Diabetes insipidus symptoms

Diabetes insipidus symptoms

Diabetes insipidus is caused by the deficit in regulation of the water balance which leads to production of > 3 litre per day of diluted /insipid urine due to impairment of the water resorption ability of the kidney and loss of the kidney concentrating ability.

The above condition is caused by reduced secretion of vasopressin /ADH hormone from the posterior pituitary gland or impair response of the kidney to the ADH/ vasopressin . ADH or also known as vasopressin is a hormone that involves in absorption of Na+ and water as well as excretion of H+ and K+ ions.

Diabetes insipidus is divided into cranial/central diabetes insipidus and nephrogenic diabetes insipidus. Cranial diabetes insipidus is caused by reduced or inadequate secretion of the ADH/vasopressin hormone while nephrogenic diabetes insipidus is caused by insensitivity response of the collecting duct of the kidney to ADH. Both of these conditions will lead to hypotonic polyuria.

Cranial diabetes insipidus is caused by several factors which include idiopathic causes in more than 50%, trauma such as head injury, neurosurgery, autoimmune hypophysitis or hypophysectomy. Any temporary trauma of the distal pituitary stalk which later leads to the grow of the proximal nerve ending search for capillaries in the scar tissue and begin secretion again may also leads to diabetes insipidus. Vascular causes such as haemorrhage, Sheehan syndrome or pituitary infarction form shock resulted from postpartum haemorrhage and sickle cell disease may also contribute to cranial diabetes insipidus. Infiltration (amyloidosis, histiocytosis, sarcoidosis and tuberculosis) and infection (encephalitis or meningitis) may as well lead to cranial diabetes insipidus. Cranial diabetes insipidus may also associate with Craniopharyngioma, pituitary tumour and metastases. Cranial diabetes insipidus may also related to familial causes such as DIDMOAD syndrome which is an autosomal recessive condition where the patient suffers from diabetes insipidus, optic atrophy, deafness and diabetes mellitus . It can also be inherited in an autosomal dominant pattern with more than 20 mutations detected. Defect in ADH gene synthesis may also lead to cranial diabetes insipidus.

Nephrogenic diabetes insipidus is another form of diabetes insipidus. It may be inherited in an autosomal dominant pattern which leads to a defect in the encoding of the aquaporin 2 gene which involves in the function of the ADH responsive water channel. Nephrogenic diabetes insipidus may also be inherited in an X linked pattern which leads to a defect in the V2 receptor which bind to ADH. Certain drugs may also lead to nephrogenic diabetes insipidus such as dexamethasone, lithium, democycline, dopamine, olfloxacin, amphothericin B and orlistat. Metabolic abnormalities such as hypercalcemia or hypokalemia may also cause diabetes insipidus, Interstitial kidney disease, chronic renal failure and post obstructive uropathy , pregnancy, pyelonephritis and osmotic diuresis (diabetes mellitus) may also lead to nephrogenic diabetes insipidus.

Diabetes insipidus is associated with another disorder such as paraneoplastic syndrome and Hand- Schuller - Christian (2-5 years old, lytic lesion and exopthalmus and diabetes insipidus.)

Pregnancy may also be associated with diabetes insipidus due to an increase ADH/ vasopressin breakdown from the effect of vasopressinase from the placenta.

In terms of epidemiology, the prevalence of diabetes insipidus is 4 per 100 000. The congenital form of diabetes insipidus is 1 per 100 000. 90% of diabetes insipidus is mostly inherited in an X linked disorder. Male is more commonly affected with a median age of onset is 24 years old. Besides that 18.3% of patients following transphenoidal microsurgery may develop diabetes insipidus. Deficiency of ADH occurs at any age including infant and children. Nephrogenic diabetes insipidus will manifest mostly in male during infancy which reflect x-linked mode of inheritance.

