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: FR-PO928

Association of Serum Uric Acid with Podocyte Injury and Kidney Histopathologic Lesions

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Rosan, Sophia H., Boston Medical Center, Boston, Massachusetts, United States
  • Verma, Ashish, Boston Medical Center, Boston, Massachusetts, United States
  • Claudel, Sophie E., Boston Medical Center, Boston, Massachusetts, United States
  • Palsson, Ragnar, Massachusetts General Hospital, Boston, Massachusetts, United States
  • Srivastava, Anand, University of Illinois Chicago, Chicago, Illinois, United States
  • Huber, Tobias B., Universitat Hamburg Medizinische Fakultat, Hamburg, Hamburg, Germany
  • Stillman, Isaac Ely, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Henderson, Joel M., Boston Medical Center, Boston, Massachusetts, United States
  • Waikar, Sushrut S., Boston Medical Center, Boston, Massachusetts, United States
  • Schmidt, Insa Marie, Boston Medical Center, Boston, Massachusetts, United States
Background

Hyperuricemia may impair podocyte function by promoting oxidative stress and inflammatory responses, but these effects have not been comprehensively studied in patients with chronic kidney disease (CKD). This study explores the association between serum uric acid (SUA) levels, histopathologic lesions, and podocyte injury evidenced by foot process effacement (FPE) in patients with biopsy-confirmed kidney disease.

Methods

We measured SUA levels in 519 individuals enrolled into the Boston Kidney Biopsy Cohort, a cohort of individuals with biopsy-confirmed semi-quantitative assessment of histopathology. We assessed the correlation between SUA, estimated glomerular filtration rate (eGFR), and proteinuria using Spearman correlation coefficients. Multivariable linear regression models tested the associations of SUA levels with histopathologic lesion severity and FPE.

Results

The mean SUA level was 8.3±2.6 mg/dL, the mean eGFR was 57±36 ml/min/1.73m2, and the median proteinuria [IQR] was 3.0 [0.4–4.0] g/g creatinine. SUA levels correlated negatively with eGFR and positively with proteinuria (r = -0.28, p<0.001 and r = 0.18, p<0.001, respectively) (Figure 1a). After multivariable adjustment for age, sex, race, and eGFR, more severe segmental sclerosis was associated with higher SUA levels (β= 0.64, p=0.020) (Figure 1b). More severe FPE was also associated with higher SUA levels. This relationship remained consistent in multivariable models after adjustment for demographics, eGFR, and proteinuria (β = 0.52, p = 0.048) (Figure 1c).

Conclusion

This study demonstrates an association between hyperuricemia and podocyte injury. Further research is needed to determine whether urate-lowering therapy could help reduce podocyte injury and potentially delay the onset of CKD.

Figure 1.