2016/01/14 by Anna Zuk, Anna Żuk, Joseph V. Bonventre · 766 citations
Medicine · #Acute Kidney Injury Research #Acute kidney injury #Bioinformatics #Biology #Chronic Kidney Disease and Diabetes #Dialysis #Dialysis and Renal Disease Management #Disease #Fibrosis #Immunology #Inflammation #Intensive care medicine #Internal medicine #Kidney disease #Medicine #Pathology #Pathophysiology
paper · pdf · doi:10.1146/annurev-med-050214-013407
published in Annual Review of Medicine 67(1), 293-307 (Annual Reviews)
openalex publication_date 2016/01/14 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
Acute kidney injury (AKI) is a global public health concern associated with high morbidity, mortality, and healthcare costs. Other than dialysis, no therapeutic interventions reliably improve survival, limit injury, or speed recovery. Despite recognized shortcomings of in vivo animal models, the underlying pathophysiology of AKI and its consequence, chronic kidney disease (CKD), is rich with biological targets. We review recent findings relating to the renal vasculature and cellular stress responses, primarily the intersection of the unfolded protein response, mitochondrial dysfunction, autophagy, and the innate immune response. Maladaptive repair mechanisms that persist following the acute phase promote inflammation and fibrosis in the chronic phase. Here macrophages, growth-arrested tubular epithelial cells, the endothelium, and surrounding pericytes are key players in the progression to chronic disease. Better understanding of these complex interacting pathophysiological mechanisms, their relative importance in humans, and the utility of biomarkers will lead to therapeutic strategies to prevent and treat AKI or impede progression to CKD or end-stage renal disease (ESRD).