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Vasopressin V2 receptor antagonists. Cardiovasc Res. This content is owned by the AAFP. A person viewing it online may make one printout of the material and may use that printout only for his or her personal, non-commercial reference. This material may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in any medium, whether now known or later invented, except as authorized in writing by the AAFP.
Contact afpserv aafp. Want to use this article elsewhere? Get Permissions. Read the Issue. Sign Up Now. Next: Diethylstilbestrol Exposure. May 15, Issue. Management of Hyponatremia. Significant ECF fluid losses also cause release of vasopressin , causing water retention by the kidneys, which can maintain or worsen hyponatremia. It causes various symptoms, including hypotension and hyperpigmentation, and can lead to adrenal crisis Salt-losing nephropathy encompasses a loosely defined group of intrinsic renal disorders with primarily renal tubular dysfunction.
This group includes interstitial nephritis Tubulointerstitial Nephritis Tubulointerstitial nephritis is primary injury to renal tubules and interstitium resulting in decreased renal function. The acute form is most often due to allergic drug reactions or to infections Almost all forms are Renal causes of hypovolemic hyponatremia can usually be differentiated from extrarenal causes by the history. Common causes In metabolic alkalosis, urine chloride concentration frequently differentiates renal from extrarenal sources of volume depletion.
Diuretics may also cause hypovolemic hyponatremia. Once volume depletion occurs, the nonosmotic release of vasopressin causes water retention and worsens hyponatremia. Concomitant hypokalemia shifts sodium intracellularly and enhances vasopressin release, thereby worsening hyponatremia. This effect of thiazides may last for up to 2 weeks after cessation of therapy; however, hyponatremia usually responds to replacement of potassium and volume deficits along with judicious monitoring of water intake until the drug effect dissipates.
Older patients may have increased sodium diuresis and are especially susceptible to thiazide-induced hyponatremia, particularly when they have a preexisting defect in renal capacity to excrete free water. Rarely, such patients develop severe, life-threatening hyponatremia within a few weeks after the initiation of a thiazide diuretic.
Loop diuretics much less commonly cause hyponatremia. In euvolemic dilutional hyponatremia, total body sodium and thus ECF volume are normal or near-normal; however, TBW is increased. Because normal kidneys can excrete up to 25 L urine a day, hyponatremia due solely to polydipsia results only from the ingestion of large amounts of water or from defects in renal capacity to excrete free water.
Patients affected include those with psychosis or more modest degrees of polydipsia plus renal insufficiency. Euvolemic hyponatremia may also result from excessive water intake in the presence of Addison disease Addison Disease Addison disease is an insidious, usually progressive hypofunctioning of the adrenal cortex.
It is diagnosed by clinical features such as a typical facial appearance, hoarse slow speech, and dry skin and by low levels of thyroid hormones Postoperative hyponatremia most commonly occurs because of a combination of nonosmotic vasopressin release and excessive administration of hypotonic fluids after surgery.
Certain drugs eg, cyclophosphamide , nonsteroidal anti-inflammatory drugs, chlorpropamide potentiate the renal effect of endogenous vasopressin , whereas others eg, oxytocin have a direct vasopressin -like effect on the kidneys.
MDMA acts primarily on neurons that produce and release serotonin, but it also affects A deficiency in water excretion is common in all these conditions. Diuretics can cause or contribute to euvolemic hyponatremia if another factor causes water retention or excessive water intake. Hypervolemic hyponatremia is characterized by an increase in both total body sodium and thus ECF volume and total body water with a relatively greater increase in TBW.
Cirrhosis is characterized by regenerative nodules surrounded by dense It is more common among children and has both primary and secondary In each of these disorders, a decrease in effective circulating volume results in the release of vasopressin and angiotensin II.
The following factors contribute to hyponatremia:. The antidiuretic effect of vasopressin on the kidneys. The syndrome of inappropriate ADH vasopressin secretion is attributed to excessive vasopressin release. It is defined as less-than-maximally-dilute urine in the presence of plasma hypo-osmolality hyponatremia without volume depletion or overload, emotional stress, pain, diuretics, or other drugs that stimulate vasopressin secretion eg, chlorpropamide , carbamazepine , vincristine , clofibrate, antipsychotic drugs, aspirin , ibuprofen in patients with normal cardiac, hepatic, renal, adrenal, and thyroid function.
