Related Experiment Videos
Recurrent pregnancy-induced polyuria and thirst due to hypothalamic diabetes insipidus: an investigation into
Insights
A patient with hypothalamic diabetes insipidus experienced thirst and increased urination during pregnancy due to a lowered thirst threshold, not renal issues. This highlights pregnancy
Area of Science:
- Endocrinology
- Reproductive Medicine
- Nephrology
Background:
- A patient with a history of hypothalamic diabetes insipidus (DI) since infancy, treated with vasopressin, presented with recurrent symptoms during pregnancy.
- The patient exhibited normal osmoregulation and thirst mechanisms when not pregnant, despite a history of DI.
Observation:
- During pregnancy, the patient experienced increased thirst and polyuria, with lower basal plasma osmolality and a reduced osmolar thirst threshold.
- Renal concentrating ability remained intact, and circulating vasopressinase activity was ruled out as a cause.
Findings:
- Lowered basal plasma osmolality and thirst threshold during pregnancy were observed.
- Plasma arginine vasopressin (AVP) concentrations were reduced after osmotic stimulation in the pregnant state.
- The renal concentrating mechanism was not impaired, suggesting a central osmoregulatory adaptation.
Implications:
- Pregnancy-induced hormonal changes may alter central osmoregulation, leading to thirst and polyuria in individuals with underlying DI.
- The findings suggest a potential mechanism involving a lowered thirst threshold and suppressed AVP secretion during pregnancy.
- Further research is needed to fully elucidate the interplay between pregnancy, osmoregulation, and AVP dynamics in DI patients.
Abstract:
A young patient developed hypothalamic diabetes insipidus due to histiocytosis in infancy and was satisfactorily treated with Pitressin. As a teenager she no longer had thirst or polyuria after treatment was stopped. These symptoms only returned during her two pregnancies. When non-pregnant her urine output was 1.7-2.0 1/24 h, basal plasma osmolality 288-290 mOsm/kg, and during pregnancy 24 h urine volume was 4.5-5.21, plasma osmolality 278-280 mOsm/kg. Studies on osmoregulation of thirst and AVP release, and on renal sensitivity to the V2 agonist desmopressin and endogenous vasopressin were performed in pregnant and non-pregnant states. She had no circulating antibodies to AVP, and the effect of pregnancy-associated vasopressinase was eliminated. Results showed lowered basal plasma osmolality and osmolar thirst threshold in pregnancy but no failure of the renal concentrating mechanism. Plasma AVP concentrations after osmotic stimulation were lower in pregnancy. We propose that she developed thirst and polyuria during pregnancy because of lowering of her osmolar thirst threshold to plasma osmolalities which caused her to drink sufficient quantities of fluid to further reduce AVP secretion. We cannot exclude, however, the possibility that there was increased clearance of circulating AVP.