Excretion kidneys

Hydroxy vitamin D pools ia the blood and is transported on DBF to the kidney, where further hydroxylation takes place at C-1 or C-24 ia response to calcium levels. l-Hydroxylation occurs primarily ia the kidney mitochondria and is cataly2ed by a mixed-function monooxygenase with a specific cytochrome P-450 (52,179,180). 1 a- and 24-Hydroxylation of 25-hydroxycholecalciferol has also been shown to take place ia the placenta of pregnant mammals and ia bone cells, as well as ia the epidermis. Low phosphate levels also stimulate 1,25-dihydtoxycholecalciferol production, which ia turn stimulates intestinal calcium as well as phosphoms absorption. It also mobilizes these minerals from bone and decreases their kidney excretion. Together with PTH, calcitriol also stimulates renal reabsorption of the calcium and phosphoms by the proximal tubules (51,141,181—183). 

Mexifitene is well absorbed from the GI tract and less than 10% undergoes first-pass hepatic metabolism. In plasma, 60—70% of the dmg is protein bound and peak plasma concentrations are achieved in 2—3 h. Therapeutic plasma concentrations are 0.5—2.0 lg/mL. The plasma half-life of mexifitene is 10—12 h in patients having normal renal and hepatic function. Toxic effects are noted at plasma concentrations of 1.5—3.0 lg/mL, although side effects have been noted at therapeutic concentrations. The metabolite, /V-methy1mexi1itene, has some antiarrhythmic activity. About 85% of the dmg is metabolized to inactive metabolites. The kidneys excrete about 10% of the dmg unchanged, the rest as metabolites. Excretion can also occur in the bile and in breast milk (1,2). 

The elimination of drag s from the body is called excretion. After the liver renders drag s inactive, the kidney excretes the inactive compounds from the body. Also, some dragp are excreted unchanged by the kidney without liver involvement. Fhtients with kidney disease may require a dosage reduction and careful monitoring of... 

Kidney Excretion and glu-coneogenesis Gluconeogenesis Free fatty acids, lactate, glycerol Glucose Glycerol kinase, phosphoenolpyruvate carboxy kinase... 

Because the kidneys excrete less than 1% of the estimated 13,000 mEq of H+ ions generated in an average day, renal failure can be present for prolonged periods before life-threatening... 

Ammonia buffers protons in the tubules of the kidney to prevent formation of an acidic urine, when the kidney excretes (secretes) protons to control the pH of the blood. 

A plethora of methods has been developed to evaluate renal function by dynamic renography and remote analysis of the excretion of renal function markers. The underlying principle is that the kidneys excrete a majority of small hydrophilic molecules and their clearance, secretion, or fixation in the kidney is quantifiable. When a renal marker in plasma is filtered through the glomeruli, the accumulation of the filtrate in the Bowman s capsule. One or more of the following events may occur in the renal tubule once a marker is filtered or is in plasma [171] ... 

Each hormone is the center of a hormonal regulation system. Specialized glandular cells synthesize the hormone from precursors, store it in many cases, and release it into the bloodstream when needed (biosynthesis). For transport, the poorly water-soluble lipophilic hormones are bound to plasma proteins known as hormone carriers. To stop the effects of the hormone again, it is inactivated by enzymatic reactions, most of which take place in the liver (metabolism). Finally, the hormone and its metabolites are expelled via the excretory system, usually in the kidney (excretion). All of these processes affect the concentration of the hormone and thus contribute to regulation of the hormonal signal. 

Pharmacokinetics-. Rapidly metabolized after IV administration to mesna disulfide, which is reduced to mesna in kidney. Excreted in urine. Half-life 24 min. 

Thiamphenicol is a synthetic chloramphenicol analogue with a molecular structure that appears to preserve tlie antibacterial properties, decrease markedly the metabolism by the liver, enhance kidney excretion, and eliminate tlie occurrence of aplastic anemia, although it is probably more liable to cause dose-dependent reversible depression of the bone marrow (15). These properties make it preferable in certain cases to chloramphenicol (36, 37). 

Local anesthetics are usually eliminated by hydrolyzing or breaking apart the drug molecule. This metabolic hydrolysis is catalyzed by hepatic enzymes or enzymes circulating in the plasma (e.g., the plasma cholinesterase). Once metabolized, the kidneys excrete the polar drug metabolites. 

It has been generally assumed that the amount of aluminum absorbed by healthy individuals is dependent on elimination in the urine, whereby low body levels of this element are maintained. However, it is unknown whether the normal kidney excretes all the metal absorbed when individuals are given large oral aluminum loads [16]. 

