Cleve Clin J Med. Maghnie M, Altobelli M, di Iorgi N, et al. Diabetes insipidus results from a deficiency of vasopressin (antidiuretic hormone [ADH]) due to a hypothalamic-pituitary disorder (central diabetes insipidus) or from resistance of the kidneys to vasopressin (nephrogenic diabetes insipidus). We will also discuss treatment strategies for CDI, with analysis of potential complications of treatment.Diabetes insipidus (DI) is a rare disorder of water homeostasis characterized by the excretion of abnormally large volumes of hypotonic urine.
To prevent over dehydration and severe hypernatraemia, patients should be weighed at baseline, and 2 hourly thereafter; a drop in body weight of 5% from baseline indicates serious loss of body water, and the test should be abandoned.
Ye L, Li X, Chen Y, et al. 2012;77(2):69-84.
In clinical practice, it needs to be distinguished from renal resistance to the antidiuretic effects of AVP (nephrogenic DI), and abnormalities of thirst appreciation (primary polydipsia).
Central diabetes insipidus (CDI) is characterized by hypotonic polyuria due to impair ‐ ment of AVP secretion from the posterior pituitary. The test is best performed in a specialised centre.
Urine volumes fall and urine osmolality should rise to over 750 mOsm/kg, provided that a sufficient osmotic stimulus to AVP secretion (plasma osmolality > 295 mosm/kg) is attained at the conclusion of dehydration.
Patients with nephrogenic DI are resistant to the antidiuretic effects of desmopressin and do not respond with urinary concentration.
Water intake which is in excess of physiological needs cannot be lost through the kidneys and accumulates, causing dilutional hyponatraemia. Recent prospective multicenter trial data on copeptin measurement suggests this surrogate marker improves diagnostic accuracy in polyuric syndromes and its measurement after hypertonic saline infusion may soon become part of routine diagnostic algorithms, in specialised centres.
In adipsic DI, the demonstration of absent osmoregulated thirst during WDT or hypertonic saline infusion is the gold standard for diagnosis of the condition.Once a diagnosis of CDI is made, MRI imaging of the hypothalamo‐pituitary region is required to establish whether there is a structural lesion which is responsible for AVP deficiency.
Autosomal dominant neurohypophyseal diabetes insipidus with linkage to chromosome 20p13 but without mutations in the AVP-NPII gene.
dDAVP is a synthetic analogue specific for the V2 receptor, which has been modified from AVP in two ways; the amino group of the cysteine has been removed to prolong half‐life,Acute onset of CDI usually occurs in the neurosurgical setting, 2‐3 days following hypothalamic/pituitary insult. We will also review the treatment strategies to manage polyuria, while avoiding hyponatraemia.Central DI is the clinical manifestation of destruction of the neurons of the hypothalamus/posterior pituitary axis, with consequent loss of AVP secretion. Copeptin is the C‐terminal locus of the AVP precursor, prepro‐vasopressin, and it is co‐secreted from the neurohypophysis in equimolar amounts with AVP, in response to osmotic and haemodynamic stimuli (Figure In a prospective study of 55 patients, the Swiss group further demonstrated that a baseline plasma copeptin concentration of >21.4 pmol/L differentiates NDI from other causes of polyuria, with a sensitivity and specificity of 100%, thus mitigating the need for WDT in this circumstance.
There are many possible causes of this damage, including an inherited … In addition, the measurement of thirst ratings can help the differentiation between CDI and primary polydipsia.
Because they are losing a lot of water in the urine, these patients are at risk for dehydration.Patients who have diabetes insipidus have increased thirst and tend to drink a great deal of water.
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