Diabetes Insipidus

ADH from the posterior pituitary stimulates water uptake from the distal convoluted tubule and collecting ducts of the kidney and so conserves water. Release is regulated by:

• Osmoreceptors in the hypothalamus.
• Volume receptors in the hypothalamus.

A deficiency of ADH is known as Diabetes insipidus. May be:

• Central: failure to synthesise or release ADH.
• Nephrogenic: Failure of the nephrons to respond to ADH present in the kidney.

Clinical Signs

• Marked polyuria; 5-20X normal output, often resulting in nocturia and incontinence.
• Marked polydipsia; animal will search for water.
• Dehydration.
• Weight loss.
• Anorexia.
• Neurological signs if neoplastic in origin.

Differential diagnosis:

Presents similarly to Psychogenic polydipsia. Patients drink excessively leading to overhydration and a functional lack of ADH (none is released as water does not need to be conserved). The kidney in this case will have decreased ability to concentrate urine due to medullary washout. The hypertonicity within the medulla is abolished by the excess water.

Diagnosis:

• Urine specific gravity is low (1.001-1.005)
  Solute is absorbed in excess of water thus demonstrating a good tubular function.
• Dehydration so see mildly elevated PCV and TP.

Psychogenic polydipsia: plasma osmolality decreased due to excess water in contrast to increased plasma osmolality with DI due to dehydration.

• Water deprivation test: Aims to measure urine osmolality after 12-24 hours water deprivation to determine whether ADH is indeed deficient.
  • Collect initil urine and plasma samples for osmolality.
  • Weigh patient.
  • Withhold food and fluid.
  • Collect urine and plasma after 6 hours and thence 2 hourly.
  • STOP when:
    • Patient displays concentraing ability.
    • Patient loses >5% bodyweight.
    • 24 hours have passed.

A positive test for diabetes insipidus is a failure to concentrate urine >1.010 after 12-24 hours.

If psychogenic polydipsia is suspected then gradually restrict water for 3 days prior to test to avoid medullary washout giving a false positive test.

• ADH response test: Administer Desmopressin i/m. Monitor specific gravity of urine 2 hourly.
  • Central diabetes insipidus will concentrate urine >1.020.
  • Nephrogenic diabetes insipidus will not be able to concentrate the urine at all in response to the synthetic ADH. SG <1.010.
    Nb. A positive ADH response test means nothing unless preceded by a water deprivation test to prove the presence of diabetes insipidus.

Treatment:

• Desmopressin: Central disease only. Expensive.
• Thiazide diuretics: Paradoxical effect. By inhibiting the reabsorption of sodium in the proximal convoluted tubule the volume of fluid within the ECF will fall and hence the GFR will also decrease, reducing water loss.
• Chlorpropamide: Potentiates effect of ADH on the tubules.
• Carbemazepine: Acts similarly to chlorpropamide.
• No therapy: Animals kept outdoors with free access to water at all times.

Prognosis:

Congenital central diabetes insipidus has a favourable prognosis and can be treated with desmopressin. Nephrogenic diabetes insipidus has a more guarded prognosis.

Any expanding tumour, particularly if neurological signs are present, carries a poor prognosis.

Central diabtetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.