Diabetes insipidus in a Puppy

A 21-month-old, male, neutered cross-breed (Figure 1) presented to the practice having been adopted from Greece two-and-a-half months before. He had been a stray and living in a foster home.

Figure 1. Lolan that the 21-month-old, male, neutered crossbreed.

The owner reported that, while Lolan seemed fine, he had been polydipsic and polyuric. He had suffered two episodes of nocturia. However, if he was left by the owner during the daytime, he suffered from incontinence.

A clinical examination didn’t reveal any abnormalities. Lolan weighed 12.9kg and was set a goal weight of 11kg. A free-flow urine sample revealed very dilute urine of 1.005.

The results for electrolytes, haematology, biochemistry and C-reactive protein were within normal limits. No signs of polydipsia-induced hyponatraemia was noted.

The following week, a free-flow morning urine sample was provided, and the urine specific gravity was retested and found to be 1.008 (Table 1).

Lolan was declared for a water deprivation test. He had been put at a little, newspaper bed kennel to discourage urination and was not permitted access to water (Table two).

In the end point of the test, a pee sample was taken. The pee was nearly colourless (Figure 2) and the specific gravity was 1.005.

Urine microscopy revealed the existence of casts. A symmetric dimethylarginine test revealed a very slightly raised effect of 15ug/dL (1μg/dL into 14μg/dL) and a basal cortisol was within normal limits — 31.2nmol/L (25nmol/L into 125nmol/L).

With a diagnosis of diabetes insipidus looking extremely likely, Lolan was declared again to get a desmopressin (antidiuretic hormone analogue) response test to differentiate between central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI). He had been awarded 0.5ml of desmopressin IV and, again, water was withheld (Table 3).

The test was stopped when the specific gravity attained 1.024, as it was deemed to demonstrate a sufficient improvement in urine concentration to make a analysis of CDI.

Table 1. Urine analysis.

Desmopressin tablets were prescribed in a dose rate of 0.1mg twice daily.

Three days after although the pills had been responded to by Lolan and was urinating and drinking a lot less, he’d developed diarrhoea. He was in himself and revealed no symptoms. It was advised that the dose of desmopressin was decreased to 0.1mg twice a day, he had been moved into a dull diet plus that he took a probiotic supplement for three times.

The owner phoned two weeks to report his faeces had returned to normal and Lolan was better. 1 month later, Lolan proceeds to succeed on only 0.1milligrams desmopressin twice a day.


Diabetes insipidus is a rare endocrine disease characterised by antidiuretic hormone (ADH) dysregulation, excessive polyuria, polydipsia, and also the absence of hyperglycaemia and glucosuria. ADH is a nanopeptide.

It’s then transported to and stored in the posterior lobe of the pituitary gland, which then releases it.

ADH’s two principal functions would be to retain water within the body and to constrict blood vessels.

Diabetes insipidus contains two presentations and is distinct to diabetes mellitus.


Table two. Water deprivation test.

CDI, in which ADH amounts are inadequate, can be due to:

  • Hypothalamic-pituitary trauma.
  • Post-transsphenoidal surgery for correctionof hyperadrenocorticism.
  • Dorsally Growing cysts, inflammatory granuloma and lymphocytic hypophysitis.
  • Congenital malformation and neoplasms, such as craniopharyngioma, pituitary chromophobe adenoma.
  • Pituitary chromophobe adenocarcinoma and metastatic tumours, such as metastatic mammary carcinoma, lymphoma, malignant melanoma and pancreatic carcinoma.

The web result of central diabetes insipidus is a deficiency of antidiuretic hormone generation, causing persistent hyposthenuria (urine certain gravities less than or equivalent to 1.006) and severe diuresis, and can result in severe dehydration. Given the patient’s young age and the absence of any neurological signs, there was a mass deemed very improbable.


NDI is because of nephron impairment as a result of genetic or acquired disorder. This ends in the nephrons being conducive to ADH activity. Plasma ADH concentrations are normal or raised in animals. Main (hereditary) NDI is an uncommon disorder of puppies resulting from a congenital defect involving the cellular mechanisms responsible for insertion of aquaporin-2 water stations into the luminal cell membrane.

Secondary (obtained) NDI includes a variety of metabolic and renal disorders that interfere with the normal interaction between ADH and its renal tubular receptors, affecting renal tubular cell function, or decreasing the hypertonic renal medullary interstitium, resulting in a loss of the normal osmotic gradient.

Clinical indications of diabetes insipidus

Figure 2. Lolan’s urine sample.

