MPN-associated IgA nephropathy and IL-6/IL-11 mesangial axis
Current understanding
A proposed mechanism whereby JAK-STAT-driven IL-6 and IL-11 signaling in MPN promotes glomerular mesangial cell proliferation while aberrant clonal hematopoiesis contributes to dysregulated IgA production, together predisposing to IgA nephropathy. Evidence to date is a single case report of ruxolitinib treatment in a PV patient producing reduction in proteinuria and stabilization of renal function, providing preliminary clinical support that JAK inhibition can attenuate this glomerular pathway. This extends the systemic renal consequences of MPN beyond lysozyme-associated proximal tubular injury to a glomerular/mesangial compartment.
Evidence log
- 2026-04-27 — JAK Inhibitor-Induced Improvement of IgA Nephropathy in a Patient With Polycythemia Vera: A Case Report.: cross-connection with lysozyme-associated-nephropathy-mechanism: Both describe distinct MPN-driven renal injury mechanisms — glomerular/mesangial (IL-6/IL-11, IgA immune complexes) versus proximal tubular (lysozyme overload) — jointly framing the kidney as a shared end-organ target of MPN clonal and inflammatory output. (novelty: 4)