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Kidney Week

Abstract: SA-PO124

Urinary Follistatin Is a Marker Reflecting the Severity of Tubular Damage in Patients with AKI

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • 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
  • Nagata, Daisuke, Division of Nephrology, Department of Internal Medicine, Jichi Medical University, Shimotsuke, 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

Follistatin is an activin-binding protein that antagonizes the function of activin A, a member of TGF-beta superfamily. In animal models of acute kidney injury (AKI), the blockade of activin A by exogenous follistatin has been shown to attenuate kidney damage and improve renal function, suggesting that endogenous activin A negatively regulates tubular repair after AKI. Follistatin acts as a local modulator of activin A in many tissues. However, the role of follistatin in the kidney remains unknown.

Methods

To address this issue, we examined the localization of follistatin in normal human kidney and measured urinary follistatin in patients with AKI to test if urinary follistatin is useful as a marker for AKI. Patients with AKI (n=131) and healthy adults (n=13) were enrolled in this study. Serum and urinary follistatin was measured by ELISA. Correlations of urinary follistatin with other clinical parameters were analyzed.

Results

Follistatin was localized in renal tubules of normal kidney. Follistatin-producing cells were positive for Na-Cl co-transporter and uromodulin but were negative for aquaporin 1 or aquaporin 2. Urinary follistatin, undetectable in healthy adults, was significantly increased in patients with AKI (0.00 ± 0.00 vs. 458.1 ± 150.4 pg/mL, p<0.05) and was positively correlated with the severity of AKI. Urinary follistatin was significantly increased in patients requiring renal replacement therapy compared to those who did not. There was a significant correlation of urinary follistatin with urinary protein, alpha1-microglobulin, urinary NGAL, but not with urinary KIM-1, urinary L-FABP, urinary NAG, urinary beta2-microglobulin, serum creatinine. No correlation between urinary and serum follistatin was observed, suggesting that urinary follistatin is originated from the kidney but not from blood.

Conclusion

Collectively, follistatin produced by distal tubules of the kidney become detectable in the urine of AKI patients. Urinary follistatin might be useful to monitor the severity of acute tubular damage.