Modulation of experimental renal dysfunction of hereditary fructose intolerance by circulating parathyroid hormone.
In a woman with hereditary fructose intolerance and intact parathyroid function, the experimental administration of fructose at different dosage schedules invariably induced the dose-dependent, complex dysfunction of the proximal renal tubule now recognized as characteristic. But in a woman with hereditary fructose intolerance and hypoparathyroidism given similar amounts of fructose, the experimental dysfunction was strikingly attenuated or nondemonstrable unless or until fructose and parathyroid hormone were administered in sustained combination. Thereupon, a renal dysfunction of characteristic type and severity occurred invariably and almost immediately. Thus, the concentration of circulating parathyroid hormone can modulate the functional expression of the experimental renal disorder. This effect of parathyroid hormone, which appears to involve more than simple physiologic summation, may have important clinical implications.
D000328:Adult; D001639:Bicarbonates / Q000097:blood / Q000652:urine; D002118:Calcium / Q000097:blood / Q000652:urine; D002239:Carbohydrate Metabolism, Inborn Errors / Q000150:complications*; D005246:Feedback; D005260:Female; D005632:Fructose / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007011:Hypoparathyroidism / Q000503:physiopathology; D007684:Kidney Tubules / Q000503:physiopathology*; D009584:Nitrogen / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood / Q000502:physiology*; D015499:Renal Tubular Transport, Inborn Errors / Q000209:etiology*; D014527:Uric Acid / Q000097:blood
D001639:Bicarbonates; D010281:Parathyroid Hormone; D014527:Uric Acid; D005632:Fructose; D009584:Nitrogen; D002118:Calcium