Beyond creatinine: biomarkers of kidney recovery after acute kidney injury.

Purpose

OF REVIEW Recovery from acute kidney injury (AKI) is currently assessed via traditional diagnostic tests (i.e. serum creatinine) despite increasing recognition that restoration of kidney function does not necessarily correlate with resolution of underlying injury. This editorial summarizes recent advances in biomarkers of kidney recovery after AKI and their potential role in predicting long-term outcomes. RECENT

Findings

Emerging evidence suggests that AKI recovery is determined by several biological processes, including persistent injury, inflammatory signalling, tubular repair and onset of fibrosis. Biomarkers reflecting these pathways have shown promise in identifying patients at risk of maladaptive recovery and progression to chronic kidney disease (CKD). Albuminuria and urinary CCL14 provide information on ongoing injury and incomplete recovery while soluble TNFR1 and 2, urine MCP-1 and YLK-40 have emerged as markers of persistent inflammation associated with long-term kidney disease progression. Uromodulin and epidermal growth factor may identify adaptive repair whereas markers of extracellular matrix turnover such as endotrophin and PRO-C3 offer insight into fibrotic remodelling. SUMMARY Contrary to traditional diagnostic tests, novel biomarkers provide mechanistic information and may improve risk stratification after AKI; their integration with imaging and clinical phenotyping represents a promising strategy to better define recovery trajectories and identify therapeutic targets to prevent AKI-to-CKD transition.