Sodium kidneys excreting excess

Metabolic acidosis involves a build-up of hydrogen ions in the blood, thus lowering blood pH. Under normal physiological conditions, the kidneys excrete excess hydrogen ions, and release more bicarbonate ions into the bloodstream to buffer the excess acid. However, in renal failure, or in diabetic ketoacidosis, this mechanism either fails, or is unable to compensate to an adequate extent. Hence, metabolic acidosis is usually treated with sodium bicarbonate, either intravenously (1.26% or 8.4% i.v. solution) or orally (typically 1 g three times a day). Sodium bicarbonate 1.26% intravenous solution is isotonic with plasma (and with sodium chloride 0.9%), so may be given in large volumes (1-2 L) by peripheral venous catheter to correct metabolic acidosis and provide fluid replacement at the same time. Sodium bicarbonate 8.4% may only be given by central venous catheter. 

Using highly salted foods forces the body to get rid of excess sodium chloride, usually through the kidneys, in order to keep the proper overall balance of electrolytes, the right acid/alkaline balance, and the right amount of water in the body. The problem is that when sodium is excreted, it doesn t depart all by itself. 

The patient receives sodium when food is absorbed in the GI tract. Typically, a patient takes in more sodium than the patient s daily requirement. The kidneys regulate the sodium balance by retaining urine when the sodium concentration is low and excreting urine when the sodium concentration is high. Most excess sodium is excreted in urine although sodium also leaves the patient as perspiration and in feces. 

Psychogenic polydipsia, or compulsive water drinking (generally > 10 L/d), causes reduced serum sodium because of the excessive free water intake and because the kidney excretes sodium to maintain euvolemia. The urine sodium level may be elevated, but urine osmolality is appropriately low because the kidney is attempting to excrete the excess water and ADH secretion is suppressed. 

B. Chronic intoxication may occur in patients on stable therapeutic doses. Lithium is excreted by the kidney, where it is handled like sodium any state that causes dehydration, sodium depletion, or excessive sodium reabsorption may lead to increased lithium reabsorption, accumulation, and possibly intoxication. Common states causing lithium retention include acute gastroenteritis, diuretic use, use of nonsteroidal anti-inflammatory drugs or angiotensinconverting enzyme (ACE) inhibitors, and lithium-induced nephrogenic diabetes insipidus. 

Licorice was one of the first substances that Western physicians used to treat Addison s disease, an ailment of the adrenal glands. Addison s sufferers don t produce enough cortisol, a hormone that helps regulate blood pressure and water retention. Glycyrrhizic acid interferes with an enzyme that normally breaks down excess cortisol in the kidneys when this enzyme is rendered inactive, cortisol levels rise, and this can cause hypertension. Furthermore, high cortisol levels cause retention of sodium and excretion of potassium. Sodium retention, in... 

Sodium is absorbed in the intestines from foods and fluids ingested, as well as from many medications. The intake of sodium commonly far exceeds the needs of the human body, but an individual with healthy kidneys seldom will experience a buildup because excess sodium is excreted by the kidneys as needed to restore balance. A few basic facts about sodium concentration in the body include the following ... 

Relatedly, malfunction of one of the sodium-water control mechanisms, such as a kidney that normally excretes excess water, can result in fluid retention and dilutional hyponatremia. The pituitary gland and hypothalamus function to release ADH (which controls water reabsorption), and the cortex of the adrenal gland seaetes aldosterone (which controls sodium reabsorption). An alteration in the function of either of these hormone systems will alter the body s regulation of sodium or water and can result in hyponatremia. 2 For example, in the syndrome of inappropriate antidiuretic hormone (SIADH), excessive ADH is produced (usually by a tumor or some pulmonary diseases such as tuberculosis or bacterial pneumonia), and the kidneys reabsorb excessive fluids, resulting in dilutional hyponatremia. Conditions causing decreased aldosterone secretion include... 

The administration of a diet restricted in sodium chloride induces a normal response of the kidney and reduced electrolytes in urine, but the sweat glands continue to excrete excessive amounts of electrolytes. As a result, patients with cystic fibrosis are oversensitive to heat in that they lose large amounts of sodium chloride in the sweat. The loss of sodium leads to a reduction of the extracellular fluid with vascular collapse. The situation is readily reversed by the intravenous administration of saline [139]. 

Sodium. This element is vital to life, so it is fortunate that the human body has remarkable ways of conserving it when dietary intakes are low. However, the ability to conserve short supplies, or to excrete excesses in the urine, varies considerably among different people, and the processes also vary according to the condition of health. For example, some of the people who consume moderate to large excesses of sodium may fail to excrete completely such excesses and, therefore, suffer such consequences as buildup of excessive fluid in the blood and tissues, damage to the kidneys, heart failure, and/or high blood pressure. There is evidence that susceptibility to these sodium-induced disorders may be a trait that runs in certain families. 

