Abstract
Among the many biochemical defects associated with disease of the kidneys, there exists a profound abnormality of carbohydrate metabolism characterized by fasting hyperglycemia and a diabetic-type glucose tolerance. Studies, which included tests for insulin, glucose, and galactose tolerance and glycolytic response to epinephrine and glucagon, were performed in an effort to distinguish the defect in patients with kidney disease from that seen in diabetes mellitus. Three groups of hospitalized patients were compared 1st, a group with a wide variety of renal diseases, the majority of whom had azotemia; secondly, a smaller group of known diabetics; finally, a control group comprising patients with various illnesses not including disease of the liver, kidney, or pancreas. The demonstration in patients with kidney disease of hypoglycemia, epinephrine and glucagon unresponsiveness suggests a deficiency in hepatic glycogen storage or release. That this is the result of a block in glycogen production is further suggested by the normal transfer of serum phosphorus associated with a delayed blood glucose clearance and supported by the finding of a diminished hepatic uptake of galactose. Further evidence that a failure in glycogenesis is implicated is obtained from studies of liver glycogen in rats made hyperglycemic by partial nephrectomy. Attention is called to the possible relationship of this defect to the change in insulin requirement frequently observed in diabetes complicated by renal insufficiency.