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It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor). [1] It is stimulated by angiotensin II and aldosterone, and inhibited by atrial natriuretic peptide. It is very efficient, since more than 25,000 mmol/day of sodium is filtered into the nephron, but only ~100 mmol/day, or less than 0.4% remains in the final urine.
The kidneys can also generate dilute urine to balance sodium levels. [8] These electrolytes must be replaced to keep the electrolyte concentrations of the body fluids constant. Hyponatremia, or low sodium, is the most commonly seen type of electrolyte imbalance. [12] [13]
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.
This illustration demonstrates the normal kidney physiology, including the Proximal Convoluted Tubule (PCT), Loop of Henle, and Distal Convoluted Tubule (DCT). It also includes illustrations showing where some types of diuretics act, and what they do. Renal physiology (Latin renes, "kidneys") is the study of the physiology of the kidney.
The fractional excretion of sodium (FE Na) is the percentage of the sodium filtered by the kidney which is excreted in the urine. It is measured in terms of plasma and urine sodium , rather than by the interpretation of urinary sodium concentration alone, as urinary sodium concentrations can vary with water reabsorption .
Renal compensation is a mechanism by which the kidneys can regulate the plasma pH. It is slower than respiratory compensation, but has a greater ability to restore normal values. Kidneys maintain the acid-base balance through two mechanisms: (1) the secretion of H + ions into the urine (from the blood) and (2) the reabsorption of bicarbonate ...
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Hyponatremia occurs 1) when the hypothalamic-kidney feedback loop is overwhelmed by increased fluid intake, 2) the feedback loop malfunctions such that ADH is always "turned on", 3) the receptors in the kidney are always "open" regardless of there being no signal from ADH to be open; or 4) there is an increased ADH even though there is no ...