Since idiopathic IgA nephropathy was first reported a quarter of a century ago it has evolved from being a curiosity to becoming the commonest form of glomerulonephritis in industrialised countries. A recent international meeting held to mark the 25 years of study of IgA nephropathy concentrated on its aetiology and pathogenesis but had also to acknowledge that nephrologists still do not know how to treat the disease.1

Clinical observation over two decades has shown that spontaneous remission may occur but that 15-20% of patients develop end stage renal failure within 10 years of diagnosis. The risk factors for progression are impaired renal function at presentation, heavy proteinuria, hypertension, and (curiously) absence of the typical symptom - recurrent macroscopic haematuria. The systemic nature of IgA nephropathy is shown convincingly by its recurrence in patients who receive a kidney transplant and, more remarkably, by the disappearance of IgA deposits when a kidney from someone with the disease is inadvertently transplanted into someone with renal failure from another cause.

When IgA nephropathy was first described, IgA itself - and the fact that it was produced by mucosal cells - had been discovered only a few years earlier. The deposition of this immunoglobulin in glomeruli was explained as an immune complex disease in which …