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Journal Article Review Epublish 28 citations

PubMed: 38339031 DOI: 10.3390/ijms25031755

From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease.

Int J Mol Sci 25(3)

Authors: Tzu-Hsuan Yeh, Kuan-Chieh Tu, Hsien-Yi Wang, Jui-Yi Chen

Affiliations

  • Division of Nephrology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
  • Division of Cardiology, Department of Internal Medicine, Chi Mei Medical Center, Tainan 71004, Taiwan.
  • Department of Sport Management, College of Leisure and Recreation Management, Chia Nan University of Pharmacy and Science, Tainan 71710, Taiwan.
  • Department of Health and Nutrition, Chia Nan University of Pharmacy and Science, Tainan 71710, Taiwan.

Abstract

This article provides a thorough overview of the biomarkers, pathophysiology, and molecular pathways involved in the transition from acute kidney injury (AKI) and acute kidney disease (AKD) to chronic kidney disease (CKD). It categorizes the biomarkers of AKI into stress, damage, and functional markers, highlighting their importance in early detection, prognosis, and clinical applications. This review also highlights the links between renal injury and the pathophysiological mechanisms underlying AKI and AKD, including renal hypoperfusion, sepsis, nephrotoxicity, and immune responses. In addition, various molecules play pivotal roles in inflammation and hypoxia, triggering maladaptive repair, mitochondrial dysfunction, immune system reactions, and the cellular senescence of renal cells. Key signaling pathways, such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ, promote fibrosis and impact renal function. The renin-angiotensin-aldosterone system (RAAS) triggers a cascade leading to renal fibrosis, with aldosterone exacerbating the oxidative stress and cellular changes that promote fibrosis. The clinical evidence suggests that RAS inhibitors may protect against CKD progression, especially post-AKI, though more extensive trials are needed to confirm their full impact.

MeSH

Kidney Diseases, Cellular Senescence, Stress, Physiological, Fibrosis, Aldosterone, Acute Kidney Injury

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