Acidification, of urine

Hexanedione is usually measured as total 2,5-hexanedione, a free form accounting for about 10% of the total and 4,5-dihydroxy-2-hexanone, which is converted to 2,5-hexanedione upon acid treatment (acidification of urine samples is routinely performed in order to hydrolyze conjugates that can interfere with analysis). 2,5-Hexanedione has also been detected after acid treatment of urine from individuals not occupationally exposed to w-hcxane (Fedtke and Bolt 1986a Perbellini et al. 1993). A reference value for 2,5-hexanedione in acid-treated urine in a non-occupationally exposed Italian population (n=123,... 

Acidification of urine The point was made earlier that the pH of the fluid in the PCT is approximately 6.8, only slightly below that of blood. In contrast, urinary pH may vary considerably but is usually approximately pH 6. Acidification of the urine occurs mainly in the distal portion of the nephron. 

Is treatment with an antibiotic necessary Symptomatic patients always need treatment. Asymptomatic bacteriuria (=10 bacteria/ml in two separate urine cultures) only needs treatment in pregnancy, in children and in obstructions of the urinary tract. Obstmctions in urinary flow must be treated before an antibiotic is started. There is no clear evidence that hydration or acidification of urine improves the results of antimicrobial therapy. 

Ammonium chloride increases urinary volume with acidification of urine. The excretion of amphetamine is decreased in relatively alkaline urine and has proved useful in the treatment of amphetamine intoxication. ... 

The local anesthetics are converted in the liver (amide type) or in plasma (ester type) to more water-soluble metabolites, which are excreted in the urine. Since local anesthetics in the uncharged form diffuse readily through lipid membranes, little or no urinary excretion of the neutral form occurs. Acidification of urine promotes ionization of the tertiary amine base to the more water-soluble charged form, leading to more rapid elimination. 

FIGURE 1.13 Elimination of drug following alkalinization or acidification of urine. 

Acidification of urine is affected in renal tubular acidosis. This condition may be due to an inborn error of metabolism or to an acquired tubular lesion. The defect may be related either to the secretion of hydrogen ions or to the diffusion of hydrogen ions into the blood as a result of increased permeability of the distal tubule cell wall to secreted hydrogen ions. Because renal tubular acidosis is primarily a defect in hydrogen ion secretion, the formation of ammonia by tubule cells is not affected. 

Acidification of urine —increases ionization of weak bases —> increases renal elimination. Alkalinization of urine — increases ionization of weak acids —> increases renal elimination. 

Acidification of urine —> increases ionization of weak bases —> increases renal elimination. 

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. 

Much less data are available on the adsorption of elements onto surfaces from blood or urine samples. Stoeppler (1980) did not detect any loss of added Ni from urine samples onto polyethene container walls. Concentrations of nickel or chromium in urine samples, spiked with small concentrations of the metals and stored for 6 months at 4°C did not show a decrease (Kiilunen et al.. 1987). The lUPAC reference method for nickel in urine calls for acidification of urine quality control samples with nitric acid and storage in polypropene tubes with a screw-cap at -20°C (Brown et al., 1981). No adsorption of cadmium onto container walls (type not specified) was seen from urine acidified to pH < 2 (Stoeppler and Brandt, 1980). 

The mercurial diuretics essentially contain in an organic molecule. They usually inhibit sodium reabsorption in the proximal tubuler and ascending loop of Henle. There may be slight effect in the distal tubule where inhibition of chloride reabsorption also occurs. The mercurials have been foimd to enhance excretion though potassium loss is less than that produced by many other diuretics. However, the overall action of mercurial diuretics is invariably increased by acidification of urine. The mercurial diuretics are not very much used in clinical practices due to their pronormced and marked side-effects viz., mercurialism, hypersensitivity and excessive diuresis which may lead to electrolyte depletion and vascular complications. Most of the mercurials are administered by intramuscular route and the availability of orally active diru etics has limited their use. 

In 1937, it was proposed that the normal acidification of urine was caused by secretion of hydrogen ions by the tubular cells of the kidney. These ions were provided by... 

Amantadine crosses the blood-brain barrier and is distributed in saliva, nasal secretions, and breast milk (20). Approximately 90% of the drug is excreted unchanged by the kidney, primarily through glomerular filtration and tubular secretion, and there are no reports of metabolic products. Acidification of urine increases the rate of amantadine excretion. The half-life of the drug is 15 to 20 hours in patients with normal renal function. 

It is noteworthy that adding a methyl group to the 5-position relative to quaternary ammonium in ACh has led to significant selectivity at the nicotinic receptor (5-methylacetylcholine Fig. 16.5). All these agents are cleared mainly via the kidneys, and acidification of urine (e.g. by ingestion of ascorbic acid) enhances excretion. 

---