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Henoch–Schönlein purpura (HSP) is in most cases a self-limiting disease, however the development of chronic renal insufficiency is a real dilemma that should be prevented where possible. During the early stages of the disease, renal involvement can be diagnosed in up to 40% of patients. Unfortunately, no biomarkers are currently available that would allow for the identification of patients whose condition is likely to improve spontaneously or who are at risk of developing chronic renal failure. A kidney biopsy, usually performed in cases with gross proteinuria, may define the extent of glomerular involvement. Studies have shown that patients with 50% or more crescent formation in Bowman's capsule will have an unfavourable prognosis.1 Because these features represent already chronic and irreversible changes, many investigators have advocated the need for an earlier intervention strategy.
Despite the great gap in knowledge about the pathomechanism of HSP and the missing molecular target(s) for treatment, the study reported on by Dudley et al2 is of great interest and importance. In contrast to case series and mostly uncontrolled smaller reported studies, Dudley et al conducted the largest randomised, placebo-controlled, double-blind trial to date in order to answer the question of whether an early intervention of 2 weeks of prednisone has any impact on HSP nephropathy after 12 months. Unfortunately, the study did not give a concept for steroid use or for the dose and duration of treatment, but employed a …
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