diabetes%20insipidus
DIABETES INSIPIDUS
Treatment Guideline Chart
Diabetes insipidus is a polyuric disease characterized by excretion of a large volume of hypotonic urine and hypernatremia. It is due to the absence of antidiuretic hormone.
Central (hypothalamic or neurohypophyseal) diabetes insipidus is the inability to secrete & produce vasopressin in the neurohypophyseal system. It is due to damage to the pituitary gland & hypothalamus, may be due to diseases, head injuries, neurosurgery, infection or genetic or autoimmune disorders.
In nephrogenic diabetes insipidus, there is inappropriate renal response to vasopressin. Kidney function may be impaired by drugs & by chronic disorders like polycystic kidney disease, sickle cell disease, kidney failure, partial ureteral block, hypokalemia, hypocalcemia, low protein diet & genetic disorders.
Primary polydipsia have abnormal increase in fluid intake.

Diabetes%20insipidus Treatment

Principles of Therapy

  • Choice of therapy depends on the severity of polyuria

Goals

  • Determine and treat the underlying cause
  • Adequate hydration and replacement of free water deficit
  • Replacement of deficient hormone
 

Pharmacotherapy

Central DI

Desmopressin

  • 1st-line pharmacotherapy agent
  • Analogue of naturally occurring vasopressin
    • Antidiuretic effect is greater and more prolonged than vasopressin
    • Urine volume is decreased and osmolality is increased
    • Less vasopressor activity than vasopressin
  • Oral, intranasal and parenteral forms are available

Chlorpropamide

  • Use is limited to patients who have partial central DI
    • Patient still secretes vasopressin but in insufficient quantity
  • May work by increasing sensitivity of renal tubules to circulating endogenous vasopressin
  • Side effects and limited antidiuretic effect limit their use

Thiazide and Related Diuretics

  • Use should be combined with low-osmolar and low-Na diet 
  • May work by reducing extracellular Na and decreasing glomerular filtration
  • Side effects and limited antidiuretic effect limit their use

Carbamazepine

  • May enhance the response to ADH
  • Can lower urine output by as much as 25-60%

Clofibrate

  • Stimulates secretion of AVP

Nephrogenic DI

Desmopressin

  • Treatment option for patients with partial nephrogenic DI

Thiazide and Related Diuretics

  • Use should be combined with low-osmolar and low-Na diet
  • Increase Na loss at the cortical diluting tubule by inhibiting Na reabsorption
  • Can reduce urine output by almost 70%
  • May combine with potassium (K)-sparing diuretic if hypokalemia occurs

Potassium-Sparing Diuretics

  • Eg Amiloride 
  • Act on the distal renal tubules, cause an increase in the excretion of Na and reduce the secretion of K
  • No untoward effects reported when combined with thiazide diuretics to correct hypokalemia

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

  • Eg Indomethacin, Tolmetin and Ibuprofen
  • Prostaglandin synthetase inhibitors which reduce urine flow
  • Treatment option for patients not responsive to thiazides and Amiloride
  • May have an additive effect with thiazide diuretics in reducing water excretion in some patients

 Carbamazepine

  • Increase endogenous secretion of AVP

 

Non-Pharmacological Therapy

Central DI

  • Small children with DI may have rapid changes in osmolality
  • Family needs to be educated to gauge appropriate fluid intake and urine output
    • Daily weight may be used as index of fluid balance
    • Regular measurement of electrolytes may be required especially during beginning stages of treatment
  • A low-Na and low-protein diet is recommended
  • Appetite, linear growth and temperature should be monitored during all clinic visits

Familial

  • Genetic counseling and follow-up

Nephrogenic DI

Drug-Induced

  • Discontinue offending agent
    • May take a few weeks to see improvement

Familial

  • Infants: Human milk is preferred because of protein content (6%)
    • Decrease Na intake to 0.7 mEq/kg/day
  • Children: 8% of total daily calories should be from protein
    • Na intake should be <0.7 mEq/kg/day
  • Low-Na and low-osmolar diet
  • Appetite, linear growth and temperature should be monitored during all clinic visits
  • Genetic counseling and follow-up
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