High blood pressure—Sometimes, this condition results from a failure of the kidneys to excrete excess sodium, which promotes the accumulation of water in the body. Certain people appear to be overly susceptible to the effects of only moderate excesses of dietary sodium, so they should restrict their salt intake in order to avoid high blood pressure. 

Sodium Excess. Most of the sodium ingested is excessive, and for the most part it is excreted by the kidneys in combination with bicarbonate or phosphate. However, under some circumstances sodium accumulates in the extracellular fluid and causes edema since the retention of sodium is accompanied by water retention. Such conditions include (1) cardiac or renal failure, (2) adrenal tumors which secrete excessive cortical hormones, and (3) adrenocorticotropic hormone (ACTH) or steroid hormone therapy. In these conditions, individuals benefit from sodium-restricted diets. 

The maintenance of plasma volume and plasma osmolarity occurs through regulation of the renal excretion of sodium, chloride, and water. Each of these substances is freely filtered from the glomerulus and reabsorbed from the tubule none is secreted. Because salt and water intake in the diet may vary widely, the renal excretion of these substances is also highly variable. In other words, the kidneys must be able to produce a wide range of urine concentrations and urine volumes. The most dilute urine produced by humans is 65 to 70 mOsm/1 and the most concentrated the urine can be is 1200 mOsm/1 (recall that the plasma osmolarity is 290 mOsm/1). The volume of urine produced per day depends largely upon fluid intake. As fluid intake increases, urine output increases to excrete the excess water. Conversely, as fluid intake decreases or as an individual becomes dehydrated, urine output decreases in order to conserve water. 

Sodium chloride (hypotonic) - 0.45% Sodium chloride (hypotonic) is primarily a hydrating solution and may be used to assess the status of the kidneys, because more water is provided than is required for salt excretion. It also may be used in the treatment of hyperosmolar diabetes where the use of dextrose is inadvisable and there is a need for large amounts of fluid without an excess of sodium ions. 

Water Intoxication. Ether an increased intake of water or a decreased output of water can cause an excess of body water. Because healthy kidneys have outstanding ability to increase water excretion, a condition of water intoxication usually occurs because of a disability to excrete water (hyponatremia). Frequently impairment may not be the result of disease or damage to the kidneys per se, but rather due to faulty processing of stimuli by the kidneys. Excessive renal reabsorption of water can result from the action of antidiuretic hormone (ADH) or by the excessive reabsorption of sodium in the proximal tubules. Under such conditions, the excretion of water and sodium will be low. Retention of salt and water causes an expansion of the ECF, usually resulting in edema and effusions. 

Water Deficiency. This condition occurs when water output exceeds intake. Water is continually losl by way of the lungs, skin, and kidneys and dius a deficiency of body water will occur if a critical minimal supply is not maintained. Decreased intake when water is available is uncommon. Very rarely, a brain malfunction may interfere with one s sense of diirst. Increased output of water can result from many causes. For example, a person with diabetes insipidus who lacks ADH (antidiuretic hormone) or a person whose kidneys do not respond normally to ADH, as in instances of nephrogenic diabetes insipidus, will increase water output Other diseases which may cause excess excretion of water include osmotic diuresis, hypercalcemia, hypokalemia, chronic pyelonephritis, and sickle cell anemia, among others. Excessive water losses are also experienced in some cases with advanced age and in some burn cases. Two clinical features are good measures of dehydration—weight loss of the patient and an elevation of the serum sodium concentration. In situations of dehydration, the body initiates mechanisms which manipulate the transfer of water from one compartment to the next, retaining water in those cells and organs where it is most needed. 

Excessive retention of sodium ions in the body leads to increased release of antidiuretic hormone and a resulting increase in body water. Many diuretics such as chlorothiazide (i) and clopamide (2) inhibit sodium and chloride ion resorption in the kidney tubules and promote potassium depletion, whereas amiloride (J) and triamterene ( 4) diminish the excretion of potassium while causing a loss of sodium ions6. Other diuretics such as acetazolamide (5) and dichlorphenamide (6) inhibit the ion-exchange reaction catalysed by the zinc-containing enzyme carbonic an-hydrase. 

The most potent type of diuretic, loop diuretics are named after the loop of Henle, a component of a nephron. The nephrons are the filtering units of the kidney, and are responsible for moving fluids and waste out of the bloodstream, resulting in urine formation. The loop of Henle is a branch within each nephron where sodium and potassium are reabsorbed back into the bloodstream instead of being filtered into the urine. Loop diuretics inhibit this action and promote excretion of the sodium and potassium instead, along with calcium and magnesium. Since excess sodium causes excess fluid build-up, this results in fluid loss. Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex), and ethacryinic acid (Edecrin) are all loop diuretics. 

