Table 1.

Teaching points

1.The pathogenesis of minimal change disease remains obscure.

2.Because of the relapsing nature of minimal change disease, patients are often exposed to long-term, repeated courses of nontargeted immunosuppressive therapies (steroids, calcineurin inhibitors, cyclophosphamide, rituximab, mycophenolate mofetil), with variable rates of response and with considerable short- and long-term side effects.

3.Contemporary research into the pathogenesis of minimal change disease points to dysregulation of the CD80-CTLA-4 axis.

4.Elevated urinary CD80 has been shown to be a reliable biomarker to distinguish patients with minimal change disease from those with focal segmental glomerulosclerosis.

5.In our patient with minimal change disease and elevated urinary CD80, abatacept has dramatically decreased the number of relapses, and allowed significant reduction in the doses of coadministered tacrolimus and prednisone.

6.Anti-CD80 therapy (abatacept) may represent the first available targeted, mechanistic-based approach to the treatment of patients with minimal change disease associated with elevated urinary CD80.