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Rituximab with prednisone reduced proteinuria in Sjögren's syndrome-associated membranous nephropathy caseRituximab treatment reduced kidney protein loss in one Sjögren's syndrome patient

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Key Takeaway
Consider this single case report as very low-certainty evidence suggesting an association, not efficacy.

A case report with literature review describes a 48-year-old female hospitalized with primary Sjögren's syndrome and nephrotic-range proteinuria, diagnosed with secondary membranous nephropathy. The patient received prednisone (30 mg/day) and rituximab (two 1 g infusions two weeks apart, with an additional 1 g infusion six months later). No comparator was reported.

The main outcome was 24-hour urinary protein level. After initial treatment, proteinuria decreased from 8.5 g to 2.2 g. Following the additional rituximab infusion six months later, it further decreased to 1.3 g. No effect sizes, p-values, or confidence intervals were reported. Secondary outcomes were not specified.

Safety and tolerability data were not reported. No adverse events, serious adverse events, or treatment discontinuations were documented. Key limitations include the single-case design, absence of a control group, and lack of detailed follow-up information beyond the timing of the additional infusion. Funding and conflicts of interest were not reported.

This report shows an association between treatment and reduced proteinuria in one patient. The very low certainty evidence from a single case cannot establish causation, effectiveness, generalizability, or a safety profile for this treatment strategy in secondary membranous nephropathy due to Sjögren's syndrome.

This is a detailed report about one patient's treatment. A 48-year-old woman with primary Sjögren's syndrome developed a serious kidney complication called secondary membranous nephropathy. This caused her to lose large amounts of protein in her urine. Doctors treated her with a steroid (prednisone) and a medication called rituximab, given by infusion.

After the initial treatment, the amount of protein in her 24-hour urine sample dropped from 8.5 grams to 2.2 grams. She received another rituximab infusion six months later, and her protein loss decreased further to 1.3 grams. The report did not mention any side effects or safety problems from the treatment.

It is very important to understand what this report means. This is the story of just one person. There was no comparison to other treatments or to patients who got no treatment. We do not know the long-term results or if this would work for anyone else. The findings are a starting point for future research, not proof that this is an effective treatment.

Readers should see this as a preliminary medical observation. It suggests rituximab might be a treatment option worth studying in larger, controlled trials for this specific kidney problem linked to Sjögren's. It does not provide evidence for how well or how safely it works for the general population.

What this means for you:
A treatment helped one patient, but more research is needed to know if it works for others.

Study Details

Study typeSystematic review
EvidenceLevel 1
PublishedMar 2026
View Original Abstract ↓
Primary Sjögren’s syndrome (pSS) is a chronic autoimmune disease characterized by lymphoplasmacytic infiltration of exocrine glands, leading to dry eyes and mouth. Renal involvement, particularly glomerulonephritis, occurs in approximately 5% of pSS patients. Membranous nephropathy (MN) is one of the less common forms of renal involvement in pSS. A 48-year-old female with a history of oral and ocular dryness for several years and bilateral symmetrical lower extremity edema for three months was admitted to our hospital. Laboratory findings revealed moderate anemia, hypoalbuminemia, and nephrotic-range proteinuria. Schirmer’s test, tear break-up time, and lip biopsy confirmed the diagnosis of pSS. Renal biopsy demonstrated widespread mesangial hypercellularity and mesangial matrix expansion, thickening of the glomerular basement membrane(GBM) with prominent spikes, and subepithelial, intramembranous and mesangial electron-dense deposits under electron microscopy. Immunofluorescence showed diffuse fine granular deposits of IgG (predominantly IgG1 and IgG2). Based on these findings, secondary membranous nephropathy due to pSS was diagnosed. The patient was treated with prednisone (30 mg/day) and two infusions of rituximab (1 g each, administered 2 weeks apart). After treatment, her 24-hour urinary protein level decreased from 8.5 g to 2.2 g. The dose of glucocorticoids was gradually tapered off. During follow-up, an additional 1 g of rituximab was administered six months later, resulting in a further reduction of proteinuria to 1.3 g/24 hours. This case highlights the effectiveness of rituximab in managing secondary membranous nephropathy associated with pSS. Further studies are needed to clarify the underlying mechanisms and optimize treatment strategies for this condition.
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