Diabetes Insipidus

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Introduction

Anti-Diuretic Hormone (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 and volume receptors in the hypothalamus. A deficiency of ADH is known as Diabetes insipidus.

Causes of deficiency may be:

Central: Central DI is characterized by decreased secretion of antidiuretic hormone (ADH)—also known as arginine vasopressin (AVP)—which gives rise to polyuria and polydipsia by diminishing the patient’s ability to concentrate urine.

Diminished or absent ADH can be the result of a defect in 1 or more sites involving the hypothalamic osmoreceptors, the supraoptic or paraventricular nuclei, or the supraopticohypophyseal tract.

Nephrogenic: failure of the nephrons to respond to ADH present in the kidney.Is characterized by a decrease in the ability to concentrate urine due to a resistance to ADH action in the kidney. Nephrogenic DI can be observed in chronic renal insufficiency, lithium toxicity, hypercalcemia, hypokalemia, and tubulointerstitial disease, rarely, diabetes insipidus may be hereditary.

Psychogenic diabetes insipidus (psychogenic polydipsia) : It results from a neurological disorder of thirst control or as a result of some behavioral problem that triggers excessive water intake. In either case, the abnormally large volume of excreted urine in animals with psychogenic polydipsia is caused by excessive water intake (polydipsia), rather than by some primary problem with kidney, pituitary or hypothalamic function.

Clinical Signs

There will be a marked polyuria, 5-20X normal output, often resulting in nocturia and incontinence. There will also be a desperate polydipsia, animal will search for water.

Other clinical signs include dehydration, weight loss, anorexia and neurological signs if neoplastic in origin.

Diagnosis

The differential diagnosis of psychogenic polydipsia must be excluded. In this disease, 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.

A urine sample should be taken. In Diabetes insipidus, urine specific gravity is low (1.001-1.005).

Blood tests will show dehydration so will see mildly elevated PCV and TP.

When other differentials have been excluded, it may be necessary to perform a water deprivation test: This aims to measure urine osmolality after 12-24 hours water deprivation to determine whether ADH is indeed deficient.

Steps: Collect initial urine and plasma samples for osmolality and weigh patient. Withhold food and fluid. Collect urine and plasma after 6 hours and thence 2 hourly. This test can be damaging to the animals health and must not be performed unless diagnosis is strongly presumed as it can become an animal welfare issue if not. STOP when: patient displays concentrating ability or patient loses >5% bodyweight or 24 hours have passed.

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

An ADH response test can also be performed. Administer Desmopressin i/m and monitor specific gravity of urine 2 hourly. Central diabetes insipidus will concentrate urine (>1.020) whereas 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

A few different treatment options have been described for this disease such as Desmopressin: used for central disease only as is expensive.

Thiazide diuretics work by paradoxical effect by inhibiting the reabsorption of sodium in the proximal convoluted tubule. The volume of fluid within the extracellular fluid (ECF) will fall and hence the GFR will also decrease, reducing water loss. Chlorpropamide works by potentiating the effect of ADH on the tubules. Carbemazepine acts similarly to chlorpropamide.

Many owners choose not to medicate and will manage the disease by keeping animal 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 diabetes insipidus secondary to head trauma varies in prognosis and spontaneous recovery may occur.


Diabetes Insipidus Learning Resources
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References

Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition) W.B. Saunders Company

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2) W.B. Saunders Company

Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.




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