Proposed pathophysiological crosstalk between MAFLD and CKD.
<p>This schematic illustrates the proposed pathophysiological crosstalk between Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Chronic Kidney Disease (CKD). <b>Panel A depicts organ-specific mechanisms:</b> in the <i>liver</i>, steatosis (lipid-laden h...
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2025
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| Summary: | <p>This schematic illustrates the proposed pathophysiological crosstalk between Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Chronic Kidney Disease (CKD). <b>Panel A depicts organ-specific mechanisms:</b> in the <i>liver</i>, steatosis (lipid-laden hepatocytes) progresses through inflammation (Kupffer cell activation, TNF-α/IL-6 release) to fibrosis (stellate cell activation, collagen deposition); in the <i>kidney</i>, lipotoxicity (podocyte fatty acid influx) leads to podocyte injury (effacement, apoptosis) and glomerulosclerosis (collagen IV accumulation). <b>Panel B highlights systemic mediators</b>: insulin resistance (hyperinsulinemia-driven hepatic gluconeogenesis and renal sodium retention), dyslipidemia (VLDL/ApoB glomerular deposition), and key mediators (fetuin-A, adiponectin deficiency, uric acid-induced NLRP3 activation). Bidirectional interactions amplify organ damage through direct (lipotoxicity, fibrosis) and systemic (metabolic, inflammatory) pathways, suggesting shared therapeutic targets for dual hepatic-renal protection.</p> |
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