a 65-year-old woman
Anti-PLA2R-negative membranous nephropathy with nephrotic-range proteinuria, driven by idiopathic multicentric Castleman disease (iMCD-NOS, intermediate severity, HHV-8 negative), alongside Sjogren's syndrome and progressive polyneuropathy
She first got rituximab combined with cyclophosphamide and dexamethasone, but her nerve symptoms got worse (even though her VEGF level was falling). The anti-IL-6 medicine that guidelines prefer was out of reach because of cost. So doctors switched to rituximab on its own and kept it up for nine cycles over 24 months. By January 2024 her protein in the urine was gone, her inflammation markers were almost back to normal, and her nerves recovered.
In one 65-year-old woman, rituximab given by itself put her Castleman-driven kidney disease and nerve damage into remission after the guideline-preferred IL-6 drug was too costly to get.
- Her nephrotic-range proteinuria and nerve symptoms started ten days after a COVID-19 vaccination and led to a diagnosis of iMCD-NOS.
- Her kidney problem was anti-PLA2R-negative membranous nephropathy, meaning the usual membranous-nephropathy antibody test was negative, and it came bundled with Sjogren's syndrome.
- The first combination (rituximab plus cyclophosphamide plus dexamethasone) actually made her nerves worse, even as her VEGF level dropped.
- When the preferred anti-IL-6 medicine was not affordable, rituximab alone became the fallback and was continued for nine cycles over 24 months.
- By January 2024 her proteinuria resolved, her inflammation markers were nearly normal, and her nerves recovered, which the authors call clinical remission.
Why it might work
Castleman disease is an immune-system disorder where the body's immune signals, including a protein called IL-6, run out of control and can damage many organs at once, including the kidneys and nerves. Guidelines aim straight at IL-6, but that was not an option here because of cost. Rituximab works differently: it clears out B cells, the immune cells that help drive this overactive signaling. The paper frames the idea that quieting those B cells can calm the whole immune storm enough to let the kidney and nerve damage heal, which is what appeared to happen over her 24 months of treatment.
The honest limits
- This is a single patient (n=1), so it cannot tell us how often rituximab alone works for others with this condition.
- The abstract reports no actual numbers: no proteinuria grams, no IL-6 or VEGF values, and no eGFR, so 'resolution' and 'near-normalization' are the authors' words, not measured figures we can check.
- It took nine cycles over two years, and the first drug combination made her nerves worse before the single-drug approach helped, so the path was slow and not smooth.
- The abstract does not disclose any funding sources or author conflicts of interest, and the text is cut off at 'The delayed re...', so part of the authors' reasoning is missing.
- My kidney biopsy points to membranous nephropathy but the PLA2R antibody is negative. Should we look for an underlying cause like Castleman disease?
- If an anti-IL-6 drug is recommended but not affordable or available for me, is rituximab a reasonable alternative for my situation, and what are the trade-offs?
- How would we track whether treatment is working, such as which proteinuria, inflammation, or kidney-function numbers you would follow and how often?