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Prolonged hypernatremia triggered by hyperglycemic hyperosmolar state with coma: A case report.

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Summary

Severe hyperglycemia can trigger lithium-induced nephrogenic diabetes insipidus (NDI) years after lithium cessation. Patients with prior lithium use need monitoring for hypernatremia after hyperglycemic events.

Keywords:
HyperglycemiaHypernatremiaHypertonicityLithiumNephrogenic diabetes insipidus

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Area of Science:

  • Nephrology
  • Endocrinology
  • Pharmacology

Background:

  • Lithium is a mood stabilizer with known renal side effects, including nephrogenic diabetes insipidus (NDI).
  • NDI is characterized by the kidneys' inability to concentrate urine, leading to excessive water loss.
  • Past lithium therapy can have long-term implications on renal function.

Observation:

  • A patient with a history of prolonged lithium use presented with hyperglycemic hyperosmolar state (HHS).
  • Following HHS treatment, the patient developed persistent hypernatremia with polyuria and low urine osmolality.
  • The condition was unresponsive to desmopressin and vasopressin, indicating NDI.

Findings:

  • Severe hyperglycemia can precipitate symptomatic NDI, even years after lithium discontinuation.
  • The patient's NDI resolved with fluid intake and diuretic therapy (amiloride and hydrochlorothiazide).
  • This suggests a complex interplay between hyperglycemia and latent lithium-induced renal dysfunction.

Implications:

  • Patients with a history of lithium use require careful monitoring of serum sodium levels after hyperglycemic episodes.
  • This is crucial regardless of a prior NDI diagnosis, as NDI can manifest late.
  • Early recognition and management are essential to prevent severe hypernatremia and its complications.