Uric acid urinary

Since allopurinol blocks xanthine conversion to uric acid, urinary xanthine excretion is increased, creating a risk of xanthine crystal formation in the urinary system or even in muscles this can result in nephrolithiasis (12). It is still an open question whether a predisposition to renal disease or renal disease itself is required to precipitate these adverse effects. It is also not known whether increased excretion of orotic acid, due to an interaction of allopurinol with pyrimidine formation, has any consequences for these adverse effects or for its role in reducing glucose tolerance. 

In summary these children had features in common which made it difficult to identify the underlying enzyme abnormality and its relationship to their presentation in renal failure. Both had raised plasma uric acids not unusual in severe renal failure but in these children the magnitude was the important factor The crystals or stones causing the nephropathy could both have been identified as uric acid Urinary uric acid on a creatinine basis was not raised in either The severe renal damage at such an early age in both underlines the importance of early and correct identification of these defects, especially APRT deficiency, which can be treated successfully with allopurinol and such severe renal damage need never occur. ... 

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). 

DRUGS USED FOR GOUT. The nurse encourages a liberal fluid intake and measures the intake and output. The daily urine output should be at least 2 liters. An increase in urinary output is necessary to excrete the urates (uric acid) and prevent urate acid stone formation in the genitourinary tract. 

If the test is positive, the urine is examined microscopically for red blood cells. If no red blood cells are found, a tentative diagnosis of myoglobinuria is made, serum chemistries are obtained, and the patient is held to rule out rhabdomyolysis. If the uric acid and creatinine kinase (CK) values are normal, and the patient is asymptomatic, he/she is discharged from the hospital. Routine toxicology tests include urinary PCP, serum alcohol, and hypnotic screen. 

Uric acid - Normal urinary excretion in humans ... 

About two-thirds of the uric acid produced each day is excreted in the urine. The remainder is eliminated through the GI tract after enzymatic degradation by colonic bacteria. A decline in the urinary excretion of uric acid to a level below the rate of production leads to hyperuricemia and an increased miscible pool of sodium urate. 

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. 

Prophylactic treatment can be withheld if the first episode of acute gouty arthritis was mild and responded promptly to treatment, the patient s serum urate concentration was only minimally elevated, and the 24-hour urinary uric acid excretion was not excessive (less than 1,000 mg/24 hours on a regular diet). 

If the patient had a severe attack of gouty arthritis, a complicated course of uric acid lithiasis, a substantially elevated serum uric acid (greater than 10 mg/dL), or a 24-hour urinary excretion of uric acid of more than 1,000 mg, then prophylactic treatment should be instituted immediately after resolution of the acute episode. 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. 

Drug/Lab test interactions Methyidopa may interfere with tests for Urinary uric acid by phosphotungstate method serum creatinine by alkaline picrate method AST by colorimetric methods. Because methyidopa causes fluorescence in urine samples at the same wavelengths as catecholamines, falsely high levels of urinary catecholamines may occur and will interfere with the diagnosis of pheochromocytoma. 

Pharmacology Thiazide diuretics increase the urinary excretion of sodium and chloride in approximately equivalent amounts. They inhibit reabsorption of sodium and chloride in the cortical thick ascending limb of the loop of Henie and the early distal tubules. Other common actions include Increased potassium and bicarbonate excretion, decreased calcium excretion and uric acid retention. At maximal therapeutic dosages all thiazides are approximately equal in diuretic efficacy. 

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. 

Pharmacology A uricosuric and renal tubular blocking agent, probenecid inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum uric acid levels. 

Adverse reactions may include headache anorexia nausea vomiting urinary frequency hypersensitivity reactions sore gums flushing dizziness anemia hemolytic anemia (possibly related to G-6-PD deficiency) nephrotic syndrome hepatic necrosis aplastic anemia exacerbation of gout uric acid stones with or without hematuria renal colic or costovertebral pain. 

Administration generally results in a fall in both serum and urinary uric acid within 2 to 3 days. The magnitude of this decrease is dose-dependent. One week or more of treatment may be required before the full effects of the drug are manifested likewise, uric acid may return to pretreatment levels slowly following cessation of therapy. 

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