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Neurological complications are rare during the course of Henoch-Schönlein purpura (HSP). We report a 7-year-old girl with HSP who presented with seizures, loss of vision and disturbance of consciousness. Magnetic resonance imaging (MRI) showed high signal intensity in the gray and white matter over the left parietal and both occipital lobes, compatible with MRI findings of cerebral vasculitis. The eye fundi revealed multiple branches of retinal artery occlusion. Intravenous pulse methylprednisolone (MTP) followed by oral steroid therapy was initially administered for HSP nephritis. Cerebral vasculitis developed 10 days post-MTP treatment, with progressive worsening of consciousness. Oral steroid was discontinued and plasmapheresis was performed alone. Her level of consciousness dramatically improved after plasmapheresis. The brain MRI and eye fundi findings were consistent with her clinical improvement. To the best of our knowledge, this is the first description of MRI abnormalities and multiple retinal artery branch occlusion of cerebral vasculitis in a patient with HSP that was successfully treated by plasmapheresis alone. In conclusion, we propose that plasmapheresis may be used as a first-line therapy or rescue therapy for cerebral vasculitis in HSP.

The high prevalence of arterial calcification in end-stage renal disease (ESRD) is far beyond the explanation by common cardiovascular risk factors such as aging, diabetes, hypertension, and dyslipidemia. The finding relies on the fact that vascular and valvular calcifications are predictors of cardiovascular diseases and mortality in persons with chronic renal failure. In addition to traditional cardiovascular risk factors such as diabetes mellitus and blood pressure control, other ESRD-related risks such as phosphate retention, excess calcium, and prolonged dialysis time also contribute to the development of vascular calcification. The strategies are to reverse “calcium paradox” and lower vascular calcification by decreasing procalcific factors including minimization of inflammation (through adequate dialysis and by avoiding malnutrition, intravenous labile iron, and positive calcium and phosphate balance), correction of high and low bone turnover, and restoration of anticalcification factor balance such as correction of vitamin D and K deficiency; parathyroid intervention is reserved for severe hyperparathyroidism. The role of bone antiresorption therapy such as bisphosphonates and denosumab in vascular calcification in high-bone-turnover disease remains unclear. The limited data on sodium thiosulfate are promising. However, if calcification is to be targeted, ensure that bone health is not compromised by the treatments.

We report a case of nephrotic syndrome and acute renal failure apparently induced by sunitinib. A 67-year-old man with a history of metastatic renal cell carcinoma presented with progressive kidney dysfunction with proteinuria, general edema, and body weight gain of 21 kg after undergoing 3 weeks of sunitinib therapy. The patient had taken no other over-the-counter medications, and all other possible causes of nephrotic syndrome were excluded. The Naranjo Adverse Drug Reaction Probability Scale score for this event was 6, indicating a high probability that the observed presentations were associated with use of the drug. However, despite the discontinuation of sunitinib, his condition deteriorated, and hemodialysis was initiated for respiratory distress. A renal biopsy was performed, which revealed ischemic acute tubular necrosis with minimal change nephropathy. In conclusion, nephrologists and oncologists should be aware that nephrotic syndrome with ischemic acute tubular necrosis is a possible adverse effect of sunitinib. For early diagnosis of this condition and to avoid renal damage, we recommend differential diagnosis of serum creatinine and proteinuria in patients undergoing sunitinib therapy.

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