Spontaneous hypoglycemia has been observed on rare occasions in renal failure. We observed episodes of spontaneous hypoglycemia in nondiabetic subject with renal failure.
A fourty-two-year old housewife was admitted because of dyspnea of sudden onset on Nov. 10, 1975. She had the history of acute glomerulonephritis and toxemia gravidarum. Her BUN was 137mg/dl, Na 137 mEq/L, K 5.5 mEq/L, Cl 105 mEq/L, creatinine 21.4mg/dl. s-GOT s-GPT and bilirubin levels were normal. s-cortisol, s-ACTH and h-GH levels were above normal. Thyroid function was normal. She undewent hemodialysis with gradual clinical improvement,
However early in the morning on Jan. 14, 1976 she developed severe hypoglycemia, less than 10mg/dl, with loss of consciousness and positive Babinski reflex of the left site, without hemiparesis. Intravenous glucose infusion resulted in gradual clearing of her mentsl ssatus and complete disappearance of abnormal neurological findings. The hypoglycemia was preceded three weeks by a transient rise of s-GOT (574 U), s-GPT (230 U) and al-P (32.6 K-AU) without icterus. However hepatic hypoglycemia was unlikely Hypoglycemia developed in the beginning and middle of February, and the beginning of April also. She died on April 20, 1976 because of heart failure. At autopsy, pancreatic adenoma could not be found, and liver cell glycogen centent was low in some part on PAS stain. The thyroid, the adrenal gland and the pancreas was morphologically normal.
Glucose tolerance test with fifty gram oral glucose revealed borderline blood sugar curve with maximal blood sugar level 156mg/dl at 120 minutes, and fair, delayed IRI response and paradoxical rise of h-GH. The IRI response was in the normal range during tolbutamide infusion, however blood sugar drop was only 8% at 20 minutes and blood sugar remained low even at 120 minutes. This might suggest some disturbances in recovery mechanism from hypoglycemia. Hypoglycemia developed fifteen hours after tolbutamide infusion. Blood sugar response to intravenous glucagon was poor; only 23mg/dl rise at 20 and 60 minutes. Glycogen deficiency in the liver cell must be the major cause of her hypoglycemia, whether it was resulted from renal failure itself or impaired caloric intake. Insulin tolerance test showed slightly prolonged half time disappearance of insulin (12 minutes) with slight blood sugar drop and rather high basal IRG. The first hypoglycemia on Jan, 14 did not seem to reflect increased insulin secretion, high insulin sensitivity or impaired caloric intake.
These results were essentially consistent with those of usual renal failure except for poor blood sugar response to glucagon. Probable glycogen deficiency in the liver cell might be the cause of hypoglycemia, and some disturbances in the recovery mechanism from hypoglycemia could be also. But these could not be adequate explanation for her hypoglycemia. Some unknown factor (s) in renal failure might be also responsible for hypoglycemia.