X-linked hypophosphatemic rickets is caused by abnormal reabsorption of phosphate in the proximal renal tubule, resulting in excessive excretion of phosphate and hence hypophosphatemia. There may also be blunting of the normal increase in calcidiol 1 -hydroxylase activity in response to hypophosphatemia. The gene responsible for the condition has been identified (the PHEX gene) its product is a membrane-bound endopeptidase that normally acts to clear the hormone phosphatonin from the circulation. Phosphatonin acts to decrease the activity of the sodium/phosphate cotransporter in the kidney (Drezner, 2000). 

Amounts of dietary sodium in excess of the kidney s ability to dilute and to excrete it in the urine leads directly to hypertension and indirectly to coronary heart disease and stroke. Although sodium chloride is required at about 1 g day, a typical Western diet, in fact, may contain from 8 to 12 g day. If renal transport is impaired, sodium ion accumulates and the osmotic pressure of the blood rises. Dietary reduction of salt can ameliorate some but not all of the problems. A wide variety of low-salt food products is now available. 

The body can absorb about 500 mg of ascorbic acid daily with any excess immediately excreted by the kidneys. Large doses may cause diarrhea or other gastrointestinal disturbances. Damage to the teeth has also been reported. However, no adverse effects have been reported at the levels employed as an antioxidant in foods and pharmaceuticals. The WHO has set an acceptable daily intake of ascorbic acid, potassium ascorbate, and sodium ascorbate, as antioxidants in food, at up to 15mg/kg body-weight in addition to that naturally present in food. ... 

The mineralocorticoids have a main action on the distal tubules in the kidney to increase sodium absorption, with concomitant increased excretion of K and H. Aldosterone is the main endogenous mineralocorticoid. It is produced in the outermost layer of the adrenal cortex (the zona glomerulosa). An excessive secretion of mineralocorticoids (e.g. in Conn s syndrome) causes marked salt and water retention, with a resultant increase in the volume of extracellular fluid, alkalosis, hyperkalaemia and often hypertension. A decrease in secretion (e.g. Addison s disease) causes a disproportional loss of Na compared to fluid loss, so osmotic pressure of the extracellular fluid is reduced. This results in an increase in intracellular compared to extracellular fluid volume. The concomitant decrease in excretion of K results in hyperkalaemia with some decrease in bicarbonate. The control of synthesis and release of aldosterone is complex and involves both the renin-angiotensin system and the electrolyte composition of the blood. As with other... 

Sodium is the major cation of extracellular fluid. Because it represents approximately 90% of the 154mmol of inorganic cations per liter of plasma, Na is responsible for almost one half the osmotic strength of plasma. It therefore plays a central role in maintaining the normal distribution of water and the osmotic pressure in the extracellular fluid compartment. The normal daily diet contains 8 to 15 g (130 to 260 mmol) of NaCl, which is nearly completely absorbed from the gastrointestinal tract. The body requires only 1 to 2 mmol/day, and the excess is excreted by the kidneys, which are the ultimate regulators of the amount of Na" (and thus water) in the body. 

Excessive urinary losses of magnesium from the kidneys are important causes of magnesium deficiency. Clinically important causes include alcohol, diabetes meUitus (osmotic diuresis), loop diuretics (furosemide), and aminoglycoside antibiotics. Increased sodium excretion (parenteral fluid therapy) and increased calcium excretion (hypercalcemic states) also result in renal magnesium wasting. 

Rationale An excess of ADH leads to hyponatremia, because it interferes with the ability of the kidneys to excrete a water load normally. This test is useful if SIADH is suspected in a patient with normal or near-normal serum sodium and plasma osmolality or in a patient with reset osmostat. This test should not be performed in patients who are already significantly hyponatremic because of the danger that the water load will worsen the hyponatremia. 

Last, ammonia is excreted in the urine in the form of ammonium salts. Normally, however, this is relatively small, but it may be increased in metabolic acidosis, if kidney tubular function is normal. Ammonia is synthesized from glutamine by the kidney as required in order to conserve fixed base, e.g., sodium or potassium or to neutralize excessive amounts of acid excreted in the urine as, for example, in acidosis. 

Hyponatremia (serum sodium <135 mEq/L) is the most common electrolyte abnormality in hospitalized patients, with a reported incidence of about 2.5%. ° Brain injury results from either the acute effects of hypo-osmolality or from too rapid correction of hypo-osmolality in patients with symptomatic hyponatremia, and is associated with a 20% incidence of significant morbidity and a mortality rate as high as 25%. Hyponatremia is predominantly the result of an excess of extracellular water relative to sodium because of impaired water excretion. The kidney normally has the capacity to excrete large volumes of dilute urine after ingestion of a water load. Nonosmotic... 

The sodium-to-water ratio in the body must be properly balanced or unfortunate effects may result. The hypothalamus area of the brain is fairly efficient at regulation of this ratio when sodium is high, thirst results when excess urination causes loss of water, the body also excretes sodium to help maintain the balance. People traveling long distances in desert or other dry climates may ingest salt (NaCl) as a way to retain water in their systems. The kidneys also play a role in sodium regulation. 

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