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the physiologic response to a decrease in kidney perfusion is an increase in sodium reabsorption to control hyponatremia, often caused by volume depletion or decrease in effective circulating volume (e.g. low output heart failure). above 2% [citation needed] or 3% [2] acute tubular necrosis or other kidney damage (postrenal disease)
Patients with extra-renal salt losses complicated by hyponatremia were found to be common-place, and consistent with McCance's description, they excreted urine virtually free of sodium. [22] In 1950, Sims et al, published their work that suggest observed relation between hyponatremia and pulmonary tuberculosis.
The PRISMA flow diagram, depicting the flow of information through the different phases of a systematic review. PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) is an evidence-based minimum set of items aimed at helping scientific authors to report a wide array of systematic reviews and meta-analyses, primarily used to assess the benefits and harms of a health care ...
Antipsychotics have been reported to cause hyponatremia in a review of medical articles from 1946 to 2016. [25] Available evidence suggests that all classes of psychotropics, i.e., antidepressants, antipsychotics, mood stabilizers, and sedative/hypnotics can lead to hyponatremia. Age is a significant factor for drug induced hyponatremia. [26]
Hypoosmolar hyponatremia is a condition where hyponatremia is associated with a low plasma osmolality. [1] The term "hypotonic hyponatremia" is also sometimes used.[2]When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states: low volume, normal volume, or high volume.
The term "cerebral hyponatremia" was suggested in the work of Epstein, et al. 1961. Inappropriate release of endogenous vasopressin is probably responsible for hyponatremia in tuberculous meningitis. Inability to excrete water normally is also a feature of the salt wasting of certain hyponatremic patients with pulmonary tuberculosis.
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