Urine acidification

Vanillylmandelic acid human urine acidification, centrifugation ion-pair CIS Affix EC 65... 

Domino, E.F., and Wilson, A.E. Effects of urine acidification on plasma and urine phencyclidine levels in overdosage. Clin Pharmacol Ther 22(41 421-424, 1977. 

Consider forced diuresis, urine acidification, or alkalinization if specific antidotes are not available Hemodialysis or charcoal hemoperfusion may be appropriate for rapid elimination if antidotes are not available... 

Urine pH is an important determinant of renal elimination of PCP. In a study in which urine pH was uncontrolled (6.0 to 7.5), the average total clearance of PCP was 22.8 4.8 L/h after intravenous administration.4 In the same study, renal clearance was 1.98 0.48 L/h. When the urine was made alkaline, the renal clearance of PCP was found to decrease to 0.3 0.18 L/h. If the urine was acidified (pH 6.1) in the same subjects, renal clearance increased to 2.4 0.78 L/h.13 Aronow et al.14 determined that if the urine pH was decreased to <5.0, renal clearance increased significantly to 8.04 1.56 L/h. There is disagreement about the utility of urine acidification in the treatment of PCP overdose, even though excretion may be increased by as much as 100-fold.15 It should be noted that acidification may increase the risk of metabolic complications.16... 

Ammonium chloride 60-250 mg/kg, once daily (urine acidification) p.o. 

Adequate supportive care should be assured in the phencyclidine-intoxicated patient. There is no antidote for phencyclidine overdose. The patient should be isolated from all sensory stimuli as much as possible and protected from self-inflicted injury. Benzodiazepines should be administered liberally and titrated until the phencyclidine-intoxicated patient calms. Adequate hydration should be assured to maintain the urine output at l-2cckg h. Although urine acidification theoretically enhances phencyclidine elimination, it is not recommended because of the high frequency of rhabdomyolysis and myoglobinuric renal failure seen with significant intoxication. Seizures should be treated with... 

Treatment of PCP toxicity is supportive. Severe agitation or seizures may respond to diazepam severe psychoses may require a neuroleptic drug, such as haloperidol. " For the most serious cases, continuous nasogastric suction to help remove PCP may be beneficial urine acidification to hasten eEmination has been advocated by some but is controversial. ... 

Treatment of the adverse effects of PCP is difficult for several reasons. PCP has a very high volume of distribution (6.2 liters per kilogram (L/kg) in humans) and its clearance is primarily by metabolism (Cook et al. 1982) with only a small contribution from renal excretion. Its major sites of action in the central nervous system (CNS) are far removed from the beneficial effects of most traditional treatment methods such as dialysis. In addition, there is no specific antagonist for PCP s adverse effects. These pharmacokinetic and receptor-medicated characteristics make it very difficult to develop effective treatment strategies. Some of the current methods for treatment of overdose are urine acidification, diazepam administration to control convulsions (Aronow and Done 1978 ... 

Peterson and Stillman 1978), and simply waiting for the patient to get better. Nevertheless, Mayersohn (1985) predicts that even under ideal conditions, urine acidification would only increase systemic clearance (Cis) by about 28 percent and would only decrease the half-life (t ) by about 23 percent (t in humans averages about 17 hrs, but can range from 7 to 58 hrs Cook et al. 1985). This small change in kinetic parameters is not surprising due to PCP s very high volume of distribution and low renal clearance (Mayersohn 1985). 

Urine Acidification with nitric acid dilution addition of La matrix modifier GFAAS 0.13 mg/L 98.8-101.5 Burguera et al. 1999... 

Ascorbic acid, a water-soluble vitamin (1(X) to 250 mg p.o. daily), is indicated in the treatment of frank and subclinical scurvy in extensive bums, delayed fracture or wound healing, postoperative wound healing severe febrile or chronic disease states and in prevention of ascorbic acid deficiency in those with poor nutritional habits or increased requirements. In addition, ascorbic acid has been used for potentiation of meth-enamine in urine acidification and as an adjunctive therapy in the treatment of idiopathic methemoglobinemia. 

