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Urinary Podocyte Loss is Associated With Treatment Response in Patients With Primary Nephrotic Syndrome

Year: 2025
Type: article
Study design: Observational Study
Abstract: Introduction: The disease course of primary nephrotic syndrome (PNS) is highly variable, and is difficult to predict at onset. PNS is characterized by podocyte injury and loss. We hypothesized that measurement of urinary podocyte loss is associated with treatment response in patients with PNS. Methods: = 42). MCD and FSGS were considered manifestations of the same disease entity, and analyzed as one group. Patients' baseline clinical and follow-up data were recorded. Urinary sediments were collected and stained for podocyte-specific markers, and analyzed using fluorescence-activated cell sorting (FACS). Results: In patients with MCD/FSGS, the respective partial and complete remission rates were 24% and 59% during a median follow-up of 12.9 months, and all patients received immunosuppressive treatment. In patients with MN, the respective partial and complete remission rates were 64% and 19% during a median follow-up of 15.5 month, and the majority of patients received immunosuppressive treatment. Patients with PNS had elevated levels of podocyturia when compared with controls, and repeat measurements revealed that podocyturia follows proteinuria course over time, normalizing following complete proteinuria remission. In treatment-responsive immunosuppresive-treated patients with MCD/FSGS, podocyturia at baseline significantly differentiated between early and late treatment responders at 4 weeks, contrary to proteinuria and serum albumin. In symptomatically treated patients with MN, low levels of podocyturia at baseline were associated with spontaneous remission. Conclusion: Patients with PNS have increased podocyturia compared with healthy individuals. Quantitative detection of podocyturia may have prognostic relevance in patients with PNS.
Language: English
Subfield: Nephrology
Field: Medicine
Open Access status: gold
Estimated APC paid: $2,800
Award: G419155335
OpenAlex ID: W4416410896
FWCI:
Cites: 39
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