker for risk stratification, and potentially as a therapeutic target.
Health & Medical Research Fund (Ref: 12232596)
Acknowledgment
Supported by the Health and Medical Research Fund (Ref: 12232596) of HKSAR Government
Funding
- Government Support – Non-U.S.