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Anti Diuretic hormone (ADH)

Basic physiology

 

Desmopressin acts via V1 and V2 receptors.

  1. Actions Via V1 are
    1. Blood vessel = Constricts, causes increase BP in high doses.
    2. Other smooth muscle constriction, causes increases GIT movement
    3. Liver increase hepatic glycogenolysis
    4. Increase platelet aggregation
  2. Action Via V2 are
    1. Collecting tubules – action by regulating aquaporin 2, 3, 4
    2. Liver : release of factor VIII (  that’s why it is used in hemophilia)
    3. Endothelium : causes release of V.W. Factor

Diabetes insipidus

This is the passage of big volumes [polyuria (>3L/day) of dilute urine due to impaired water resorption by the kidney, because of reduced ADH secretion from the posterior pituitary (cranial DI), or impaired response of the kidney to ADH (nephrogenic DI).

 

Causes of cranial DI.

  1. Idiopathic (>50%).
  2. Congenital: X-link recessive, DIDMOAD syndrome
  3. Tumour: craniopharyngioma
  4. Trauma: hypophysectomy, head injury.
  5. Infiltration: histiocytosis, sarcoidosis.
  6. Vascular: Sheehan's syndrome.' haemorrhage
  7. Infection: meningoencephalitis, 

Important Point: Multiple sclerosis is not a cause of DI

 

Causes of nephrogenic DI

  1. Hereditary X-link recessive (LQ 2012)
  2. Drugs: Lithium (FAQ), Demeclocycline,  Methoxyflurane, Amphotericin B,  Aminoglycosides, Cisplatin, Rifampin, Foscarnet
  3. Chronic renal disease.
  4. Post-obstructive uropathy.
  5. Hypokalemia, Hypercalcemia (FAQ) 

Diagnosis

 

The water deprivation test.

  1. In this test patient is hospitalized and his water intake is stop completely.
  2. If patient urine out put is reduce that indicates psychogenic cause of polyuria.
  3. If still urine out put is high then injection ADH is given.
  4. Now If patient’s urine output is reduce that indicate cranial cause of diabetes insipidus.

If still urine out is high than it is most likely nephrogenic diabetes insipidus. In that case treat the basic cause.

 

Laboratory differentiation of polyuria

 

Lab parameters

Psychogenic Polydipsia

Central DI

Nephrogenic DI

(LQ 2012)

Osmotic Diuresis

Serum Na

N or

(LQ 2012)

N or

Posm

N,

N,

Uosm

(LQ 2012)

Plasma ADH

Uosm after ADH

Increase

Increase

Nil (LQ 2012)

Slight increase

 

How to approach a cause of Polyuria (>3L / 24 hrs)

 

Urine osmolality

  1. Decreased < 250 mosmol
    1. Low serum sodium, · Plasma osmolality Normal or Low = Psychogenic polydipsia
    2. Increased serum sodium, Increased plasma osmolality = 
      1. ↑ plasma ADH = No response in urine osmolality after ADH administration = Nephrogenic DI (LQ 2012)
      2. ↓ plasma ADH = Increase in urine osmolality after ADH administration =  Central DI
  2. Increased (>300 mosm/kg) = Solute Diuresis  
    1. Serum Sodium / Serum Osmolality is usually increased
    2. During solute diuresis more water is lost than sodium thereby causing hypernatremia and hypertonicity.
    3. Solute Diuresis
      1. Glucose (Diabetes Mellitus)            
      2. Mannitol (Osmotic Diuretic)
      3. Urea (High protein feeding)            
      4. Resolving ATN
      5. Medullary Cystic Disease                        
      6. Diuretics

TABLE Response to Water Deprivation Test

 

Diagnosis

Increase in Urine Osmolality above 280 mOsm/kg with Dehydration

Further Increase in Urine Osmolality in Response to ADH

Normal

+

-

Central DI

-

+

Nephrogenic DI

-

-

 


Treatment

  1. Cranial DI: desmopressin (LQ 2012), a synthetic analogue of ADH.
  2. Nephrogenic: Treat the cause- Treatment with conventional doses of a thiazide diuretic and/or amiloride in conjunction with a low-sodium diet and a prostaglandin synthesis inhibitor (e.g., indomethacin) usually reduces the polyuria and polydipsia (Ref. Hari. 18th ed., Pg-2907)




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