Transition from acute kidney injury to chronic kidney disease: mechanisms, models, and biomarkers.
A substantial proportion of acute kidney injury episodes progress to chronic kidney disease through maladaptive repair, and emerging tubular biomarkers may allow earlier identification of patients at risk.
Background
Acute kidney injury (AKI) and chronic kidney disease (CKD) are increasingly recognized as interconnected conditions that share overlapping pathophysiological mechanisms. AKI, even when followed by apparent recovery, is an established risk factor for the later development of CKD and end-stage disease. This review examines the molecular mechanisms, experimental models, and biomarkers relevant to understanding and managing the AKI-to-CKD transition.
Key recommendations
The progression from AKI to CKD is driven by maladaptive repair processes, persistent inflammation, and fibrosis, with both conditions sharing common pathways involving cell death, inflammation, and extracellular matrix deposition. Current animal models, including ischemia-reperfusion injury and nephrotoxic models, help elucidate these mechanisms but have limitations in replicating the full complexity of human disease. The authors emphasize the need for improved models and validated biomarkers to enhance clinical translation.
Clinical implications
Emerging biomarkers such as kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and soluble tumor necrosis factor receptors (TNFRs) show promise for early detection and monitoring of disease progression. Advancing the understanding of the AKI-to-CKD transition through refined research approaches and targeted therapies holds potential to improve patient outcomes, although clinically validated interventions remain to be established.
Category
Research
Source
Am J Physiol Renal Physiol
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