ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

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

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO1899

Clonal Hematopoiesis of Indeterminate Potential Is Associated with Worse Kidney Function and Anemia in a Cohort of Patients with Advanced CKD

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology

Authors

  • Vlasschaert, Caitlyn, Queen's University, Kingston, Ontario, Canada
  • Mcnaughton, Amy J. M., Queen's University, Kingston, Ontario, Canada
  • Hopman, Wilma M., Queen's University, Kingston, Ontario, Canada
  • Kestenbaum, Bryan R., University of Washington, Seattle, Washington, United States
  • Robinson-Cohen, Cassianne, Vanderbilt University, Nashville, Tennessee, United States
  • Moran, Sarah Margaret, Queen's University, Kingston, Ontario, Canada
  • Garland, Jocelyn S., Queen's University, Kingston, Ontario, Canada
  • Holden, Rachel M., Queen's University, Kingston, Ontario, Canada
  • Lanktree, Matthew B., McMaster University, Hamilton, Ontario, Canada
  • Rauh, Michael J., Queen's University, Kingston, Ontario, Canada
Background

Clonal hematopoiesis of indeterminate potential (CHIP) is an inflammatory premalignant disorder resulting from acquired genetic mutations in hematopoietic stem cells. CHIP is common in aging populations and associated with cardiovascular morbidity and overall mortality, but its role in chronic kidney disease (CKD) has not been investigated.

Methods

We performed targeted sequencing to detect CHIP mutations in a cohort of 87 adults with advanced CKD (eGFR < 60 ml/min/1.73m2). Kidney function, hematologic, and mineral bone disease parameters were assessed cross-sectionally at baseline, and a total of 2,091 creatinine measurements and 3,382 hemoglobin measurements were retrospectively collected over the following 12-year period.

Results

At baseline, 20 of 87 (23%) cohort participants had CHIP detected. Those with CHIP had lower baseline eGFR (22.3 ± 2.5 vs. 28.2 ± 1.4 ml/min/1.73 m2, P = 0.04) in age- and sex-adjusted regression models. Individuals with CHIP had a 2.5–fold increased risk of a 50% decline in eGFR or ESKD in a Cox proportional hazard model adjusted for age and sex (95% confidence interval, 1.3–4.7). Further, those with CHIP had lower hemoglobin at baseline (11.6 ± 0.3 vs. 12.8 ± 0.2 g/dL, P = 0.0003) and throughout the follow-up period despite a greater use of erythropoiesis-stimulating agents. Mean cell volume was associated with variant allele fraction, suggesting CHIP may contribute to defective erythropoiesis in CKD.

Conclusion

CHIP was associated with lower eGFR, progression of CKD, and anemia in individuals with advanced CKD. Further assessment of the direction of causality between CHIP and CKD and validation in additional cohorts is required.

Funding

  • Private Foundation Support