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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)
There are nine supplemental features: 1) a low BUN; 2) a low uric acid; 3) a normal creatinine; 4) failure to correct hyponatremia with IV normal saline; 5) successful correction of hyponatremia with fluid restriction; 6) a fractional sodium excretion >1%; 7) a fractional urea excretion >55%; 8) an abnormal water load test; and 9) an elevated ...
Hyponatremia means that the concentration of sodium in the blood is too low. It is generally defined as a concentration lower than 135 mEq/L. [ 3 ] This relatively common electrolyte disorder can indicate the presence of a disease process, but in the hospital setting is more often due to administration of Hypotonic fluids.
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.
Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. [4] It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. [3] [8] Symptoms can be absent, mild or severe.
Exercise-associated hyponatremia (EAH) is a fluid-electrolyte disorder caused by a decrease in sodium levels (hyponatremia) during or up to 24 hours after prolonged physical activity. [1] This disorder can develop when marathon runners or endurance event athletes drink more fluid, usually water or sports drinks, than their kidneys can excrete. [2]
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.
Primary polydipsia and psychogenic polydipsia are forms of polydipsia [1] characterised by excessive fluid intake in the absence of physiological stimuli to drink. [2] Psychogenic polydipsia caused by psychiatric disorders—oftentimes schizophrenia —is frequently accompanied by the sensation of dry mouth .