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Altered renal handling of electrolytes in a child with central diabetes insipidus (CDI)
Y Sebsibe1, Y Elias, L Zerihun
1Department of Paediatrics, Faculty of Medicine, Addis Abeba University.
Insights
This case study presents a child with central diabetes insipidus, a condition causing excessive urination and thirst. Treatment with a vasopressin analogue effectively managed the symptoms, highlighting its therapeutic role.
Area of Science:
- Pediatrics
- Endocrinology
- Nephrology
Background:
- Central diabetes insipidus (CDI) is characterized by inadequate antidiuretic hormone (ADH) secretion, leading to polyuria and polydipsia.
- Diagnosis often involves water deprivation tests and response to vasopressin administration.
- Management focuses on fluid replacement and ADH analog therapy.
Observation:
- A 12-year-old female presented with a three-year history of severe polyuria and polydipsia.
- Water deprivation failed to concentrate urine, with elevated basal plasma osmolality and sodium levels.
- Urine analysis revealed low osmolality and altered sodium and potassium concentrations.
Findings:
- Intramuscular administration of lypressin (a vasopressin analogue) significantly increased urine osmolality to 586 mOsm/kg.
- Symptoms resolved following vasopressin analogue treatment.
- The case suggests potential alterations in renal electrolyte handling and an abnormal response to vasopressin in CDI.
Implications:
- This case underscores the importance of prompt diagnosis and management of central diabetes insipidus in pediatric patients.
- Effective treatment with vasopressin analogues can significantly improve quality of life.
- Further research into the pathophysiology of electrolyte imbalances in CDI may be warranted.
Abstract:
A 12-year-old female child, with a history of polyuria and polydipsia of about three years duration, was admitted to Ethio-Swedish Paediatric Hospital, in Addis Abeba. Urine output in 24 hours averaged 5-6 litres, with a frequency of 15 times during the day and 7-8 times during the night. Random urine analysis showed an osmolality of 60 mOsm/kg, Na+ 27.1 mmol/L and K+ was 7.6 mmol/L. Basal plasma osmolality was 313 mOsm/kg with Na+ being 156 mmol/L and K+ 4.06 mmol/L. Water deprivation for nine hours failed to produce a concentrated urine, which was only 138 mOsm/kg at the end of the test, with a corresponding plasma osmolality of 336 mOsm/kg. After nine hours of water deprivation, urine Na+ increased from 27.1 to 37.3 mmol/L while K+ increased from 7.1 to 18.7 mmol/L. Lypressin, a vasopressin analogue, at a concentration of 0.3 IU/kg injected intramuscularly, resulted in a marked increase in urine osmolality to 586 mOsm/kg within two hours, associated with relief of symptoms. Urinary excretion of K+ was markedly increased during the vasopressin test while Na+ excretion was little affected. A case of central diabetes insipidus of undefined etiology is presented and the possibility of altered renal handling of electrolytes and an abnormal response to vasopressin in such cases is noted. The problem of management and the currently available treatment options are summarized.