RHI levels in patients with a history of HSP were similar to the control group. This finding fits with the known history of patients with HSP who usually develop no long-term damage in the affected organs. We demonstrate that more than half of patients with HSP had abnormal endothelial dysfunction compared to only 30% in the control group although this differences didn’t reach significance (p = 0.06). Our results suggest that endothelial damage may take a long time to recover possibly years. The only clinical feature that correlated with decreased RHI was corticosteroid therapy, which may suggest that patients with severe HSP may have greater endothelial damage. Several in vitro studies [25–27] demonstrated that circulating serum growth factor, adhesion molecules, or other markers of endothelial cell damage were elevated in the acute phase of HSP, especially in severe forms developing IgA nephritis. These vascular abnormalities reduce the availability of nitric oxide, which induces structural and mechanical changes, and may offer important insights into the development and progression of vasculitis initiated end-organ damage. The present study did not include patients with renal impairment, since we wanted to rule out other factors that may affect the endothelial function. Further study is needed to clarify differences between patients with and without renal impairment.