ArticlePediatric nephrology (Berlin, Germany)2009
Increased nitric oxide production by T- and B-cells in idiopathic nephrotic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- The effect of systemic corticosteroids on the innate and adaptive immune system in children with steroid responsive nephrotic syndrome.European journal of pediatrics · 2016Trial
- Immunosuppressive Agent Options for Primary Nephrotic Syndrome: A Review of Network Meta-Analyses and Cost-Effectiveness Analysis.Medicina (Kaunas, Lithuania) · 2023Review
- Successful management of post-transplant focal segmental glomerulosclerosis with therapeutic plasma exchange and rituximab.Clinical and experimental nephrology · 2019Article
- Minimal change nephrotic syndrome and prohibitin-2 gene polymorphism.Clinical and experimental nephrology · 2017Article
- Pathogenesis of childhood idiopathic nephrotic syndrome: a paradigm shift from T-cells to podocytes.World journal of pediatrics : WJP · 2015Review
- Long-term outcome of children treated with rituximab for idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2013Article
- Rituximab in post-transplant pediatric recurrent focal segmental glomerulosclerosis.Pediatric nephrology (Berlin, Germany) · 2013Article
- The factors that may predict response to rituximab therapy in recurrent focal segmental glomerulosclerosis: a systematic review.Journal of transplantation · 2011Article
- Nephrotic syndrome and rituximab: facts and perspectives.Pediatric nephrology (Berlin, Germany) · 2009Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of idiopathic nephrotic syndrome (INS) remains unclear. To study the role of nitric oxide (NO) in INS, we measured intracellular NO produced by T- and B-cells using a novel fluorescent indicator. Twelve children with INS (mean age 7.3 years; group A-1: in relapse, group A-2: in remission) were enrolled in the study together with 16 children with other renal diseases (9.5 years; group B) and 42 healthy control children (7.7 years; group C). The amount of NO produced by CD3+ cells (T-cells) and CD19+ cells (B-cells) and of plasma NO(x) was measured by flow cytometry and colorimetry, respectively. The average amount of NO produced by CD3+ and CD19+ cells in group A-1 subjects was significantly higher than that produced by these cells in group A-2 and B patients and the healthy controls (group C), respectively (P < 0.01), and it decreased after the patients achieved remission (P < 0.01). Plasma NO(x) levels in group A-1 patients was also highest among the different groups (P < 0.01). There were no significant differences in intracellular NO and plasma NO(x) among group A-2, B, and C subjects (P > 0.05). A significant correlation between plasma NO(x) and urinary protein excretion was found only in group A patients and not in group B patients. We conclude that an aberrant immune system may exist not only in T-cells but also in B-cells, and NO may play some role in INS.
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Registered trials
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