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. 

Two of the ketone bodies are acids, and their accumulation in the blood as ketosis worsens results in a condition of acidosis called ketoacidosis because it is caused by ketone bodies in the blood. If ketoacidosis is not controlled, the person becomes severely dehydrated because the kidneys excrete excessive amounts of water in response to low blood pH. Prolonged ketoacidosis leads to general debiUtation, coma, and even death. 

A singly charged positive ion formed during protein metabolism. Under alkaline conditions, the ammonium ion may be converted to ammonia gas under acid conditions, it forms salts. Also, the ammonium ion is a nontoxic means by which the kidney excretes excess acid. 

Metabolic alkalosis is maintained by abnormal renal function that prevents the kidneys from excreting excess bicarbonate. 

More accurate assessment of the ability of the kidney to appropriately regulate plasma tonicity and/or respond appropriately to antidiuretic hormone (ADH) can be made by calculation of electrolyte-free water clearance (ECh2o)- This formula takes into account only water needed to excrete excess effective os-molytes (in general, monovalent electrolytes and their associated anions) and is calculated as follows ... 

In aquatic animals, ammonia diffuses out of the body through the skin, but land animals excrete excess ammonia either as urea or uric acid. Ammonia is excreted by humans on high meat diets as a strategy to conserve Na+ and K +. Excess PO4- and SO4- produced from phosphoproteins and S-containing amino acids are excreted as ammonium salts Na+ and K+ are exchanged for NH in the kidney. The excretion of urea requires a plentiful supply of water, as it is normally excreted in solution, whereas uric acid is very insoluble and is excreted as a solid by birds and reptiles. Thus, in animals in which weight, or the conservation of water, is important (e.g., birds), excess ammonia is excreted as uric acid. 

The kidneys will excrete excess acid equivalents in the urine. At acidic pH, LSD will become protonated and therefore no longer slip back across the tubule epithelium into the circulation this will lead to accelerated elimination of LSD. We here have another example of the principle of non-ionic diffusion , which we have previously discussed in the context of drug absorption. 

Although potassium supplementation is necessary in some individuals being treated with a potassium-depleting diuretic, the initiation of therapy with such a diuretic must not be viewed as a mandate to provide potassium supplementation. This decision should be based on a consideration of the individual patient s situation and the appropriate parameters should be periodically monitored. It must be recognized that dangers exist if hyperkalemia occurs as a result of excessive supplementation. Although the kidneys are usually able to excrete excessive amounts of potassium rapidly, hyperkalemia may develop, especially in patients with diminished renal function. 

Ammonia arises in the body principally from the oxidative deamination of amino acids. In addition to its uptake in the reactions mentioned above, ammonia is also excreted in the urine as ammonium salts. This is not derived directly from the blood ammonia but is formed by the kidney from glutamine by the action of glutaminase. In metabolic acidosis, ammonia production and excretion by the kidney is greatly increased, and conversely it is decreased in metabolic alkalosis. This may be an important means of excreting excess ammonia. It must be remembered that ammonia formed by the action of intestinal bacteria on the protein hydrolyzates in the intestine can be also absorbed. The contribution of the ammonia formed in this way to the total ammonia in the body is unknown. Since this ammonia drains into the portal circulation, it is promptly removed by the liver. 

Extra magnesium may be required by individuals with conditions that cause excessive urinary loss of Mg, such as chronic malabsorption or severe diarrhea. Certain medications can also cause the kidneys to excrete excessive Mg, such as diuretics, and Cisplatin, which is used as a chemotherapeutic agent for cancer, as well as certain antibiotics. 

The kidneys excrete >95% of eliminated Al, presumably as the citrate. Less than 2% appears in bile. Reduced renal function in the very young, elderly and renally impaired humans increases the risk of Al accumulation. In humans, the terminal elimination half life appears to be in excess of one year (Priest etal. 1995). This probably reflects the slow Al clearance from bone. 

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. 

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... 

Hypermagnesemia, a rare condition, is an elevation of the serum magnesium level higher than 2.5 mEq/L (1.25 mmol/L). Since the kidneys are very effective in excreting excess magnesium, hypermagnesemia occurs very rarely. Therefore, the most common occurrences of hypermagnesemia would be in patients whose... 

Metabolic acidosis results when there is an excess of acid relative to the base (i.e., bicarbonate) in the body. Additionally, conditions that result in a decreased total amount of base, commonly bicarbonate, relative to the acid in the body will cause metabolic acidosis. Conditions that reduce the ability of the kidneys to excrete acid cause the kidneys to excrete excessive bicarbonate, as well as conditions that result in increased production of acids, will contribute to the development of metabolic acidosis. 

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. 

Sometimes, these effects may be prevented by extra dietary vitamin D, or by exposure to sunlight. However, newborn infants, whose kidneys do not excrete excess phosphate as well as those of older infants and children, may develop high blood levels of phosphate and have seizures when they are fed evaporated milk containing phosphate additives.The seizures are attributed to the fact that cow s milk contains almost four times the calcium and over six times the phosphorus present in human breast milk. Furthermore, extra phosphate is often added to evaporated milk to lengthen its shelf life. Hence, newborn babies fed evaporated milk (diluted with an equal volume of water) may receive between seven and eight times the phosphorus they would get from the same amount of human breast milk. An elevation of the blood level of phosphate causes a corresponding drop in the level of ionized calcium. The direct cause of the milk-induced seizures is the lack of sufficient ionized calcium in the blood. 

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. 

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

Copper is an essential trace element. It is required in the diet because it is the metal cofactor for a variety of enzymes (see Table 50—5). Copper accepts and donates electrons and is involved in reactions involving dismu-tation, hydroxylation, and oxygenation. However, excess copper can cause problems because it can oxidize proteins and hpids, bind to nucleic acids, and enhance the production of free radicals. It is thus important to have mechanisms that will maintain the amount of copper in the body within normal hmits. The body of the normal adult contains about 100 mg of copper, located mostly in bone, liver, kidney, and muscle. The daily intake of copper is about 2—A mg, with about 50% being absorbed in the stomach and upper small intestine and the remainder excreted in the feces. Copper is carried to the liver bound to albumin, taken up by liver cells, and part of it is excreted in the bile. Copper also leaves the liver attached to ceruloplasmin, which is synthesized in that organ. 

Nitrogen compounds commonly determined are creatinine, urea, and uric acid. Creatinine is an end product of the energy process occurring within the muscles, and is thus related to muscle mass. Creatinine in urine is commonly used as an indicator and correction factor of dilution in urine. Creatinine in serum is an indicator of the filtration capacity of the kidney. Urea is the end product of the nitrogen luea cycle, starting with carbon dioxide and ammonia, and is the bulk compoimd of urine. The production of uric acid is associated with the disease gout. In some cases, it appears that the excess of uric acid is a consequence of impaired renal excretion of this substance. 

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