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Feedback Endocrinology

 Diabetes insipidus (DI)

DI may be due to lack of hormone ( Central ) or inadequate response to hormone (  Nephrogenic )

Physiology

– Normal concentrations cause reduction of diuresis in kidney tubules via aquaporin 2.

– High concentration causes vasoconstriction in vascular tissue

– ADH (anti- diuretic hormone) is supressed below 280mOsm/kg

– Max ADH action is achieved at 295 mOsm/kg

– Thirst is achieved at 295 mOsm/kg

Etiology  
  • Central – idiopathic, head trauma, vascular disorders,
  • Nephrogenic – idiopathic, hypercalcemia, hypokalaemia, chronic kidney disease, pregnancy
  • Congenital – Wolfram syndrome (WFS1 mut) – DI, DM, optic atrophy, deafness

Clinical features

  • Polyuria, nocturia, polydipsia, dehydration, impaired consciousness
  • DI may be masked by cortisol deficiency. Give hydrocortisone to see if DI apparent (symptoms still present)

Diagnosis

  • Fluid deprivation test  
    • Healthy patients
      • Normal plasma osmolality and increased urine (600 mOsm/kg)
    • DI
      • High plasma Osm and normal/low urine Osm.
      • Corrected with Desmopressin  (cranial)
      • If not corrected (nephrogenic)

Treatment

  • Desmopressin – intranasal [20-40mcg], oral [100-200mcg], I.M
    • Doesn’t cause vasoconstriction.
  • Thiazides
    • Sensitise s renal collecting ducts. Good for nephrogenic type.
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