Acid urine

The nurse measures the fluid intake and output, especially when the primary health care provider orders an increase in fluid intake or when a kidney infection is being treated. The primary health care provider may also order daily urinary pH levels when methenamine or nitrofurantoin is administered. These drugs work best in acid urine failure of the urine to remain acidic may require administration of a urinary acidifier, such as ascorbic acid. 

Uric acid excretion is reduced in patients with chronic kidney disease, putting them at risk for hyperuricemia. In patients with persistently acidic urine and hyperuricemia, uric acid nephrolithiasis can occur in up to 25% of patients in severe cases, uric acid stones can cause nephropathy and renal failure. Extreme hyperuricemia can occur because of rapid tumor cell destruction in patients undergoing chemotherapy for certain types of cancer (see Chap. 85). 

Decreased urinary output, dehydration, or renal failure Preexisting hyperuricemia Acidic urine... 

N-Hydroxy arylamines readily form glucuronide conjugates, but in contrast to the N-hydroxy arylamides, these are N-glucuronides which are unreactive and stable at neutral pH. The N-glucuronides are readily transported to the lumens of the urinary bladder and intestine where they can be hydrolyzed to the free N-hydroxy arylamines by mildly acidic urine or by intestinal bacterial 3-glucuronidases (13,14). Non-enzymatic activation of N-hydroxy arylamines can occur in an acidic environment by protonation (15,16) of the N-hydroxy group (VIII) as well as by air oxidation (reviewed in 17) to a nitrosoarene (IX). 

Uric acid nephrolithiasis occurs in 10% to 25% of patients with gout. Predisposing factors include excessive urinary excretion of uric acid, acidic urine, and highly concentrated urine. 

Omnivores excrete a more acidic urine than herbivores. Investigators have demonstrated increased urinary acid and calcium by feeding acid-producing chemicals. 

Many animal species excrete more calcium if fed an acid or acidforming compounds. In the calf, Steenbock and coworkers (13) observed hypercalciuria and acidic urine after feeding hydrochloric acid to the calf. Stehle (14) pointed out that calcium represented the main long-term fixed base to be lost in the urine of the dog loaded with excessive amounts of hydrochloric acid. Walzer and Browder (15) demonstrated that when infused with a sulfate containing solution, the dog excreted several fold more acid and calcium than saline-infused controls the increased calcium loss returned to normal upon removal of the sulfate. Marone, et al. (16) demonstrated increased excretion of calcium in the acidotic dog. Correction of the acidosis reduced the excessive fractional calcium excretion rate, but did not alter sodium excretion. 

The lacto-ovo vegetarian diet that these S.D.A. women follow would produce a slightly alkaline urine compared with the acidic urine associated with the consumption of. a meat diet. 

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. 

Ammonia can diffuse freely into the urine through the tubule membrane, while the ammonium ions that are formed in the urine are charged and can no longer return to the cell. Acidic urine therefore promotes ammonia excretion, which is normally 30-50 mmol per day. In metabolic acidosis (e.g., during fasting or in diabetes mellitus), after a certain time increased induction of glutaminase occurs in the kidneys, resulting in increased NH3 excretion. This in turn promotes H"" release and thus counteracts the acidosis. By contrast, when the plasma pH value shifts towards alkaline values alkalosis), renal excretion of ammonia is reduced. 

Urinary alkalinization- Urates tend to crystallize out of an acid urine therefore, a liberal fluid intake is recommended, as well as sufficient sodium bicarbonate (3 to 7.5 g/day) or potassium citrate (7.5 g/day) to maintain an alkaline urine continue alkalization until the serum uric acid level returns to normal limits and tophaceous deposits disappear. Thereafter, urinary alkalization and the restriction of purine-producing foods may be relaxed. 

Uses Suppress/eluninate bacteriuria associated w/ chronic/recurrent UTI Action Converted to formaldehyde ammonia in acidic urine nonspecific bactericidal action Dose Adults. Hippurate 0.5-1 g bid. Mandelate 1 g qid PO pc hs Peds 6-12 y. Hippurate 25-50 mg/kg/d PO bid. Mandelate 50-75 mg/kg/d PO qid (take w/ food, ascorbic acid w/ adequate hydration) Caution [C, +] Contra Renal insuff, severe hepatic Dz, severe dehydration sulfonamide allergy Disp Tabs SE Rash, GI upset, dysuria, t LFTs EMS Monitor BP for hypovolemia and dehydration OD Sxs unknown symptomatic and supportive... 

Renal function studies BUN, UA, serum uric acid urine CrCl before, during therapy... 

Renal function studies BUN, serum uric acid, urine CrCl, electrolytes, input and output ratio... 

When carbonic anhydrase inhibitors block the enzyme in the kidney, HjCOj formation— and consequently the availability of H3O+ (i.e., protons)—decreases. Since the Na+ ions in the filtrate cannot be exchanged, sodium is excreted, together with large amounts of water, as a result of ion hydration and osmotic effects. The result is diuresis, accompanied by a dramatic increase in urine volume. There is also failure to remove HCOj" ions because there is no H3O+ to form HjCOj, which would decompose to COj -1- HjO. Therefore, the normally slightly acidic urine becomes alkaline. The strong carbonic anhydrase inhibitors also increase K+ excretion, an undesirable effect. 

It is bacteriostatic and but bactericidal against many gram positive and negative organisms in higher concentration and acidic urine. Pseudomonas aeruginosa and various strains of Proteus are resistant. It... 

