CASE PRESENTATION: A 5-month-old Hispanic girl was found to have a large, hemorrhagic, suprasellar
glioblastoma causing
obstructive hydrocephalus. Prior to mass resection, she developed
central diabetes insipidus. Postoperatively, she continued to have
central diabetes insipidus and concurrent cerebral
salt wasting soon after. She was managed with a
vasopressin infusion,
sodium supplementation,
fludrocortisone, and urine output replacements. Despite resolution of her other major medical issues, she remained in the pediatric intensive care unit for continual and aggressive management of water and
sodium derangements. Starting on postoperative day 18, her
polyuria began increasing dramatically and did not abate with increasing
vasopressin. Nephrology was consulted. Her blood
urea nitrogen was undetectable during this time, and it was thought that she may have developed a depletion of inner medullary
urea and osmotic gradient: a "gradient washout." Supplemental
dietary protein was added to her
enteral nutrition, and her fluid intake was decreased. Within 4 days, her blood
urea nitrogen increased, and her
vasopressin and fluid replacement requirements significantly decreased. She was transitioned soon thereafter to subcutaneous
desmopressin and transferred out of the pediatric intensive care unit.
CONCLUSIONS: Gradient washout has not been widely reported in humans, although it has been observed in the mammalian kidneys after prolonged
polyuria. Although not a problem with
aquaporin protein expression or production, gradient washout causes a different type of secondary
nephrogenic diabetes insipidus because the absence of a medullary gradient impairs water reabsorption. We report a case of an infant who developed complex water and
sodium imbalances after
brain injury. Prolonged
polyuria resulting from both water and solute diuresis with low enteral
protein intake was thought to cause a
urea gradient washout and secondary
nephrogenic diabetes insipidus. The restriction of fluid replacements and supplementation of enteral
protein appeared adequate to restore the renal osmotic gradient and efficacy of
vasopressin.