Galectin-9 reduces tissue damage in certain immune-mediated glomerular diseases. However, its role in structural and functional renal changes in patients with varying types of chronic kidney disease (CKD) is less clear.


To investigate the association between plasma galectin-9 levels, proteinuria, tubulointerstitial lesions, and renal function in different CKD stages.


We measured plasma galectin-9 levels in 243 patients undergoing renal biopsy for determining the CKD etiology. mRNA and protein expression levels of intrarenal galectin-9 were assessed by quantitative real-time polymerase chain reaction and immunostaining. Relationships between plasma galectin-9, clinical characteristics, and tubulointerstitial damage were analyzed with logistic regression. We investigated galectin-9 expression patterns in vitro in murine J774 macrophages treated with differing stimuli.


To analyze the relationship between galectin-9 and clinical features, we divided the patients into 2 groups according to median plasma galectin-9 levels. The high galectin-9 group tended to be older, have decreased renal function, higher proteinuria, and greater interstitial fibrosis. After multivariable adjustment, elevated plasma galectin-9 levels were independently associated with stage 3b or higher CKD. An analysis of gene expression in the tubulointerstitial compartment in the biopsy samples showed a significant positive correlation between intrarenal galectin-9 mRNA expression and plasma galectin-9 levels. Immunohistochemistry confirmed increased galectin-9 expression in the renal interstitium of patients with advanced CKD, and most galectin-9–positive cells were macrophages, as determined by double-immunofluorescence staining. In vitro experiments showed that galectin-9 expression in macrophages was significantly increased after interferon-γ stimulation.


Our findings suggest that plasma galectin-9 is a good biomarker for diagnosing advanced CKD.

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The core facility is funded by the Academia Sinica Core Facility and Innovative Instrument Project (AS-CFII-108-118). This study was financially supported in part by funding from the Ministry of Science and Technology R.O.C. (MOST 109-2314-B-075-071, 109-2314-B-010-056-MY3, and 110-2628-B-075-011-), Taipei Veterans General Hospital (V109B-020, V110C-149, V110C-151, VTA110-V1-3-1, VTA 110-V1-3-2, V108D42-001-MY3-3, and V108D42-004-MY3-3), and Institute of Biomedical Sciences, Academia Sinica (IBMS-CRC110-P04 and AS-VTA-110-03). This study was also supported by the Foundation for Poison Control (FPC-111-003).

Tsai and R-B Yang contributed equally to this manuscript.

The authors have no relevant financial interest in the products or companies described in this article.

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