|Title:||Novel insights into acute kidney injury-chronic kidney disease continuum and the role of renin-angiotensin system||Authors:||Chou, Yu-Hsiang
|Keywords:||Acute kidney injury; Chronic kidney disease; Renin–angiotensin system; Acute Kidney Injury; Animals; Biomarkers; Cell Cycle Checkpoints; Epigenesis, Genetic; Humans; Mitochondria; Renal Insufficiency, Chronic; Renin-Angiotensin System||Issue Date:||Sep-2017||Publisher:||ELSEVIER TAIWAN||Journal Volume:||116||Journal Issue:||9||Start page/Pages:||652-659||Source:||Journal of the Formosan Medical Association = Taiwan yi zhi||Abstract:||
Acute kidney injury (AKI) is an independent risk factor for chronic kidney disease (CKD). If injury is mild, a repair process can be adaptive and lead to complete renal recovery. However, severe injury will be accompanied by a maladaptive repair which usually leads to nephron loss, fibrosis, vascular rarefaction, and chronic inflammation. Although various mechanisms underlying AKI-CKD transition have been explored, no intervention has been proved effective to block the transition until very recently. A lack of consensus for monitoring renal function and defining renal recovery after AKI should be the reasons for the slow advance in the discovery of a timely pharmacologic treatment to block AKI-CKD transition. Recently, animal studies have shown the activation of renin-angiotensin system (RAS) after AKI. In patients with complete renal recovery after AKI defined as the decrease of serum creatinine level to within 0.3?mg/dL above the baseline, administration of RAS inhibitor can prevent the ensuing CKD. In this review, we will discuss the renal recovery after AKI and the mechanisms underlying AKI-CKD transition. We will then highlight the promising effect of RAS inhibitor on CKD prevention in patients with complete renal recovery from AKI based on the recent clinical evidence.
|Appears in Collections:||醫學教育暨生醫倫理學科所|
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