Diabetes Insipidus

Diabetes insipidus (DI) is a syndrome characterized by polyuria and polydipsia. DI reflects reduced action or secretion of ADH; four different types are distinguished (Table 1), described below.

Table1. Types of diabetes insipidus (DI)

Pituitary Diabetes Insipidus

 The most common type is pituitary diabetes insipidus, also known as hypothalamic, neurogenic, or central diabetes insipidus, in which reduced ADH production and secretion are usually related to agenesis or irreversible destruction of the neurohypophysis that may be due to a variety of genetic or acquired alterations. However, it is idiopathic in about 50% of cases (Table 2). Reduced ADH secretion results in renal free water reabsorption failure with the consequent elimination of high amounts of poorly concentrated urine. As a result, there is an increase in plasma osmolality, which stimulates thirst for osmoreceptors, causing polydipsia.

Table2. Causes of pituitary diabetes insipidus

Primary Polydipsia

 Primary polydipsia is a clinical condition characterized by an excessive and unmotivated introduction of fluids (ingestion of more than 3 liters of fluids/day), usually water, resulting in polyuria. The picture is observed mainly in patients with chronic psychiatric diseases, which is also defined as psychogenic polydipsia. The increased intake of liquids leads to a slight reduction in plasma osmolality, which deter mines a reduced secretion of ADH, leading to a reduction in urinary osmolality and an increase in urine volume; this triggers a compensatory increase in water excretion that pre vents hyperhydration.

Gestational Diabetes Insipidus

 Gestational DI is also a consequence of reduced ADH levels due to increased hormone degradation by an enzyme produced by the placenta (N-terminal aminopeptidase). Gestational DI typically develops in the third or fourth month of pregnancy and resolves 4–6 weeks after delivery. Generally, the changes are similar to those observed in pituitary DI. Plasma osmolality is usually in the normal range for a pregnant woman, which is generally about 3–4% lower than normal.

Nephrogenic Diabetes

 It is caused by altered kidney sensitivity to the action of ADH that may be genetic or acquired (Table 3), resulting in the inability to concentrate urine, polyuria, increased plasma osmolality, and polydipsia. Plasma ADH concentration is normal or increased, according to plasma osmolality.

Table3. Causes of nephrogenic diabetes insipidus

The severity of antidiuretic function defect is quite variable among patients with pituitary, gestational, and nephrogenic DI. In some individuals, the defect in ADH secretion or action is so severe as to induce high urinary flow, up to 10–15 liters per day.

Inappropriate ADH Secretion Syndrome

 Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH) is a rare disorder characterized by inappropriately elevated ADH levels associated with plasma hyperosmolarity and urinary hyperosmolarity due to an altered osmoregulatory mechanism. SIADH represents a frequent cause of hyponatremia (plasma sodium <135 mmol/L) in adults. Inappropriate ADH secretion can be of neurohypophyseal or ectopic origin. The latter represents the most frequent cause of SIADH due to neoplastic pathologies. On the other hand, the causes that can determine inappropriate secretion of ADH by the neurohypophysis are numerous and include infections, head traumas, vascular alterations, pulmonary disorders, or drug intake. The latter can determine SIADH by inducing an increase either in the release of ADH (morphine, carbamazepine, haloperidol, tricyclic antidepressants) or in the receptor sensitivity to the hormone (nonsteroidal anti-inflammatory drugs, cyclophosphamide, chlorprop amide) (Table 4).

Table4. Main causes of inappropriate ADH secretion syndrome

Four types of altered osmoregulation have been described.

• Type a (40–70%): random secretion associated with markedly increased ADH levels, independent of plasma osmolarity. There is, therefore, a complete loss of the osmoregulatory mechanism.

• Type b (20–40%): it is the classic picture of osmostat reset (literally threshold reset) characterized by a reduction in the osmolar threshold for ADH secretion. There is, therefore, a defect affecting the inhibitory component of the osmoregulation mechanism.

 • Type c (10%): low plasma osmolarity does not inhibit ADH secretion. Plasma ADH concentrations are, therefore, inappropriately high at low plasma osmolarity. There is a normal relationship between plasma osmolality and plasma ADH for physiological plasma osmolality values.

• Type d ( <5 %): it is characterized by normal osmoregulation (i.e., ADH secretion varies appropriately with plasma osmolality), but urine is concentrated even when ADH release is suppressed. The osmoregulatory mechanism of ADH secretion thus is conserved, suggesting that different alterations cause inappropriate antidiuresis. A constitutively activating mutation of the ADH receptor has been identified in some patients. There is no correlation between the etiology and the type of alteration; any of the four types described above can occur, regardless of the cause of SIADH.

The increased secretion of ADH causes increased reabsorption of free water in the distal nephron, which, in turn, causes extracellular hypervolemia, increased levels of the atrial natriuretic hormone, reduced plasma renin activity, and increased urinary sodium excretion. This natriuresis serves to balance hypervolemia but exacerbates hyponatremia. In addition, hyponatremia induces increased intracellular volume in all organs, including the brain. If hyponatremia develops slowly, patients do not have clear clinical manifestations; if, on the other hand, plasma sodium concentration drops abruptly, patients develop severe neurological manifestations.

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مواضيع ذات صلة

Antidiuretic Hormone

Prolactin

thyroid-stimulating hormone (TSH, Thyrotropin, TRH stimulation test)

thyroglobulin (Tg, Thyrogen-stimulated thyroglobulin)

thrombosis indicators

Laboratory Investigations of Growth Hormone

Growth Hormone Deficiency

Laboratory Diagnosis of Thrombophilia

thromboelastography (Thromboelastometry)

throat and nose cultures

testosterone (Dihydrotestosterone [DHT])

Biomarkers of Stroke