Nitric acid, Sulfuric acid, Phloroglucinol, Hydrochloric acid Sodium chlorate. Copper sulfate. Ammonium hydroxide. Alcohol Sodium chlorate. Copper sulfate. Ammonium hydroxide. Alcohol Sulfuric acid. Potassium nitrate, 1,3,5-Trifluorobenzene, Methylene chloride. Hexane, Charcoal, Sodium sulfate, 2-Amino-2-methylpropanone, Potassium hydrogen carbonate, 1,2-Dichloroethane, Trifluoroacetic acid. Urea, Dimethylformamide Nitric acid. Urine... 

Urea nitrate Nitric acid. Urine Secondary high explosive, Used in first World Trade Center ... 

Two main effects occur here. First, change in the pH of urine—weak bases, such as pethidine, are more easily excreted in an acid urine while alkalinisation promotes excretion of weak acids, such as salicylates and phenobarbital. Second, drugs that compete for an active excretion mechanism will reduce each other s elimination—probenecid was used in the early days of penicillin to conserve the drug, while less desirable interactions also occur, e.g. chlorpropamide and phenylbutazone interact to give increased levels of chlorpropamide and a danger of hypoglycaemia. 

Uric acid, cystine, and other weak acids are most easily reabsorbed from acidic urine. Therefore, renal excretion of cystine (in... 

Diethylcarbamazine, a synthetic piperazine derivative, is marketed as a citrate salt. It is rapidly absorbed from the gastrointestinal tract after a 0.5 mg/kg dose, peak plasma levels are reached within 1-2 hours. The plasma half-life is 2-3 hours in the presence of acidic urine but about 10 hours if the urine is alkaline, a Henderson-Hasselbalch trapping effect (see Chapter 1). The drug rapidly equilibrates with all tissues except fat. It is excreted, principally in the urine, as unchanged drug and the N-oxide metabolite. Dosage may have to be reduced in patients with persistent urinary alkalosis or renal impairment. 

On the other hand, acidic drugs tend to ionize under conditions of alkaline pH and so are unable to permeate the renal tubular epithelium and are preferentially excreted. Tire converse applies to conditions of acidic urinary pH. This has been demonstrated experimentally for many drugs weak bases are excreted more rapidly in acidic urine, whereas weak acids are excreted more rapidly in alkaline urine. In the horse, phenylbutazone, which is a weak organic acid with a pKa of 4.6, has a more delayed clearance time under conditions of aciduria than under conditions of alkaline urine. 

Aminolevulinic acid (urine, Davies method) (women < 45 years)... 

In humans, both the d- and L-forms undergo hydroxylation and A-demethylation to their respective />hy dr ox y me thainphetamine and amphetamine metabolites. Amphetamine is the major active metabolite of methamphetamine. Under normal conditions, up to 43% of a D-methamphet-amine dose is excreted unchanged in the urine in the first 24 h and 4 to 7% will be present as amphetamine. In acidic urine, up to 76% is present as parent drug10 compared with 2% under alkaline conditions. Approximately 15% of the dose was present as /7-hydroxymethamphetamine and the remaining minor metabolites were similar to those found after amphetamine administration. Urine concentrations of methamphetamine are typically 0.5 to 4 mg/L after an oral dose of 10 mg. However, methamphetamine and amphetamine urine concentrations vary widely among abusers. Lebish et al.11 reported urine methamphetamine concentrations of 24 to 333 mg/L and amphetamine concentrations of 1 to 90 mg/L in the urine of methamphetamine abusers. 

Methenamine (Hiprex, Mandelamine, Urex) exerts antibacterial properties in a unique fashion. In an acidic environment, this drug decomposes into formaldehyde and ammonia. Formaldehyde is bactericidal to almost all bacteria, and bacteria do not develop resistance to this toxin. This mechanism enables methenamine to be especially useful in treating urinary tract infections, because the presence of this drug in acidic urine facilitates the release of formaldehyde at the site of infection (i.e., within the urinary tract). Use of methenamine is safe, although high doses are associated with gastrointestinal upset and problems with urination (bloody urine, pain while urinating). 

N. Rothman, G. Talaska, R. B. Hayes, V.K. Bhatnagar, D.A. Bell, V.M. Lakshmi, S.K. Kashyap, M. Dosemeci, R. Kashyap, F.F. Hsu, M. Jaeger, A. Hirvonen, D.J. Par-ikh, B.B. Davis, T.V. Zenser, Acidic Urine pH is Associated with Elevated Levels of Free Urinary Benzidine and IV-Acetylbenzidine and Urothelial Cell DNA Adducts in Exposed Workers , Cancer Epidemiol., Biomarkers Prev., 6,1039-1042 (1997). 

Uva-ursi is known to have diuretic, urinary antiseptic, and astringent properties. Traditionally, it has been used for cystitis, urethritis, dysuria, pyelitis, lithuria, and specifically for acute catarrhal cystitis with dysuria and highly acidic urine. 

Other drugs that change the color of the urine act as follows. Logwood (hematoxylon) does not color acid urine but produces a reddish or violet color in alkaline urine. Santonin imparts a yellowish color to acid urine, with a yellow foam if the urine is made alkaline, it imparts a very pronounced pink color. Picric acid gives reddish-brown color in both acid and alkaline urine. The various coal-tar products give a brownish-black color. Methylene blue imparts a green color. 

Uric acid, cystine, and some other weak acids are relatively insoluble in, and easily reabsorbed from, acidic urine. Renal excretion of these compounds can be enhanced by increasing urinary pH with carbonic anhydrase inhibitors. In the absence of continuous bicarbonate administration, these effects of acetazolamide are of relatively short duration (2-3 days). Prolonged therapy requires bicarbonate administration. 

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