ArticlePediatric nephrology (Berlin, Germany)2026
Expression of PD-1 on T cells and its predictive value for steroid resistance in children with idiopathic nephrotic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundProgrammed cell death protein 1 (PD-1) plays a pivotal role in regulating T-cell responses. Its expression profile and clinical significance in pediatric idiopathic nephrotic syndrome (INS), particularly in steroid-resistant nephrotic syndrome (SRNS), remain unclear.
methodsPD-1 expression on CD3⁺, CD4⁺, and CD8⁺T cells was quantified by flow cytometry in 65 treatment-naive children with idiopathic nephrotic syndrome (INS): steroid-sensitive (SSNS, n = 54), steroid-resistant (SRNS, n = 11), as well as in healthy controls (HC, n = 30). Group differences, clinical correlations and PD-1's predictive value for SRNS were analyzed. Circulating T subsets, including CD3⁺PD-1⁺ T cells, CD4⁺PD-1⁺T cells, and CD8⁺PD-1⁺T were detected with multiparameter flow cytometry.
resultsThe percentage of CD4⁺PD-1⁺ T cells was significantly higher in SRNS (10.77 ± 4.62%) compared to both SSNS (5.14 ± 1.99%, P = 0.000) and HC (6.36 ± 2.02%, P = 0.028). CD3⁺PD-1⁺ T cells were also elevated in SRNS (8.13 ± 3.12%) versus SSNS (4.67 ± 1.82%, P = 0.001). No significant difference was found in CD8⁺PD-1⁺ T cells. Multivariate logistic regression identified an elevated percentage of CD4⁺PD-1⁺ T cells as an independent risk factor for SRNS (OR = 2.236, P = 0.002). Receiver operating characteristic (ROC) analysis showed that CD4⁺PD-1⁺ T cell cutoff > 7.385% predicted SRNS with an area under the curve (AUC) of 0.891, sensitivity of 81.8%, and specificity of 87.0%.
conclusionsOverexpression of PD-1, predominantly on CD4⁺ T cells, is associated with steroid resistance in pediatric INS. Elevated CD4⁺PD-1⁺ T cells may serve as a predictive biomarker for SRNS, offering a potential tool for early identification and a rationale for exploring PD-1 pathway modulation.
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