In November 1997a renal biopsy showed the pathognomic signs of Goodpasture's syndrome. Eight months earlier I had had a mysterious septicaemic illness for which no aetiological agent was ever found and from which I apparently recovered.

However, over the ensuing months the antiglomerular basement membrane (anti-GBM) antibodies were silently accumulating until they reached levels that were off the measurable scale. By the time I presented to the renal unit at Manchester Royal Infirmary, my renal function was terminally compromised.

The therapeutic plan adopted a three-fold approach. Firstly, switch off the antibody production using cyclophosphamide 150 mgs daily. Secondly, remove the existing antibodies by a process of immunoabsorption. The machines for this procedure are few and far between and rarely used. Goodpasture's syndrome is in itself a rare disease—only one person in a million develops it each year. The third part of the strategy was to protect my remaining nephrons from the dangerously high levels of …