Vasopressin-resistant diabetes insipidus
A condition which is characterised by normal renal filtration and solute excretion however there is a persistent hypotonic urine.
* Polyurea * Nocturia * Polydipsia * Failure to thrive * Weight loss * Dehydration * Bladder enlargement * Hydronephrosis
Diabetes insipidus results centrally from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture , or head trauma that damages the neurohypophyseal structures. It can also result nephrogenically from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial. (Note: Pituitary diabetes insipidus shouldn’t be confused with nephrogenic diabetes insipidus, a rare congenital disturbance of water metabolism that results from renal tubular resistance to vasopressin.) Normally, the hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable. The absence of vasopressin in diabetes insipidus allows the filtered water to be excreted in the urine instead of being reabsorbed.
Mild cases require no treatment other than fluid intake to replace fluid lost. Until the cause of more severe cases of diabetes insipidus can be identified and eliminated, administration of various forms of vasopressin or of a vasopressin stimulant can control fluid balance and prevent dehydration. Vasopressin injection is an aqueous preparation that’s administered S.C. or I.M. several times a day because it’s effective for only 2 to 6 hours; this form of the drug is used in acute disease and as a diagnostic agent.