American journal of nephrology · 2026
Galectin-9 as a Circulating Marker of Mesangial Injury and Prognosis in Biopsy-Proven Kidney Disease.
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Tsai Ming-Tsun, Li Szu-Yuan, Kim Donggun, Park Jihwan, Schmidt Insa M, Zhao Runqi, Waikar Sushrut S, Hsieh Tsung-Han, Yang Haichun, Chen Tz-Heng, Ou Shuo-Ming, Yang Ruey-Bing
Аннотация
INTRODUCTION: Galectin-9, a β-galactoside-binding protein, is elevated in various kidney diseases. While exogenous galectin-9 attenuates kidney injury in experimental models, it remains unclear whether endogenous plasma galectin-9 reflects renal histopathology and independently predicts long-term adverse outcomes in chronic kidney disease (CKD).
METHODS: Plasma galectin-9 levels were prospectively measured in 366 participants from the Taipei Renal Transcriptomics and Outcomes Investigation (TRTOI) cohort. Renal histopathology and chronicity were assessed using a modified Mayo Clinic Chronicity Score (MCCS). Major adverse renal events (MAREs) were defined as ≥40% decline in estimated glomerular filtration rate (eGFR), kidney failure, or death. Findings were validated in 549 participants from the Boston Kidney Biopsy Cohort (BKBC). In vitro, mouse mesangial cells (SV40-MES-13) were used to evaluate galectin-9 effects on TGF-β-induced mesangial activation.
RESULTS: Transcriptomic analysis showed upregulation of LGALS9 (encoding galectin-9) in fibrotic kidneys. Plasma galectin-9 positively correlated with urine protein-to-creatinine ratio and MCCS and inversely with eGFR. Elevated galectin-9 was independently associated with mesangial expansion. In vitro, exogenous galectin-9 attenuated TGF-β-induced mesangial cell activation, proliferation, and profibrotic responses; these effects were reversed by lactose, a competitive inhibitor of the carbohydrate recognition domains of galectin-9. In the TRTOI cohort, participants in the highest galectin-9 tertile had a significantly increased risk of MAREs, independent of confounders. Validation in the BKBC confirmed that higher galectin-9 levels were independently associated with increased all-cause mortality.
CONCLUSION: Elevated plasma galectin-9 is associated with mesangial expansion and predicts a higher risk of MAREs in patients with CKD.
METHODS: Plasma galectin-9 levels were prospectively measured in 366 participants from the Taipei Renal Transcriptomics and Outcomes Investigation (TRTOI) cohort. Renal histopathology and chronicity were assessed using a modified Mayo Clinic Chronicity Score (MCCS). Major adverse renal events (MAREs) were defined as ≥40% decline in estimated glomerular filtration rate (eGFR), kidney failure, or death. Findings were validated in 549 participants from the Boston Kidney Biopsy Cohort (BKBC). In vitro, mouse mesangial cells (SV40-MES-13) were used to evaluate galectin-9 effects on TGF-β-induced mesangial activation.
RESULTS: Transcriptomic analysis showed upregulation of LGALS9 (encoding galectin-9) in fibrotic kidneys. Plasma galectin-9 positively correlated with urine protein-to-creatinine ratio and MCCS and inversely with eGFR. Elevated galectin-9 was independently associated with mesangial expansion. In vitro, exogenous galectin-9 attenuated TGF-β-induced mesangial cell activation, proliferation, and profibrotic responses; these effects were reversed by lactose, a competitive inhibitor of the carbohydrate recognition domains of galectin-9. In the TRTOI cohort, participants in the highest galectin-9 tertile had a significantly increased risk of MAREs, independent of confounders. Validation in the BKBC confirmed that higher galectin-9 levels were independently associated with increased all-cause mortality.
CONCLUSION: Elevated plasma galectin-9 is associated with mesangial expansion and predicts a higher risk of MAREs in patients with CKD.