Abstract
Background: B-cell subsets may be involved in the pathogenesis of childhood steroid-sensitive nephrotic syndrome (SSNS). Horizontal control studies have shown that homeostasis of B-cell subsets changes at different stages of the SSNS. However, there is a lack of longitudinal studies that have investigated dynamic changes in B cell subpopulations.Methods: Blood samples were collected at the following time points from 15 children with SSNS treated at our hospital: before administration of steroid and after 3 days, 1 week, and 3, 6, 9, and 12 months. The proportions of circulating total B cells (CD19+), transitional B cells (CD19+CD24highCD38high), mature B cells (CD19+CD24lowCD38intermediate), and memory B cells (CD19+CD24highCD38−) were monitored by flow cytometry.Results: The proportion of CD19+ B cells before steroid administration was significantly higher than that observed at any other time point or in the healthy control (HC) group (p < 0.001). However, this proportion was significantly lower than that in the HC group at 12 months (p = 0.031). Transitional B cells before (%BL 9.5 ± 4.4) and 3 days after steroid administration (%BL 10.6 ± 5.1) were significantly higher than at any other time point or in the HC group (p < 0.001). Although these cells declined after the 3rd day the percentage was still significantly lower than that of the HC group at 12 months (p = 0.029). Memory B cells increased gradually after steroid administration and decreased to the normal range after 9 months.Conclusions: B cell subpopulations show dynamic changes in children with SSNS, suggesting that they are involved in the pathogenesis of the disorder. Further studies are required to determine whether this change can guide individualized treatment.
Highlights
Idiopathic nephrotic syndrome (INS) is the most common cause of childhood glomerular disease
Two patients were excluded from the study because of frequent relapses and three patients due to having a steroid resistant nephrotic syndrome that required additional immunosuppressive therapy
We showed that CD19+B cells were significantly higher in the initial stage of INS than that measured in the healthy control (HC) group, a finding consistent with the results of Colucci et al and Printza et al [7, 12]
Summary
Idiopathic nephrotic syndrome (INS) is the most common cause of childhood glomerular disease. The pathogenesis of SSNS is still under investigation, with a considerable volume of data suggesting that immune mechanisms may have an important role in the syndrome [1, 2]. The administration of monoclonal antibodies against CD20, a specific surface marker of B cells, has achieved remarkable results in the treatment of children with frequent relapses and steroid dependence. There is evidence that supports this role of B cells, with IgG levels shown to decrease in the acute and remission phases of children with INS. B-cell subsets may be involved in the pathogenesis of childhood steroid-sensitive nephrotic syndrome (SSNS). Horizontal control studies have shown that homeostasis of B-cell subsets changes at different stages of the SSNS. There is a lack of longitudinal studies that have investigated dynamic changes in B cell subpopulations
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