Abstract
Activin is a multifunctional cytokine belonging to the transforming growth factor (TGF)-β superfamily that regulates the growth and differentiation of cells in various organs. We previously reported that activin A, which is absent in normal kidneys, was significantly increased in the ischemic kidney, and that the blockade of activin action by follistatin, an activin antagonist, significantly enhanced tubular regeneration after renal ischemia, suggesting that activin A acts as an endogenous inhibitor of tubular repair after kidney injury in rodents. However, the role of activin A in human acute kidney injury (AKI) remains unclear. In this analysis, we measured serum and urinary activin A in human AKI (n = 39) and tested if activin A might serve as a biomarker for AKI. Urinary activin A, which was undetectable in healthy controls, was significantly increased in AKI (0.0 ± 0.0 vs. 173.4 ± 58.8 pg/mL, p < 0.05). The urinary activin A level in patients with AKI stage 3, was significantly higher than that in patients with AKI stages 1 and 2. Patients who required renal replacement therapy (RRT) had a significantly higher urinary activin A level than patients who did not require RRT. Urinary activin A might be a useful non-invasive biomarker for the severity of AKI.