In terms of pathology, cranial diabetes insipidus is associated with hypothalamic disease which leads to degeneration and loss of function of the neurosecretory neurons which makes up the post pituitary gland (neurohypophysis and pituitary stalk). These neurosecretory neurons involved in ADH /vasopressin secretion. These will lead to triphasic response. In triphasic response, the patient initially presents with polyuria due to the loss of normal control which follow by transient normalization from the stored ADH from damaged neuron and finally further polyuria will continue due to the loss of ADH synthesis and depletion Of the ADH that is stored.

Nephrogenic diabetes insipidus is associated with insensitivity of the collecting duct response to ADH / vasopressin. This will lead to the inactivation of the aquaporin / water channel which later leads to an impermeability of the luminal membrane to the water. This condition will result in polydipsia and hypotonic polyuria.

Diabetes insipidus is most commonly presented with polyuria, polydipsia, nocturia, and dehydration, symptoms of hypernatremia, the preference of the cold, icy drink, headache and visual disturbance. Central /cranial diabetes insipidus has a rapid rate of onset than nephrogenic diabetes insipidus. On examination, patients may present with signs of dehydration, such as tachycardia, reduced skin turgor, dry mucous membrane and postural hypotension.

The investigation requires in diabetes insipidus may include, urea and electrolyte studies, serum and urine osmolality and glucose.

Urea and electrolytes may reveal hypokalemia and hypercalcemia as well as hypernatremia in any cases of diabetes insipidus. Serum osmolality is measured by this formula ( 2 ( sodium ion + potassium ion ) + urea + glucose mmol/l. Normal serum osmolality is 285 - 295 mOsmol/kg. Urine osmolality is commonly twice the concentration of the serum osmolality with urine to plasma osmolality ratio is more than 2:1. In normal individual urine to plasma osmolality ratio is more than 2. Plasma osmolality is < than 295 mOsmol/kg. Urine osmolality is more preferable than urine specific gravity. Glucose level test is important to exclude diabetes mellitus.

Rarely plasma vasopressin or urinary vasopressin can be measured by osmotic stimulation from fluid restriction and hypertonic saline. Imaging test (MRI scan) is useful to defect any lesion in the brain.

Differential diagnosis of diabetes insipidus may include diabetes mellitus, psychogenic or primary polydipsia and any drug intake such as lithium, democycline or any diuretics. The primary polydipsia patient will present with polyuria and polydipsia and diluted urine. It may be due to mania, schizophrenia and lithium therapy. Hypothalamus disease such as brain tumour, injury, neurosarcoidosis, encephalitis and HIV encephalopathy may lead to primary polydipsia.

Water deprivation test is performed to test the ability of the kidney to concentrate the urine and conserve the water or producing diluted urine despite dehydration and to localize the causes of this situation.

Water deprivation test is only performed if the patient produces diluted urine > 3l/day with an increase in the urine volume and increase in the plasma sodium concentration which indicates significant water disturbance.

Basically the patient is advised not to drink tea, coffee or smoking during the test and daily breakfast is given at 6.30 am and free fluid at 7.30 am before the test start at 8.00 am. Stop the test when urine osmolality is > than 600 mOsmol/kg.

Stage 1 of the water deprivation test is performed for 8hrs and begins at 8.00 am. The purpose of this test is to confirm the diagnosis of the diabetes insipidus. The patient is asked to empty the bladder, with no fluid intake and only dry food is allowed. Weight is measured hourly. If > 3% weight loss, serum osmolality is measured. If serum osmolality is < 300 mOsmol/kg continues the test and every 2 hours urine sample is taken. Its volume and osmolality is measured. Venous sampling is taken every 4 hours and its osmolality is measured. The test is stopped at 8 hours later when urine osmolality > 600 mOsmol/kg.

