Evidence map›Paper›PMID 41307423›Full record

ArticleClinical nephrology2025

Anti-nephrin antibodies in minimal change disease: Case report series.

Maša Knehtl, Nejc Piko, Tadej Petreski, Tadej Zorman, Tina Stropnik-Galuf, Nika Kojc, Karmen Wechtersbach, Robert Ekart, Sebastjan Bevc

Abstract readCase Reports
In one paragraph

Article in Clinical nephrology, 2025. 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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5 · Who and what money

Authors and funding

9 authors.

Maša Knehtl
Nejc Piko
Tadej Petreski
Tadej Zorman
Tina Stropnik-Galuf
Nika Kojc
Karmen Wechtersbach
Robert Ekart
Sebastjan Bevc

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMinimal change disease (MCD) is one of the causes of nephrotic syndrome (NS) in adults. Recently, anti-nephrin antibodies have been detected in a certain subset of patients with MCD, supporting the proposed autoimmune etiology and appearing to be markers of disease activity. Despite their diagnostic and prognostic potential, the use of anti-nephrin autoantibodies in routine clinical practice is not yet widespread. Studies have shown that patients with anti-nephrin-associated MCD have a more fulminant NS and a better response to antibody-depleting therapy than those who are anti-nephrin-negative. MATERIALS AND

methodsWe report cases of a 79- and a 42-year-old male patient presenting with new-onset NS and acute kidney injury. Both patients had negative immunologic tests, including antibodies against phospholipase A2-receptor (anti-PLA2R) and thrombospondin-7A (anti-THSD7A). Renal biopsy was performed in both patients.

resultsIn both cases, light microscopy of kidney samples from thick-needle biopsy showed acute tubular injury attributed to severe proteinuria. Electron microscopy revealed diffuse (90%) effacement of the podocyte foot processes without electron-dense deposits. Immunofluorescence presented discrete intracytoplasmic IgG podocyte deposits with a high probability of MCD due to anti-nephrin autoantibodies. In addition to therapy with angiotensin convertase inhibitors, calcium channel blockers, and furosemide, we started treatment with low-dose oral glucocorticoids and mycophenolic acid (case 1) or oral glucocorticoids alone (case 2) depending on patients' comorbidities. We administered rituximab, resulting in a fast and complete resolution of proteinuria and improvement of kidney function.

conclusionAnti-nephrin autoantibodies have been detected in a subgroup of patients with MCD supporting the autoimmune etiology of the disease. Targeted anti-B-cell therapy with rituximab is an additional therapeutic option in patients with relapsing or treatment-resistant disease, or drug-related adverse effects to standard therapy.

Indexed as

AutoantibodiesMembrane ProteinsNephrosis, LipoidAcute Kidney InjuryAdultAgedBiopsyHumansImmunosuppressive AgentsMalePodocytesTreatment OutcomeAutoantibodiesImmunosuppressive AgentsMembrane Proteins

Identifiers

PMID41307423
PMCPMC12912638

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