Context: Preoperative localisation of insulinoma improves cure rate and reduces complications, but may be challenging. Objective: To review diagnostic features and localisation accuracy for insulinomas. Design: Cross-sectional, retrospective analysis. Setting: A single tertiary referral centre. Patients: Patients with insulinoma in the years 1990-2009, including sporadic tumours and those in patients with multiple endocrine neoplasia syndromes. Interventions: Patients were identified from a database, and case notes and investigation results were reviewed. Tumour localisation by computed tomography (CT), magnetic resonance imaging (MRI), octreotide scanning, endoscopic ultrasound (EUS) and calcium stimulation was evaluated. Main outcome measure(s): Insulinoma localisation was compared to histologically confirmed location following surgical excision. Results: Thirty-seven instances of biochemically and/or histologically proven insulinoma were identified in 36 patients, of which seven were managed medically. Of the 30 treated surgically, 25 had CT (83.3%) and 28 had MRI (90.3%), with successful localisation in 16 (64%) by CT and 21 (75%) by MRI respectively. Considered together, such imaging correctly localised 80% of lesions. Radiolabelled octreotide scanning was positive in 10 out of 20 cases (50%); EUS correctly identified 17 lesions in 26 patients (65.4%). Twenty-seven patients had calcium stimulation testing, of which 6 (22%) did not localise, 17 (63%) were correctly localised, and 4 (15%) gave discordant or confusing results. Conclusions: Preoperative localisation of insulinomas remains challenging. A pragmatic combination of CT and especially MRI predicts tumour localisation with high accuracy. Radionuclide imaging and EUS were less helpful but may be valuable in selected cases. Calcium stimulation currently remains useful in providing an additional functional perspective.European Journal of Endocrinology 162 971-978

The authors apologise for an error in the author list of the article titled above published in the journal, volume 162 on page 971. R H Reznek should be the penultimate author. The full list of authors and their affiliations for this article is as follows:Maralyn R Druce1, Vasantha M Muthuppalaniappan1, Benjamin O'Leary1, Shern L Chew1, William M Drake1, John P Monson1, Scott A Akker1, Michael Besser1, Anju Sahdev2, Andrea Rockall2, Soumil Vyas3, Satya Bhattacharya3, Matthew Matson2, Daniel Berney4, R H Reznek2 and Ashley B Grossman1Departments of 1Endocrinology, 2Radiology, 3Surgery and 4Histopathology, Barts and the London Medical School, St Bartholomew's Hospital, London EC1A 7BE, UK.

We describe the case of a 47-year-old man who developed significant acute, and subsequently chronic, kidney injury due to bilateral renal infarction. This occurred in the context of a combined inherited thrombophilia including antithrombin III deficiency and a prothrombin gene mutation. Bilateral renal artery thrombosis developed despite prophylactic treatment for thromboembolism. Arterial thrombosis is rare in the context of inherited thrombophilia and bilateral renal infarction is an unusual cause of acute kidney injury. Bilateral renal infarction due to primary renal artery thrombosis has not been previously described in antithrombin III deficiency, either as an isolated defect or in combination with other hereditary thrombophilia.

Ethnicity and race are often used interchangeably in the literature. However, the traditional definition of race and ethnicity is related to biological (bone structure and skin, hair, or eye color) and sociological factors (nationality, regional culture, ancestry, and language) respectively. Diabetes mellitus (DM) is a huge global public health problem. As the number of individuals with Type 2 DM grows, the prevalence of diabetic kidney disease (DKD), which is one of the most serious complications, is expected to rise sharply. Many ethnic and racial groups have a greater risk of developing DM and its associated macro and micro-vascular complications.

Diabetic kidney disease is the leading cause of end-stage kidney disease in the Western world. It accounts for up to 40% of patients requiring renal replacement therapy. Currently, achieving optimal glycaemic and blood pressure control are the only strategies that have been shown to prevent and retard the progression of diabetic kidney disease. Recently, the elucidation of pathophysiological mechanisms of kidney damage, involving oxidative stress in particular, have led to the development of promising therapeutic targets. It remains to be seen whether these novel therapies are effective in clinical trials.