Scholarlink

<p>Recurrent weight gain after metabolic bariatric surgery (MBS) threatens the durability of metabolic and renal benefits, yet its intricate relationship with kidney function remains underexplored. This review synthesizes evidence that weight regain (≥ 20% from nadir weight) reactivates obesity-driven kidney injury pathways, including glomerular hyperfiltration, lipotoxicity (toxic damage from lipid overload), and NOD-like receptor protein 3 (NLRP3) inflammasome activation (an immune complex driving inflammation). Consequently, albuminuria recurs in 20–35% of patients and eGFR decline accelerates. Procedure-specific dynamics modulate outcomes. Roux-en-Y gastric bypass (RYGB) offers superior kidney protection despite moderate regain (5.3–37% at 7 years). In contrast, sleeve gastrectomy (SG) shows higher regain (26.3–76% at 6 years) and weaker renal improvements. Critically, weight recurrence reactivates transforming growth factor-beta (TGF-β)/mothers against decapentaplegic homolog (SMAD) and Wnt/β-catenin fibrotic signaling, driving ectopic renal fat reaccumulation and tubular injury. Emerging strategies, including glucagon-like peptide-1 (GLP-1) agonists (27% albuminuria reduction) and endoscopic revisions, show promise in mitigating renal sequelae. However, definitional heterogeneity in weight regain and insufficient phenotyping of kidney-specific biomarkers impede clinical translation. This review underscores the urgency of personalized interventions to preserve kidney health in the context of post-bariatric weight recurrence, advocating for multidisciplinary approaches and future research into novel antifibrotic therapies.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Recurrent Weight Gain after Metabolic Bariatric Surgery (MBS): Emerging Insights on Kidney Function

  • 期刊论文

  • 发表日期：

    2025年12月3日

查看全文
  • Seyed Amirhossein Fazeli,
  • Mamdouh I. Elamy,
  • Hamed Soleimani samarkhazan

摘要

Recurrent weight gain after metabolic bariatric surgery (MBS) threatens the durability of metabolic and renal benefits, yet its intricate relationship with kidney function remains underexplored. This review synthesizes evidence that weight regain (≥ 20% from nadir weight) reactivates obesity-driven kidney injury pathways, including glomerular hyperfiltration, lipotoxicity (toxic damage from lipid overload), and NOD-like receptor protein 3 (NLRP3) inflammasome activation (an immune complex driving inflammation). Consequently, albuminuria recurs in 20–35% of patients and eGFR decline accelerates. Procedure-specific dynamics modulate outcomes. Roux-en-Y gastric bypass (RYGB) offers superior kidney protection despite moderate regain (5.3–37% at 7 years). In contrast, sleeve gastrectomy (SG) shows higher regain (26.3–76% at 6 years) and weaker renal improvements. Critically, weight recurrence reactivates transforming growth factor-beta (TGF-β)/mothers against decapentaplegic homolog (SMAD) and Wnt/β-catenin fibrotic signaling, driving ectopic renal fat reaccumulation and tubular injury. Emerging strategies, including glucagon-like peptide-1 (GLP-1) agonists (27% albuminuria reduction) and endoscopic revisions, show promise in mitigating renal sequelae. However, definitional heterogeneity in weight regain and insufficient phenotyping of kidney-specific biomarkers impede clinical translation. This review underscores the urgency of personalized interventions to preserve kidney health in the context of post-bariatric weight recurrence, advocating for multidisciplinary approaches and future research into novel antifibrotic therapies.