Disorders of Water and Salt Metabolism Associated with Pituitary Disease
Section snippets
Overview of normal water metabolism
Water metabolism is controlled primarily by arginine vasopressin (AVP), a nonapeptide that is synthesized in the neurohypophyseal magnocellular neurons of the supraoptic and paraventricular nuclei of the hypothalamus. The newly synthesized AVP prohormone is packaged into neurosecretory granules and then transported down the supraopticohypophyseal tract to the posterior pituitary, during which it is enzymatically cleaved into AVP, neurophysin, and a C-terminal glycopeptide. When release is
Hyperosmolality and hypernatremia
Hyperosmolality indicates a deficiency of water relative to solute in the extracellular fluid. Because water moves freely between the extracellular (ECF) and intracellular (ICF) fluid, this also indicates a deficiency of total body water relative to total body solute. In evaluating hypernatremia, it is helpful to classify it broadly by etiology: hypervolemic, inadequate water intake, and increased free water losses.
Diabetes insipidus
Diabetes insipidus (DI) is the most well-known manifestation of a deficiency in AVP secretion or abnormal renal response to AVP. Central DI is caused by a variety of acquired or congenital anatomic lesions that disrupt the hypothalamic-posterior pituitary axis, and include some types of tumors, trauma, hemorrhage, thrombosis, infarction, granulomatous disease, and pituitary surgery. It is unusual for pituitary adenomas to present with DI. This is because synthesis of AVP occurs in the
Hypoosmolality and hyponatremia
Hyponatremia is the most common electrolyte disorder in hospitalized adult patients. The reported incidence of hyponatremia varies depending on the age of hospitalized patients studied, and the definition of hyponatremia used. When hyponatremia is defined as a serum [Na+] less than 135 mmol/L, incidences of 6% to 22% have been reported [1]. However, when hyponatremia is defined by more stringent criteria of serum [Na+] less than 130 mmol/L, incidences fall to 1% to 4%. This cutoff likely
Hypovolemic hyponatremia
Hypovolemic hyponatremia occurs when there are simultaneous losses of body water and sodium, resulting in ECF volume depletion. The decrease in blood volume and pressure results in secondary stimulated AVP secretion, and ultimately decreased free water excretion by the kidney. Retention of water from ingested or infused fluids can then lead to the development of hyponatremia. Primary solute depletion, from either renal losses (eg, diuretics, mineralocorticoid deficiency, and various
Hypervolemic hyponatremia
In hypervolemic hyponatremia, there is an excess of total body water and total body sodium, resulting in clinically evident hypervolemia manifested by edema or ascites. Hyponatremia occurs because the increase in total body water is usually in excess of the increase in total body sodium as a result of potent AVP secretion in response to a decreased effective arterial blood volume (EABV) [32]. Hypoosmolality in these patients suggests a relatively decreased intravascular volume, leading to water
Euvolemic hyponatremia
Euvolemic hyponatremia can be caused by virtually any disorder causing hypoosmolality. The pathogenesis of euvolemic hyponatremia is typically excessive water retention, caused by either impaired water excretion from advanced renal failure, or more likely from increased secretion of AVP. Occasionally, hyponatremia can occur from over-ingestion of water, where the gastrointestinal tract absorbs water faster than the kidney's ability to excrete it. Because clinical assessments of volume status
Vasopressin receptor antagonists
A new class of agents, AVP receptor antagonists, have been recently introduced as a method of correcting hyponatremia by blocking the binding of AVP to V2 receptors in the kidney. AVP receptor antagonists are highly effective in producing a safe and predictable increased excretion of free water that increases the serum [Na+] in hyponatremic patients. Because these agents induce excretion of free water without accompanying natriuresis or kaliuresis, this effect has been termed “aquaresis,” to
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2019, Neurosurgery Clinics of North AmericaCitation Excerpt :When secreted, ADH binds to the V2 receptors in the renal collecting ducts, activating a cyclic AMP-mediated signal transduction pathway that stimulates insertion of aquaporin-2 water channels into the apical membrane of the collecting duct epithelial cells. These water channels increase water permeability that facilitates passive renal water reabsorption, which consequently alters plasma sodium levels.15 In addition, the thirst mechanism also plays an important role in maintaining water and sodium homeostasis.
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2018, Current Opinion in Endocrine and Metabolic ResearchCitation Excerpt :When DI occurs, polyuria typically starts within the 12–24 h after surgery. Acute disorders of water metabolism can manifest in a typically triphasic pattern (typical, but only occurring in a minority of patients): after an initial DI phase, a subsequent SIADH phase (with hyponatremia) develops, and a final DI phase that is usually chronic returns [13]. However, the SIADH phase may be isolated and neither preceded nor followed by DI.
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