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January 8, 2024Open Access

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

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Authors

TYTzu-Hsuan YehKTKuan-Chieh TuHWHsien‐Yi Wang

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Overview

Review uncovers molecular drivers of transition from acute kidney injury to chronic kidney disease, highlighting pathways that cause maladaptive repair and progressive renal fibrosis.

Key Points

  • To delineate the biomarkers, molecular signaling pathways, and pathophysiological mechanisms governing the progression from acute kidney injury and acute kidney disease to chronic kidney disease.
  • Categorized diagnostic and prognostic acute kidney injury biomarkers into stress, damage, and functional indicators.
  • Synthesized molecular mechanisms connecting acute insults to chronic pathology, focusing on hypoxia, inflammation, and cellular senescence.
  • Evaluated the roles of profibrotic signaling cascades and renin-angiotensin-aldosterone system inhibition in post-injury renal remodeling.
  • Renal hypoperfusion, sepsis, and nephrotoxicity initiate cascades marked by mitochondrial dysfunction, cellular senescence, and maladaptive repair.
  • Activation of the Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ pathways promotes progressive renal fibrosis and functional decline.
  • The renin-angiotensin-aldosterone system exacerbates oxidative stress and fibrogenesis, whereas renin-angiotensin system inhibitors show potential to mitigate progression after acute injury.

Cite This Study

Yeh et al. (2024) studied this question.

synapsesocial.com/papers/6a82a73f129689dedc133497https://doi.org/10.20944/preprints202401.0620.v1
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