Dextroamphetamine is a sympathomimetic amine that is used in narcolepsy and in attention-deficit disorder (ADD) in children. Dextroamphetamine releases norepinephrine and, in high doses, also dopamine. It is absorbed from the GI tract, metabolized in the liver, and excreted unchanged in the urine. Acidification of urine shortens amphetamine s half-life, whereas alkalinization of urine prolongs it. The accumulation of hydroxy metabofite of amphetamine has been thought to cause amphetamine-induced psychosis. Therapeutic doses of amphetamine may cause insomnia, tremor, and restlessness, and toxic doses of amphetamine may cause mydriasis, hypertension, and arrhythmia. Chlor-promazine is an excellent antidote in amphetamine toxicity. 

Chloroquine is well absorbed after oral, intramuscular, and subcutaneous administration. It distributes relatively slowly into a very large apparent volume (over 100 L/kg) and is extensively sequestered in tissues, particularly liver, spleen, kidney, lung, and to a lesser extent, brain and spinal cord. Chloroquine binds moderately (60%) to plasma proteins and is biotransformed via hepatic CYPs to two active metabolites, desethylchloroquine and bisdesethylchloroquine. Renal clearance of chloroquine is about half of total clearance. Unchanged chloroquine and its major metabolites account for >50% and 25% of urinary drug products, respectively, and their renal excretion is increased by urine acidification. 

Renal excretion of basic drugs such as amphetamine theoretically can be enhanced by acidification of the urine. Acidification can be accomplished by the administration of ammonium chloride or ascorbic acid. Urinary excretion of an acidic compound is particularly sensitive to changes in urinary pH if its is within the range of 3.0-7.5 for bases, the corresponding pH range is 7.5-10.5. 

C. Methenamine Methenamine mandelate and methentunine hippurate combine urine acidification with the release of the antibacterial compound formaldehyde at pH levels below 5.5. These drugs are not usually active against proteus because those organisms alkalinize the urine. Insoluble complexes form between formaldehyde and sulfonamides, and the drugs should not be used together. 

Mitchell BG, Clements lA Pottage A, Prescott LF. Mexiletine disposition individual variation in response to urine acidification and alkalinisation BrJ Clin Phannacol( 9% S) 16, 281-4. 

Adrenal insufficiency is responsible for renal sodium loss and failure of urine acidification in the tubules. Similarly, the reabsorption of sodium and the excretion of H are impaired in severe kidney disease. 

We have seen that bicarbonate is reabsorbed primarily in the proximal tubule and that the urine is acidified and ammonia excreted in the distal tubule. Any inherited or acquired injury that interferes with bicarbonate reabsorption or urine acidification will lead to acidosis. (Although interference with ammonia excretion could, in theory, also lead to acidosis, it seldom does.)... 

Similar to the gastrointestinal tract, development of renal function is not influenced by dietary content. Glomular filtration does not approximate adult values until about 3 years of age, and tubular reabsorption and urine acidification reach normal values at several months of age. However both are sufficient for healthy term infants, but contribute to fluid and electrolyte abnormalities in infants who are ill and in those who are fed an inappropriate diet. 

Specific functions of the kidney that can be assessed inclnde glomernlar filtration rate (GFR), which can be measured by quantifying the clearance of a substance that is freely filtered across the capillary wall and is neither reabsorbed nor secreted by the tubules. The optimal measurement of GFR is insnlin clearance (Arant et al., 1972). Clinically, however, GFR can be estimated by the clearance of endogenous creatinine. At serum levels of creatinine exceeding 2.0 mg/dL, changes in renal function can be monitored by the serum creatinine concentration. GFR is adequate for healthy term infants, bnt it does not approximate adult rates until about 3 years of age. Renal tubular reabsorption and urine acidification is less at birth and for several months thereafter than it is for adults. This function is adequate for healthy infants, but contributes to fluid and electrolyte abnormalities in infants who are ill or are fed an inappropriate diet (Goldsmith and Novello, 1992). 

GF-AAS urine acidification, microwave digestion with HNO3/HCI 0.05 pg/L [19]... 

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