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Hormonal and metabolic responses to intravenous glucose in children on regular hemodialysis

Insights

Children undergoing hemodialysis show impaired glucose metabolism and abnormal hormone levels, including elevated insulin and growth hormone, suggesting a link to poor glucose utilization in chronic renal failure.

Area of Science:

  • Pediatric Nephrology
  • Endocrinology
  • Metabolic Disorders

Background:

  • Chronic renal failure (CRF) impacts multiple organ systems, including metabolic regulation.
  • Children on hemodialysis often exhibit altered glucose homeostasis.
  • Hormonal dysregulation is a common complication in pediatric CRF.

Purpose of the Study:

  • To investigate the metabolic and hormonal responses to intravenous glucose in children with CRF undergoing hemodialysis.
  • To compare these responses with those of healthy children.
  • To explore potential interrelationships between metabolic and hormonal changes.

Main Methods:

  • Intravenous glucose tolerance tests were performed in 16 children on regular hemodialysis and 9 healthy controls.
  • Measurements included blood glucose, plasma nonesterified fatty acids, amino acids, immunoreactive insulin, growth hormone, and immunoreactive glucagon.
  • Fractional disappearance rate of glucose was calculated.

Main Results:

  • Patients had a reduced fractional glucose disappearance rate and elevated basal insulin, growth hormone, and glucagon levels.
  • Insulin response to glucose showed an increased late phase in patients.
  • Growth hormone rose paradoxically post-glucose, and glucagon failed to suppress.
  • Plasma nonesterified fatty acids were lower and fell more post-glucose in patients.

Conclusions:

  • Children on hemodialysis exhibit significant metabolic and hormonal disturbances, including impaired glucose utilization.
  • Elevated basal insulin, growth hormone, and glucagon, along with altered responses to glucose, suggest complex endocrine dysregulation.
  • These alterations may be interconnected and stem from a fundamental failure in normal glucose metabolism in pediatric CRF.

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