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: SA-PO467

Diabetic Kidney Disease Phenotypes and Cardiovascular Outcomes

Session Information

Category: Diabetic Kidney Disease

  • 702 Diabetic Kidney Disease: Clinical

Authors

  • Claudel, Sophie E., Boston Medical Center, Boston, Massachusetts, United States
  • Zhao, Runqi, Boston Medical Center, Boston, Massachusetts, United States
  • Schmidt, Insa Marie, Boston Medical Center, Boston, Massachusetts, United States
  • Waikar, Sushrut S., Boston Medical Center, Boston, Massachusetts, United States
  • Srivastava, Anand, University of Illinois Chicago, Chicago, Illinois, United States
  • Verma, Ashish, Boston Medical Center, Boston, Massachusetts, United States
Background

Adults with diabetic kidney disease (DKD) have high risk of major adverse cardiovascular events (MACE) and cardiovascular disease (CVD). However, variability in cardiovascular risk across DKD phenotypes remains poorly understood.

Methods

This is a longitudinal analysis of adults with diabetes from two cohorts, the National Health and Nutrition Examination Survey (NHANES, N=5,126) and the UK Biobank (N=27,059). We defined four distinct clinical phenotypes: no DKD (estimated glomerular filtration rate (eGFR)≥60ml/min and urinary albumin-to-creatinine ratio (UACR)<30mg/g), albuminuria only (eGFR≥60mg/ml and UACR≥30mg/g), decreased eGFR only (eGFR<60ml/min and UACR<30mg/g), and albuminuria plus decreased eGFR (eGFR<60ml/min and UACR≥30mg/g). We used multivariable adjusted Cox proportional hazard models to assess CVD outcomes.

Results

In NHANES, the albuminuria only phenotype and the albuminuria plus decreased eGFR phenotype were associated with a 2.71-fold higher risk of CVD mortality (hazard ratio [HR] 2.71, 95% confidence interval [CI] 1.91-3.85) and a 2.75-fold higher risk (HR 2.75, 95%CI 1.80-4.21) compared to no DKD. In the UK Biobank, the albuminuria-only phenotype had a 2.01-fold higher risk of CVD mortality (HR 2.01, 95%CI 1.75-2.32) and a 1.54-fold higher risk of MACE (HR 1.54, 95%CI 1.41-1.68) compared to no DKD. Moreover, the albuminuria plus decreased eGFR phenotype had a 3.24-fold higher risk of CVD mortality (HR 3.24, 95%CI 2.38-4.40) and a 2.06-fold higher risk of MACE (HR 2.06, 95%CI 1.64-2.59) compared to no DKD. The decreased eGFR phenotype was associated with a 1.65-fold higher risk of CVD mortality (HR 1.65, 95%CI 1.24-2.18) and a 1.30-fold higher risk of MACE (HR 1.30, 95%CI 1.06-1.59) compared to no DKD.

Conclusion

Each DKD phenotype had varying risk of CVD mortality and MACE, indicating distinct clinicopathological characteristics. These findings emphasize the need for tailored management to prevent adverse cardiovascular outcomes in DKD.

Table 1

Funding

  • Other NIH Support