diabetes%20insipidus
DIABETES INSIPIDUS
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.

Pharmacotherapy

Central DI

Desmopressin

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

Chlorpropamide

  • Use is limited to patients who have partial central DI
    • Patient still secretes vasopressin but in insufficient quantity
  • Actions: May work by increasing sensitivity of renal tubules to circulating endogenous vasopressin
  • Effects: May achieve 25-75% reduction in polyuria
  • Side effects & limited antidiuretic effect limit their use

Thiazide & Related Diuretics

  • Actions: May work by reducing extracellular Na & decreasing glomerular filtration
  • Effects: May achieve 25-50% reduction in polyuria
  • Side effects & limited antidiuretic effect limit their use
  • Use should be combined w/ low osmolar & low Na diet

Carbamazepine

  • Actions: May enhance the response to antidiuretic hormone
  • Can lower urine output by as much as 50-60%

Clofibrate

  • Actions: May increase the release of antidiuretic hormone

Nephrogenic DI

Thiazide & Related Diuretics

  • Use should be combined w/ low osmolar & low Na diet
  • Actions: Increase Na loss at the cortical diluting tubule by inhibiting Na reabsorption
  • Effects: Can usually obtain 50% reduction in polyuria
  • May combine w/ K-sparing diuretic if hypokalemia occurs

Potassium-Sparing Diuretics

  • No untoward effects reported when combined w/ thiazide diuretics to correct hypokalemia
  • Actions: Act on the distal renal tubules, cause an increase in the excretion of Na & reduce the secretion of K

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

  • Indomethacin, Tolmetin & Ibuprofen
  • May have an additive effect w/ thiazide diuretics in reducing water excretion in some patients
  • Actions: Prostaglandin synthetase inhibitors which reduce urine flow

Non-Pharmacological Therapy

Central DI

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

Familial

  • Genetic counseling & follow-up

Nephrogenic DI

Drug-Induced

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

Familial

  • Low sodium & low osmolar diet
  • 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
  • Genetic counseling & follow-up
  • Appetite, linear growth & temperature should be monitored during all clinic visits
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