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Abstract: PO1825

Minimal Change Disease Relapse Following Administration of an Anti-IgE Monoclonal Antibody, Omalizumab

Session Information

Category: Trainee Case Report

  • 1202 Glomerular Diseases: Immunology and Inflammation


  • Cowhig, Cliona, Beaumont Hospital, Dublin, Ireland
  • Sandys, Vicki K., Beaumont Hospital, Dublin, Ireland
  • Stoneman, Sinead, Beaumont Hospital, Dublin, Ireland
  • Magee, Colm, Beaumont Hospital, Dublin, Ireland

Minimal Change Disease (MCD) is incompletely understood with immune cells, circulating factors, and glomerular basement membrane all considered potential precipitants. We present the first reported case of reactivation of MCD following administration of omalizumab.

Case Description

A 59-year-old lady presented with lower limb oedema two days following a second dose of Omalizumab for treatment of severe eosinophilic asthma. Her background was significant for two previous episodes of biopsy-proven MCD. Exam was significant for bilateral lower limb pitting oedema, a blood pressure of 174/86 mmHg, and proteinuria on urine dipstick. Urine PCR was 473 mg/mmol on presentation with preserved GFR. Treatment for a presumed MCD relapse was commenced with prednisolone and diuresis and omalizumab was discontinued indefinitely. Clinical and biochemical remission was achieved at 2-weeks and maintained at 6-month follow-up.


Omalizumab is indicated as add-on therapy in patients with severe persistent allergic asthma, the primary mechanism of which is the binding of the active drug to IgE. The clinical effects of omalizumab are not accounted for solely by IgE antagonism with further immune regulatory effects hypothesised. Notably reduction in IL4, IL13, and IL8 have been described post-treatment.
Immune system dysregulation, a hypothesized circulating factor, medications, and atopy are all considered to play a role in development of MCD. Studies have supported an imbalance of T-cell subpopulations and cytokines in MCD. Of note, Th2 cytokines IL4 and IL13 can interact directly with the glomerular basement membrane and are acted upon by omalizumab. In particular IL13 has been described as being related to a nephrotic syndrome in animal studies, and high levels are seen in paediatric nephrotic syndromes, with IL13 levels increasing further in remission.
This is the first reported case of MCD in the context of omalizumab administration. IL13 and IL4 appear key to the hypothesised pathophysiology of MCD and mechanism of action of omalizumab. This case provides an insight into the interactions between MCD, atopy, and biologic medications, presenting MCD as a novel complication of omalizumab.