adrenal failure is a potentially fatal disorder , and the prevalence of primary and secondary adrenal failure is 93140 and 150280 per million , respectively . because symptoms of adrenal failure such as anorexia , nausea , vomiting , weight loss and fatigue are rather non - specific , they may well be mistaken as those occurring from other disorders in patients suffering from severe co - morbidities . we encountered a rare case of a chronic haemodialysis patient with type 2 diabetes , alcoholic cirrhosis and pancreatitis , presenting as hypoglycaemic coma due to severe adrenal failure caused by acth deficiency . a 62-year - old man was admitted in emergency in the early morning because he could not be awakened . he had started haemodialysis for diabetic nephropathy 3 years previously and had been receiving regular haemodialysis three times a week . he also suffered from hypertension , alcoholic cirrhosis and chronic pancreatitis . during the last 15 months , with progressive appetite loss and fatigue , seven weeks previously , he had experienced hypoglycaemia and was treated with intravenous ( iv ) glucose . insulin dosing was 4 u novorapid twice a day at that time , which had been stopped since then . upon arrival , the level of consciousness was glasgow coma scale 14 ( e4v4m6 ) without focal neurological deficit . he appeared malnourished ( body mass index 16 kg / m ) without skin pigmentation . his body temperature was 33.1c ( on a warm june day ) , blood pressure ( bp ) 146/78 mm hg , pulse rate 66/min , respiration rate 14/min , arterial ph 7.383 and o2 saturation 100% ( with room air ) . the general laboratory data ( table 1 ) were compatible with the known morbidities of chronic renal failure , liver cirrhosis and chronic pancreatitis , except for hypoglycaemia and a lowered hba1c for a patient with diabetes . ten grams of glucose was administered iv and , 30 min later , capillary blood glucose ( bg ) was 5.7 mmol / l , and he was fully conscious . ast , aspartate aminotransferase ; alt , alanine aminotransferase ; ldh , lactate dehydrogenase ; gtp , glutamyl transpeptidase . the patient was receiving 7500 u epogen per week.cortisol and acth were determined before breakfast on day 2 ; other endocrine data were obtained at 1000 h on day 7 when capillary blood glucose was 6.2 mmol / l ; cortisol was undetectable by radioimmunoassay ( immunotech ) with the detection limit being 5.5 nmol / l . cortisol was undetectable with a very low acth level ( table 1 ) , which established a diagnosis of adrenal failure due to acth deficiency . the magnetic resonance imaging revealed no hypothalamic or pituitary abnormality , and serum antipituitary antibody   was negative . 9 mm hg ( mean  sd , n = 17 ) during days 18 . upon diagnosing adrenal failure , 25 mg of oral hydrocortisone ( 10 mg , 10 mg and 5 mg after each meal , respectively ) was started on day 9 , which promptly restored appetite and well - being . bp was 151  18/83  14 mm hg ( n = 15 ) during days 916 with 5 mg of amlodipine , which was modestly higher than the values recorded before the treatment with hydrocortisone ( p = 0.005 for systolic bp and p < 0.001 for diastolic bp , mann hypoglycaemia did not recur , and insulin was resumed on day 11 , because bg ( mean  sd from the premeal and the midnight values ) for the preceding 2 days was 11.8  2.2 mmol / l ( n = 7 ) with 1800 kcal diet . in this patient , adrenal failure was due to acth deficiency , not due to addison s disease , hence there was no skin pigmentation . loss of appetite , general fatigue , malnutrition and previous hypoglycaemic events had been considered to be due alcoholic binge as far as we are aware , adrenal crisis or hypoglycaemic coma due to adrenal failure has not been reported in chronic haemodialysis patients . toth and lee   analysed 36 patients with uraemic hypoglycaemia in the literature and identified 19 haemodialysis patients . the number of dialysis patients is estimated to be 1.5 million and > 90% of them are receiving haemodialysis . the prevalence of primary and secondary adrenal failure is 93140 and 150280 per million , respectively . , cortisol production must have been virtually absent because plasma cortisol was undetectable despite the cortisol metabolism is depressed in haemodialysis patients . however , the patient presented with only hypoglycaemic coma and mild hypothermia , but not with circulatory collapse or electrolyte abnormalities . we consider haemodialysis had protected him from adrenal crisis because the circulating volume and electrolytes were maintained by haemodialysis . because the glucose concentration of the dialysis solution was 8.3 mmol / l , hypoglycaemia , if any , might have been relieved to some extent during each haemodialysis session . adrenal crisis develops not only in patients with addison s disease but also in patients with acth deficiency , and hyponatraemia is not rare in the latter group . this is in part due to the fact that cortisol concentration in plasma is 1000-fold higher than that of aldosterone , and cortisol elicits its effects not only through the glucocorticoid receptor but also through the mineralocorticoid receptor . because cortisol is a tonic inhibitor of antidiuretic hormone ( adh ) , adh excess is often present in adrenal insufficiency , which also contributes to hyponatraemia in adrenal failure . haemodialysis most likely protects the patients with either primary or secondary adrenal failure against volume depletion and hyponatraemia . in summary , adrenal failure should be suspected in chronic haemodialysis patients with hypoglycaemia even if other salient features of adrenal failure are absent .