Polydipsia and Polyuria are the clinical signs in dogs with diabetes insipidus.

In dogs with primary (genetic) NDI, clinical indications typically become evident at that time the dog is 8 to 12 months of age, with symptoms of polyuria, polydipsia and urinary incontinence.

Signs have been reported, dueto electrolyte disturbances or adrenal neoplasia, with melancholy and seizures detected in circumstances. Water consumption can be intense, occasionally exceeding 800ml/kg/day, together with compensatory urine production exceeding50ml/kg/day.

Blood tests are often within normal limits, but might include a polydipsia-induced hyponatraemia (not detected in this case).

Urinalysis usually shows hyposthenuria or isosthenuria, unless concurrent nephropathy is present and haematuria isn’t regularly observed. Urine culture and sensitivity is needed to eliminate underlying cystitisor pyelonephritis.


Diagnosis is initially one of exclusion of other ailments (Panel 1), followed by water deprivation tests, ADH treatment and, if possible, central nervous imaging research to diagnose CDI. The main challenge is differentiating between CDI, NDI and psychogenic polydipsia. Standard haematology and biochemistry assessments tend to be within normal limits.

Table 3. Desmopressin response test.

An answer to artificial ADH therapy and CDI might help differentiate nephrogenic. A rise in urine specific gravity by 50% or more, compared with pre-treatment certain gravities, supports the identification of CDI — especially if urine-specific gravity exceeds 1.025. Minimal improvement should be evident in dogs with main NDI. Since the plasma tends to depress ADH generation, dogs with psychogenic water consumption may exhibit a decrease in water intake and urine output.

Hypothalamic or pituitary neoplasia should be considered in elderly dogs diagnosed with CDI.

A renal biopsy may be warranted in the elderly dog thought to have NDI.


Together with hypophyseal tumours, a hypophysectomy is suggested. In dogs that develop CDI secondary into hypophysectomy, CDI may spontaneously resolve within two to four months.

Prophylactic use of desmopressin in 4μg twice daily has been shown to be effective at minimising the beginning of CDI.

In dogs with primary NDI, long-term treatment incorporates reduced sodium diet, unlimited water access, hydrochlorothiazide (usedto increase urine osmolality), or desmopressin pills or nasal spray.


Water must be made accessible to the dog. Diabetes insipidus is a permanent condition, but in cases.

The prognosis is generally good, based on the underlying disorder. Regular monitoring of functionis advisable.

  • Drugs mentioned in this article are used under the cascade.

Panel 1. Differential diagnoses of and mechanism of action

  • Diabetes mellitus — osmotic diuresis
  • Chronic renal disorder — osmotic diuresis
  • Main renal glycosuria — osmotic diuresis
  • Post-urolithiasis diuresis — osmotic diuresis, down-regulation of aquaporin-2
  • Pyometra — bacterial endotoxin-induced reduced tubular sensitivity to antidiuretic hormone (ADH)
  • Escherichia coli septicaemia — bacterial endotoxin-induced reduced tubular sensitivity to ADH
  • Hypercalcaemia — interference with action of ADH on renal tubules
  • Hepatitis — loss of medullary hypertonicity, diminished hormone metabolism
  • Hyperadrenocorticism — diminished tubular response to ADH
  • Hyperaldosteronism — diminished tubular response to ADH
  • Pyelonephritis — bacterial endotoxin-induced reduced tubular sensitivity to ADH, damaged countercurrent mechanism
  • Fanconi’s syndrome — osmotic diuresis
  • Hypokalaemia — down-regulation of aquaporin-2, loss of medullary hypertonicity
  • Hyponatraemia — loss of medullary hypertonicity
  • Hypoadrenocorticism — loss of medullary hypertonicity
  • Hyperthyroidism — loss of medullary hypertonicity
  • Leptospirosis — action unknown
  • Polycythaemia — action of natriuretic peptide
  • Pheochromocytoma — excessive catecholamines
  • Portosystemic shunt — loss of medullary hypertonicity, improved glomerular filtration rate (GFR)
  • Dwarfism — action unknown
  • Acromegaly — osmotic diuresis because of diabetes mellitus
  • Psychogenic polydipsia — loss of medullary hypertonicity
  • Intestinal leiomyosarcoma — diminished tubular response to ADH
  • Really low protein diet — loss of medullary hypertonicity
  • Gastrointestinal disease (by Way of Example, ulcerative colitis)
  • X-linked hereditary nephropathy — loss of medullary hypertonicity, improved GFR
  • Renal dysplasia — loss of medullary hypertonicity, improved GFR

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