Among the many potential contributing factors are. Nonosmotic vasopressin release due to intravascular volume depletion. In addition, adrenal insufficiency has become increasingly common among AIDS patients as the result of cytomegalovirus adrenalitis, mycobacterial infection, or interference with adrenal glucocorticoid and mineralocorticoid synthesis by ketoconazole.
SIADH may be present because of coexistent pulmonary or central nervous system infections. Hyponatremia frequently occurs in patients with brain pathology, including concussion, intracranial hemorrhage, encephalitis, meningitis, and CNS tumors. However, cerebral salt wasting has been recognized by some as a separate entity affecting a small group of these patients, especially those with subarachnoid hemorrhage Subarachnoid Hemorrhage SAH Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space.
The most common cause of spontaneous bleeding is a ruptured aneurysm. Symptoms include sudden, severe headache, usually Cerebral salt wasting is thought to be due to either decreased sympathetic nervous system function or secretion of a circulating factor that decreases renal sodium reabsorption.
Symptoms mainly involve central nervous system dysfunction. However, when hyponatremia is accompanied by disturbances in total body sodium content, signs of ECF volume depletion Volume Depletion Volume depletion, or extracellular fluid ECF volume contraction, occurs as a result of loss of total body sodium.
ECF volume expansion typically occurs in heart failure, kidney failure, nephrotic syndrome, and cirrhosis In general, older chronically ill patients with hyponatremia develop more symptoms than younger otherwise healthy patients.
Symptoms are also more severe with faster-onset hyponatremia. Sequelae include hypothalamic and posterior pituitary infarction and occasionally osmotic demyelination syndrome or brain stem herniation. Hyponatremia is occasionally suspected in patients who have neurologic abnormalities and are at risk. However, because findings are nonspecific, hyponatremia is often recognized only after serum electrolyte measurement. Serum sodium may be low when severe hyperglycemia or exogenously administered mannitol or glycerol increases osmolality and water moves out of cells into the ECF.
Serum sodium concentration falls about 1. This condition is often called translocational hyponatremia because it is caused by translocation of water across cell membranes. Pseudohyponatremia with normal serum osmolality may occur in severe hyperlipidemia Dyslipidemia Dyslipidemia is elevation of plasma cholesterol, triglycerides TGs , or both, or a low high-density lipoprotein cholesterol level that contributes to the development of atherosclerosis.
Autoanalyzers in many clinical laboratories are affected by this artifact. Methods of measuring serum electrolytes with direct ion-selective electrodes circumvent this problem. Such direct ion-selective electrodes are available in some hospital laboratories by special request, but are also used by most point-of-care bedside analyzers.
These analyzers can be used to exclude pseudohyponatremia. Formulas exist to estimate the effect these abnormalities have on sodium measurement. Identifying the cause of hyponatremia can be complex. The history sometimes suggests a cause eg, significant fluid loss due to vomiting or diarrhea, renal disease, compulsive fluid ingestion, intake of drugs that stimulate vasopressin release or enhance vasopressin action.
The volume status, particularly the presence of obvious volume depletion or volume overload, suggests certain causes see table Common Causes of Volume Depletion Common Causes of Volume Depletion Volume depletion, or extracellular fluid ECF volume contraction, occurs as a result of loss of total body sodium.
Overtly hypovolemic patients usually have an obvious source of fluid loss and typically have been treated with hypotonic fluid replacement. Overtly hypervolemic patients usually have a readily recognizable condition, such as heart failure or hepatic or renal disease.
Euvolemic patients and patients with equivocal volume status require more laboratory testing to identify a cause. Am J Med S1—S Kidney Int — J Am Soc Nephrol — J Clin Res Pediatr Endocrinol — Bockenhauer D Draining the edema: a new role for aquaretics?
Nephrol Dial Transplant i1—i Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Jean-Daniel Delbet. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Reprints and Permissions. Delbet, JD. Tolvaptan therapy to treat severe hyponatremia in pediatric nephrotic syndrome. Pediatr Nephrol 35, — Download citation. Received : 09 February Revised : 24 February Accepted : 04 March
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