Stage 2 is performed when the serum osmolality is > than 300 mOsmol/kg and urine is diluted < 600 mOsmol/kg. Desmopressin 2 microgram intramuscularly is given to the patient and the patient is asked to drink the water. 4 hours later, urine osmolality is measured every hour

Normal individuals may have normal concentrations of urine (600 mOsmol/kg) and urine to plasma ration more than 2:1. In primary polydipsia individual, the urine is concentrated but less than normal 400 -600 mOsmol/Kg. The cranial diabetes insipidus patient is responsive to Desmopressin and produce normal urine concentration while nephrogenic diabetes insipidus unresponsive to Desmopressin.

Generally the treatment of diabetes insipidus may include the control of the balance of the fluid and prevention of dehydration. Patient is weigh daily. Good skin and mouth care is provided. In cases such as nephrogenic diabetes insipidus correction of hypercalcaemia and hypokalemia is performed followed by discontinuation of causative medication.

The patient is advised to have a normal diet with free access to the fluid. The low solute formula is given to young infants with nephrogenic diabetes insipidus . Low sodium and low protein diet may reduce the urine output in nephrogenic diabetes insipidus.

Treatment of cranial diabetes insipidus may include confirmation of pituitary pathology with MRI scan and performing anterior pituitary function tests as well as consider giving Desmopressin to the patient. Desmopressin ( DDAVP - a derivative of vasopressin or synthetic vasopressin /ADH analogue ) is given intranasally 1-2 times a day in a dosage which is sufficient to control polyuria and polydipsia. It can be given orally, starting at 100 micorgram 2-4 times a day on an empty stomach and titrated to 200 - 600 microgram 2-4 times a day.

Desmopressin is used with caution in the immediate postoperative period of the intracranial lesson as it carries a possibility of developing cerebral oedema. Desmopressin overdose may lead to water intoxication and hyponatremia in patients with excessive water intake.

Treatment of nephrogenic diabetes insipidus may include treatment of the underlying disorder and hydrochlorothiazide 25 mg OD/bed. Amiloride can be added as an additional effect. NSAIDS is also beneficial as it will inhibit prostaglandin synthase that involved in the synthesis of prostaglandin that increase plasma sodium concentration and reduction in urine volume.

Chlorpropamide (Diabinase in the second line of drug use with a dosage of 125- 250 mg od/bd) will enhance the renal response to ADH. Chlorpropamide and an oral hyplycemic agent will lead to hypoglycemic episodes in diabetic patient. Clofibrate ( Atromid - s ) will increase ADH secretion in 500 mg every 6 hour dosage.

In the acute setting of diabetes insipidus, urgent urea and electrolytes and serum as well as urine osmolality is performed. Urine output is also monitored at the same time. Initial urea and electrolytes is measured twice daily with the aim to reduce the sodium concentration slowly at the rates below12 mmol/l per day with 0.9 % saline solution (150mmol/l) if sodium concentration is more than 170 mmol/l . Avoid the use of 0.45 % saline solution. Rapid reduction in sodium concentration may lead to cerebral oedema and brain injury. Then consider the trial of Desmopressin.

Complication may include complication of the underlying disorder such as tumour, histocytosis and dilation of the urinary tract due to accumulation of the urine. Congenital onset of nephrogenic diabetes insipidus is associated with mental retardation. Subnormal growth rate may also occur. Dehydration without treatment may lead to stupor coma and confusion.

The patient may require follow up at 2 -3 weeks then 3 -4 months. Treatment is adjusted based on the urea and electrolytes. Follow up treatment may include hospitalization of the patient for diagnostic test and outpatient continuous care and self medication.

The prognosis is variable depends on the causes. Most nephrogenic diabetes insipidus causes are associated with medication. Removal of the offending factors may improve the symptoms. Good prognosis depends on the underlying disorder. Cranial diabetes insipidus due to tumour may be improved by removal of the tumour.






the effect of vasopressin  on the collecting duct of the kidney in renal system which activates the water channel
the effect of vasopressin on the collecting duct of the kidney in renal system which activates the water channel

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