Hypoglycaemia is not uncommon in patients with renal failure (RF), and it is secondary to malnutrition, infections, congestive heart failure, liver disease, adrenal insufficiency and some medications. Insulinoma and RF are a rare combination. The diagnosis of insulinoma in RF is particularly difficult, since in these patients the cell polypeptides β are elevated due to reduced renal excretion and insulin resistance.1,2 There are few studies on severe hypoglycaemia treated with diazoxide in haemodialysis (HD).3–5 We present a case of hypoglycaemia with endogenous hyperinsulinism (probable insulinoma that was not identified) treated with diazoxide.

The patient was a 73-year-old woman on HD with AA amyloidosis due to deforming rheumatoid arthritis, on treatment with deflazacort 7.5mg/day but with poor therapeutic adherence, who was admitted for hypoglycaemic coma (blood glucose 18mg/dL). Cortisol and adrenocorticotropic hormone levels ruled out adrenal insufficiency, which was the first diagnostic suspicion in view of the patient's long-term steroid treatment that was recently discontinued by the patient. Laboratory tests showed blood insulin 103μIU/mL (6–27), C-peptide 39.5ng/mL (0.7–4), intact proinsulin 65.3pmol/L (0–6), β-hydroxybutyrate 0.8mg/dL (0.6–1.8), anti-insulin antibodies were negative and sulphonylureas and repaglinide undetectable in urine. These findings are consistent with endogenous hyperinsulinism, with insulinoma the most likely diagnosis, although its confirmation in RF depends to a large extent on its location. Eighty percent of insulinomas are <2cm in size, so up to 30% remain undiagnosed. Imaging tests (chest-abdominal computed tomography, abdominal magnetic resonance imaging, abdominal ultrasound, selective angiography, multislice CT angiography, positron emission tomography and octreotide scan) were negative, and the patient refused to have endoscopic ultrasound, arteriography with selective arterial calcium stimulation6 and/or surgical exploration. Since insulinoma is a neuroendocrine tumour, the following biochemical parameters were determined: chromogranin A>1140.0ng/mL (19.4–98.1); gastrin 295pg/mL (0–100), glucagon 290pg/mL (59–177), vasoactive intestinal peptide 25.3pmol/L (0–30) and neuron-specific enolase 7.9ng/mL (0–18.3). Interpretation of these results was also hampered by the elevated chromogranin A,7 gastrin and total glucagon8 in the RF.

To maintain the blood glucose >60mg/dL, the patient required 50% dextrose solution at 50mL/h and IV steroids in the form of 100mg boluses of actocortina (hydrocortisone sodium phosphate). The patient was discharged with higher doses of corticosteroids (30mg/day), but the patient was readmitted in 48h with a new episode of severe hypoglycaemia. At that time, treatment with diazoxide was initiated with a progressive increase in the doses (to avoid hypotension and fluid retention) up to 3mg/kg/day (132mg/day). Once the treatment was established, the hypoglycaemia episodes completely disappeared. On discharge, the patient was advised to have frequent meals rich in complex carbohydrates at regular intervals, and to monitor the blood glucose levels. Diazoxide opens the K+ATP channels present in the insulin-producing beta cells of the pancreas, causing a reduction in insulin release. The diazoxide therapy had no effect on the dialysis, and the blood glucose remained at normal levels. In this patient, the use of other treatments, such as somatostatin analogues, was not considered, because they attenuate the secretion of the counter-regulatory hormone which may aggravate hypoglycaemia,9 and are excreted through the kidneys.

In our experience, diazoxide is useful in HD patients as ymptomatic treatment to control and maintain blood glucose levels in patients with severe hypoglycaemia caused by endogenous hyperinsulinism suggestive of insulinoma in patients in whom surgery is not possible.10