The kidneys excrete a variety of waste products produced by metabolism, including the nitrogenous wastes urea (from protein catabolism) and uric acid (from nucleic acid metabolism). The kidneys also excrete many drugs or their metabolites, in particular those that are hydrophilic, have a small volume of distribution and a low degree of protein binding. 

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. 

The kidney excretes and reabsorbs calcium, leading to a small overall loss. The kidney also processes vitamin D into calcitrol, which assists in intestinal absorption of calcium both processes are stimulated by PTH, which also regulates calcium release from bone. 

Studies in humans have shown that approximately 66% of an intravenous injection of uranium is eliminated from the plasma within 6 min, while 99% of the uranium is eliminated from the plasma 20 hours after injection (ATSDR, 1999 Harley et al, 1999 Luessenhop et al, 1958). Another study has shown that the kidneys excrete over 90% of intravenously injected soluble hexavalent uranium salt, with less than 1% excreted in the feces approximately 70% of the dose is excreted within the first 24 h (Bassett et al, 1948). 

Most opiate drugs arc rapidly metabolized in the liver and excreted by the kidneys. Excretion of opiates is fairly rapid, with 90% excretion within a day after taking the drug. Hov e cr, traces of morphine may remain in urine for two to four days after use (Hawks C hiang, 1986). 

Hypoventilation causes retention of C02 by the lungs, which can lead to a respiratory acidosis. Hyperventilation can cause a respiratory alkalosis. Metabolic acidosis can result from accumulation of metabolic acids (lactic acid or the ketone bodies p-hydroxybutyric acid and acetoacetic acid), or ingestion of acids or compounds that are metabolized to acids (methanol, ethylene glycol). Metabolic alkalosis is due to increased HC03, which is accompanied by an increased pH. Acid-base disturbances lead to compensatory responses that attempt to restore normal pH. For example, a metabolic acidosis causes hyperventilation and the release of C02, which tends to lower the pH. During metabolic acidosis, the kidneys excrete NH4+, which contains H+ buffered by ammonia. 

D. The kidney excretes urea. If the kidney is diseased, urea will accumulate in the blood. 

C. The kidney excretes nitrogenous waste products, including urea, ammonia, creatinine, and uric acid. If the kidneys fail, these waste products will not be excreted into the urine. 

CS reacts covalently with plasma proteins to form compounds that may be antigenic. On contact with water, it hydrolyses into o-chlorobenzaldehyde and malononitrile. The kidney excretes o-chlorobenzal-dehyde as the metabolites o-chlorohippuric acid (major) and o-chlorobenzoic acid (minor). The malononitrile is metabolized to thiocyanate. The cyano groups of 2-chlorobenzylidene malononitrile are unlikely to cause systemic cyanide toxicity since no significant amounts of free cyanide appear in the plasma. 

However, a second agent shown in the PMI curves is that of D-peni-cillamine. Upon studying the speciation of that agent in blood plasma it is found that this is electrically net-neutral and therefore is able to penetrate into tissue. Further, the PMI curves indicate that it is able to complex with lead ions and to form a net-neutral lead-penicillaminate complex. This then passes out of the cell membrane into the blood plasma where it remains net-neutral and thus is not amenable to kidney excretion. 

The (metabolic) pathways of dietary vanadium, such as vanadate [H2V04], can be expressed as illustrated in Scheme 5.1 after oral uptake, vanadate reaches the gastrointestinal tract, where it is partially reduced and precipitated to vanadyl (VO ) hydroxides, which are excreted with the faeces. Another portion is absorbed and circulated in the blood, where it undergoes redox speciation and complexation by the serum proteins transferrin and albumin. Vanadate and vanadyl are finally incorporated into cells, mainly those of the liver, spleen and kidney. Excretion is achieved via the urine. Part of the vanadium is taken up by bones, where the mean retention time is comparatively long. 

The kidneys excrete 80% of the daily potassium intake. Therefore when the kidney is unable to excrete potassium appropriately, as in acute renal failure and CKD, potassium is retained and often results in hyperkalemia. Moreover, many drugs can inhibit the kidney s ability to excrete potassium by inhibiting aldosterone and thus contribute to an increase in serum potassium levels. 

Creatinine clearance—A test that measures how efficiently the kidneys excrete creatinine. Low creatinine clearance usually indicates the presence of kidney damage. 

Local anaesthetics used in podiatry are all readily absorbed from their sites of administration into the bloodstream, so potentially they can have systemic side effects. Metabolism is by enzymes in the liver, and to a lesser extent in the kidneys. Excretion occurs via the kidneys but only a small percentage of the drug appears in the urine in its original form. Therefore, the risk of adverse effects is increased in patients with hepatic or renal disorders. 

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