Etiology and pathogenesis of acute kidney disease

Abstract

Acute kidney disease (AKD), a group of clinical syndromes between acute kidney injury (AKI) and chronic kidney disease (CKD), is defined as the kidney injury from after 7 days of AKI to the onset of CKD for 90 days. The pathogenesis of AKD is closely related to multiple factors including age, race, gene, CKD and comorbidities, acute disease, and the severity and duration of AKI. The mechanism of AKD is relatively complex. At present it is considered that CKD and comorbidities, acute diseases, AKD, and other causes can cause renal ischemia, and common pathological changes of hypoxia, leading to renal endothelial cell damage, microcirculation disturbance, tubular cell G2/M cycle stagnation and cell silence , local recruitment and activation of macrophages and other immune cells, abnormal expression of a variety of genes, and especially abnormal changes of biomarkers. These factors, combining with aging and epigenetics, etc, can contribute to abnormal expression of inflammatory cytokines and cytokines, renal local persistent inflammation, and even activation of fibrosis signal pathway, tubular epithelial cell regeneration impairment, resulting in poor and repair delay after renal injury. The above mechanisms lead to the occurrence and progression of AKD. Therefore, it is of important theoretical and prevention and treatment significance to understand the etiology and pathogenesis of AKD for exploring new mechanisms of injury and repair of AKI so as to block its progression to CKD. Key words: Acute kidney disease; Acute kidney injury; Inflammation; Injury; Repair