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Kidney Week

Abstract: SA-PO123

Growth Differentiation Factor (GDF)-15, a Stress-Induced Cytokine, Is Increased in Patients with AKI

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Hamada, Takayuki, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  • Sekiguchi, Momoko, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  • Nagayama, Izumi, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  • Takayanagi, Kaori, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  • Hasegawa, Hajime, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
  • Maeshima, Akito, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Japan
Background

Growth Differentiation Factor (GDF)-15, a member of the TGF-beta superfamily, is one of the stress response cytokines that promotes cell death. Under physiological conditions, GDF-15 is expressed in high levels in the placenta, prostate, and bladder. High circulating levels of GDF-15 have been associated with chronic inflammatory conditions including lung, liver and cardiovascular diseases, rheumatoid arthritis, and cancers. In the kidney, GDF-15 is expressed in renal tubules but its role in acute kidney injury (AKI) remains unknown. To address this issue, we measured urinary GDF-15 in patients with AKI to test if GDF-15 is involved in pathophysiology of human AKI.

Methods

AKI patients (n=86) who were treated in our department (December 2020 to December 2022) and healthy adults (n=19) were enrolled in this study. Written informed consent was obtained from all patients. Serum and urinary GDF-15 were measured by ELISA. Correlations of urinary GDF-15 with renal function, urinary protein level, clinical parameters and various AKI biomarkers were analyzed. This study was approved by the Ethics Committee on Human Research of our institutions (Approval number 2487).

Results

Urinary GDF-15 was detectable in healthy adults but was significantly increased in patients with AKI (5.1 ± 1.0 vs. 18.4 ± 1.5 ng/mL, p<0.001). Especially, urinary GDF-15 was markedly elevated in patients with ischemic AKI, drug-induced AKI, lupus nephritis, and ANCA-associated vasculitis. In most cases of AKI, urinary GDF-15 was decreased after therapeutic intervention. In cases of deceased donor kidney transplant recipients, urinary GDF-15 was significantly elevated at 1 day after transplantation but was decreased with improvement of kidney function thereafter. There was a significant correlation of urinary GDF-15 with urinary neutrophil gelatinase-associated lipocalin (NGAL), urinary kidney injury molecule-1 (KIM-1), urinary NAG, urinary β2-microglobulin, and urinary protein level, but not with serum creatinine level or L-FABP.

Conclusion

Collectively, urinary GDF-15 might be useful as a marker reflecting tubular stress and/or damage in patients with AKI.