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Fasting Hypoglycemia in a Hemodialysis Patient

Hypoglycemia, though reported in nondiabetic dialysis patients, is not a common occurrence. In this particular patient, I would measure plasma glucose and insulin levels after an overnight, 12-hr fast. If the glucose is >60 mg/dL, it is unlikely that patient’s symptoms are related to hypoglycemia. If the plasma glucose is <50 mg/dL in this setting, hypoglycemia is documented unequivocally; a simultaneous insulin level of <5 pU/mL would indicate appropriate suppression of insulin secretion. In the postabsorptive state, insulin secretion is inhibited and glucagon is stimulated resulting in suppressed glucose utilization and enhanced glucose production; the latter is accomplished through glycogenolysis and gluconeogenesis. Hypoglycemia activates counter-regulatory hormones, including glucagon, epinephrine, cortisol, and growth hormone. Glucagon and epinephrine secretion are not impaired in dialysis patients, and deficiencies of these hormones are rarely if ever causes of hypoglycemia. Thus, it is conventional to measure plasma cortisol and growth hormone level in hypoglycemic states to exclude pituitary and/or adrenocortical insufficiency. In renal failure patients, insulin inhibition and glucagon stimulation are generally unimpaired. Thus, malnutrition or a combination of malnutrition and excessive ethanol ingestion are the most common causes of hypoglycemia. Diminished hepatic glycogen store would result in decreased glycogenolysis. Theoretically, impaired gluconeogenesis due to alanine deficiency can occur, but this seems unlikely because plasma alanine levels in dialysis patients are not reduced; in the few instances in which alanine kinetics were measured, turnover rate was normal or increased. Patients taking beta blocker may also be more susceptible to hypoglycemia due to its ability to inhibit hepatic glucose production. Some noninsulin producing extra-pancreatic large mesenchymal tumors may cause hypoglycemia due to excessive glucose utilization. Liver disease severe enough to cause hypoglycemia should be clinically evident. A plasma insulin >I0 pM/mL indicates an inappropriate insulin response to hypoglycemia. In this situation, I would think about factitious hypoglycemia due to self-administration of either insulin or oral hypoglycemia agent. Plasma C-peptide level is normal or low with exogenous insulin administration and elevated with sulfonylurea ingestion. Of course, insulinoma also needs to be considered in the differential diagnosis if one is assured that patients did not take either insulin or oral hypoglycemic agent. Treatment of hypoglycemia in these patients would depend on the etiology. If malnutrition is the cause, then effort should be concentrated on increasing hepatic glycogen storage by increasing nutritional intake. Glucose-containing dialysate may also be of value when symptoms occur during or just after hemodialysis.