Proposed pathophysiological crosstalk between MAFLD and CKD.

This schematic illustrates the proposed pathophysiological crosstalk between Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Chronic Kidney Disease (CKD). Panel A depicts organ-specific mechanisms: in the liver, steatosis (lipid-laden h...

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מחבר ראשי:	Zienab M. Saad (22676502) (author)
מחברים אחרים:	Hesham K. H. Keryakos (22676505) (author), Hala A. Hassanin (22676508) (author), Mahmoud M. Higazi (22676511) (author), Manar M. Sayed (22676514) (author), Doaa E. Ismail (22676517) (author), Safaa M. Abdelhalim (21398199) (author)
יצא לאור:	2025
נושאים:	Medicine Cell Biology Biotechnology Marine Biology Cancer Infectious Diseases Virology shear wave elastography patients remains underexplored mitigate progression risks higher liver stiffness 56 ± 17 43 ± 17 5 ± 28 ></ b >). ></ b >), ></ b >) shared metabolic abnormalities 9 ± 39 invasive fibrosis scores 45 ± 1 2 ± 5 mafld patients also dialysis ckd patients 108 ckd patients metabolic risk factors 5 ± 6 9 ± 1 5 ± 3 6 ± 1 xlink "> mafld xlink "> 5 %, b >< metabolic dysfunction 9 ml risk populations fibrosis severity advanced fibrosis 1 years 2 vs ckd severity 1 vs 6 vs study aimed sectional study participants stratified older age nafld score management strategies lower egfr integrated screening insulin resistance findings highlight diagnostic criteria bidirectional relationship apri score
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תיאור
סיכום:	<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>

Proposed pathophysiological crosstalk between MAFLD and CKD.

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