Pathophysiology
There are three pathologic states related to ADH. The first is the syndrome of inappropriate ADH (SIADH) and occurs when ADH is released in excessive unregulated quantities. SIADH results in excess water reabsorption and thus creates dilutional hyponatremia. Although water is retained in quantities greater than the body’s needs, these patients typically remain euvolemic and do not exhibit features of the third spacing of fluid such as edema. The mechanism behind this is that, regardless of the excess ADH present, the kidneys maintain their ability to excrete salt. As ADH signals for increased water reabsorption, the body senses the increase in extracellular volume, and natriuretic mechanisms come into play that cause increased salt excretion via the kidneys. The increased salt in the urine will osmotically attract water to be excreted as well, thus keeping the body in a euvolemic state. This increase in salt excretion also contributes to the hyponatremia seen in SIADH. Settings in which SIADH arises include malignancies (most often by autonomous production of ADH by small cell lung cancer), central nervous system (CNS) disturbances (e.g., stroke, hemorrhage, infection, trauma, etc.), drugs (e.g., selective serotonin reuptake inhibitors, carbamazepine, and others), surgery (most likely secondary to pain), and more. Patients with SIADH may be asymptomatic or present with a spectrum of severity of complaints based on their level of hyponatremia. Nausea and malaise are typically the earliest presenting symptoms and present when the sodium acutely falls below 125 to 130 mEq/L. Lower levels of sodium are associated with headache, obtundation, seizure, and even coma and respiratory arrest.[4] These symptoms arise due to the increased movement of water into neurons as the extracellular osmolarity falls. The intracellular swelling causes neuronal dysfunction.[5]
Unlike the excess ADH seen in SIADH, the remaining two pathologic states related to ADH result from either decreased ADH or resistance to its effects. A failure of ADH secretion causes central diabetes insipidus. In this scenario, ADH levels are low; thus, the collecting tubules are impermeable to water, resulting in excess water excretion. In nephrogenic diabetes insipidus, ADH secretion is normal, but there is a defect in the V receptor or other signaling mediators that makes the kidneys unresponsive to ADH. In either disease, the net effect is increased excretion of water. The depletion of water causes the production of large volumes of dilute water and the concentration of body fluids leading to hypernatremia and hyperosmolarity. This status results in polyuria, polydipsia, and the effects of electrolyte imbalances that ensue.[6]
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Central diabetes insipidus is the more common form and often seen after brain trauma or surgery that damages either the hypothalamus or posterior pituitary. Other cerebral infiltrative processes such as infection, autoimmune disease, or neoplastic disease may also cause central diabetes insipidus. Nephrogenic diabetes insipidus can be either inherited or acquired. The most common inherited form is attributed to mutations in the V receptor and often manifests in childhood. Acquired causes of nephrogenic diabetes insipidus are more often at play in adulthood expression of the disease. Most often, acquired nephrogenic diabetes insipidus is due to drugs, notably lithium and some antibiotics such as tetracyclines.[6]
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