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.
Highlights
Acute kidney injury (AKI) represents a critical and potentially devastating condition in clinical settings, and has many complicated pathophysiological features, including tubular injury [1–3]
There were no significant differences in the frequency of comorbidities between AKI patients and healthy controls
Blood urea nitrogen (BUN), serum Cr, white blood cell (WBC), and C-reactive protein (CRP) were significantly higher, while serum sodium (Na), estimated glomerular filtration rate (GFR), and hemoglobin, were significantly lower in AKI patients compared to healthy controls
Summary
Acute kidney injury (AKI) represents a critical and potentially devastating condition in clinical settings, and has many complicated pathophysiological features, including tubular injury [1–3]. Serum creatinine is a simple and useful marker of renal function, but is unreliable during acute changes in kidney function, and does not accurately reflect kidney function until a steady-state has been reached. Several molecules, such as urinary neutrophil gelatinase-associated lipocalin (NGAL) [4–8], interleukin (IL)-18 [9–11] and L-type fatty acid-binding protein (L-FABP) [12–15], have been identified as potential markers for the early detection of kidney damage, before serum creatinine increases. Kidney injury molecule-1 (KIM-1) has been proposed as a diagnostic biomarker, and as a pro-recovery marker for AKI [16–19]. Clinical biomarkers reflecting the pathophysiological phase of AKI are still lacking
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