Urine urate

B-5) Xanthine oxidase deficiency. The inability to change xanthine to urate results in xanthinuria with decreased blood and urine urate levels. Sometimes urinary xanthine stones may form. The absent enzyme may be confirmed on liver biopsy. 

EFFECT OF PURINE RESTRICTION ON SERUM AND URINE URATE IN NORMAL SUBJECTS... 

Fig. 1. Plan of study to determine changes in serum urate and mean urine urate excretion following purine restriction.

SERUM AND URINE URATE UNDER PURINE RESTRICTION 311... 

Patient Diagnosis Serum Urate Urine Urate urate Ccreatinine... 

Table II. Serum and urine urate and urine oxypurine excretion in heterozygotes for xanthine oxidase deficiency.

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. 

An amperometric urate sensor based on uricase-immobilized silk fibroin membrane was developed by Zhang [256], The biosensor can be used to measure the urate level in human serum or urine and standard additions of uric acid. F or this biosensor, the recoveries of uric acid in human serum and urine are in the range of 94.2 102.6% to 92.5 97.9%, respectively. The relative standard deviations for repeatedly monitoring standard urate solution, human serum, and urine are 2.37, 3.72, and 2.95%, respectively, based on 100 measurements. 

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. 

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Hyperuricemia may be produced by overproduction of uric acid or under-excretion of uric add by the kidneys. Kyperuricemia may progress to acute and chronic gouty arthritis if uric acid (monosodium urate) is deposited in joints and surrounding soft tissue, where it causes inflammation, Uric add is produced from excess endogenous purines as shown in Figure 1-18-5, and is also produced from dietary purines (digestion of nucleic acid in the intestine) by intestinal epithe-lia. Both sources of uric acid are transported in the blood to the kidneys for excretion in urine. 

The low solubility of uric acid has unfortunate consequences since at higher than normal concentrations it can crystallise in the body. For example, when the urine is unusually acid, calcium urate stones can form in the kidney and bladder. High levels of uric acid in the blood can result in the formation of urate crystals in the joints, which causes a very painful condition, since it results in inflammation in these joints. Gout is unlikely to develop if the urate concentration remains low (<0.4 mmol/L) but any factor that increases the rate of production or decreases that of elimination by the... 

The presence of sodium urate in the amorphous deposits in a jug found in 1903, but dating back to the Middle Ages, suggests that it was used to store urine, from which the urate precipitated as the urine evaporated. But why was urine stored in a jug in the Middle Ages Perhaps because drinking urine was highly recommended at this time for treatment of bubonic plague and other diseases Lancet, July 11, 1942). 

In healthy individuals, useful endogenous compounds that are freely filtered by the glomerulus, only appear in the urine in small quantities. These compounds are rescued by tubular reabsorption. These rescue mechanisms consist of a variety of, mostly, carrier-mediated processes at the luminal site of the tubular cell. Substances transported by reabsorptive systems include sugars [6], amino acids [7], dipeptides [8], urate [9], folate [10], nucleosides [11] and proteins [12]. 

Large doses may cause diarrhea and precipitation of cystine, oxalate, or urate renal stones if the urine becomes acidic during therapy. 

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. 

Alkalinization of urine Hematuria, renal colic, costovertebral pain, and formation of urate stones associated with use in gouty patients may be prevented by alkalization of urine and liberal fluid intake monitor acid-base balance. 

The uricosurics are most effective when used during the first few weeks after an acute attack of gout. It is to be expected that in this period high serum levels of uric acid exist with insufficient excretion of urate in the urine. Oral doses of both probenecid and sulfinpyrazone are completely absorbed. Benzbromarone has an oral bioavailability... 

The adverse effect of formation of urate stones in the kidney can be reduced by adequate hydration and alkalinization of the urine. 

As the urinary excretion of uric acid increases, the size of the urate pool decreases, although the plasma concentration may not be greatly reduced. In patients who respond favorably, tophaceous deposits of urate are reabsorbed, with relief of arthritis and remineralization of bone. With the ensuing increase in uric acid excretion, a predisposition to the formation of renal stones is augmented rather than decreased therefore, the urine volume should be maintained at a high level, and at least early in treatment the urine pH should be kept above 6.0 by the... 

Special assays (urine and plasma) lactate, orotidine, thiosulphate, carnitine, succinylacetone, hydroxyproline, urate, orotate, sialic acid, MPS, guanidino-acetate, HVA, pyroglutamate, 5H1AA, pipecolate, pyruvate, 3-hydroxybutyrate, phytanate, VLCFA, homocysteine, 7-dehydrocholesterol, phenylalanine ERNDIM 8 148... 

A 42-year-old male cancer patient undergoing radiation therapy develops severe pain in his right big toe. Laboratory analyses indicate an elevated serum uric acid level and urate crystals in his urine. This patient s pain is caused by the overproduction of the end product of which of the following metabolic pathways ... 

The contribution of lipophilic antioxidants is small. Escobar et al. (E5) found that the TAC of lipophilic antoxidants in blood plasma was 16.5 1.5 pM and corresponded almost exclusively to a-tocopherol the concentration of this compound in the blood plasma, analyzed independently, was 17.6 0.3 pM. Popov and Lewin (PI9) found TAC of lipid-soluble antioxidants in blood plasma to be 28.0 8.1 /u.M, a value comparable with the concentration of a-tocopherol (20.5 6.6 /U.M). These (and other) results confirm that a-tocopherol is the main lipid-soluble antioxidant of blood plasma (II) and indicates that the contribution of the lipid-soluble antioxidants to TAC of blood plasma is in fact negligible, taking into account that TAC of human blood plasma is of the order of 1 mM (see later). The contribution of ascorbic acid is also low. This situation may differ considerably in other biological fluids and tissue homogenates. In seminal plasma, the concentration ratio of ascorbate to urate is about 1 (G3). Ascorbate and urate contribute 29% of the fast TRAP of human seminal plasma the share of proteins and polyphenolic compounds is 57%, whereas tyrosine contributes 15% of the slow TRAP (R14) (Table 7). Ascorbate and uric acid account for about half of TAC of human tears (K3). TAC of urine is determined mainly by urate and proteins (K5). 

Increase in TAC is not always a good prognostic it may simply indicate an initial response to oxidative stress, as with concentrations of individual antioxidants and activities of antioxidant enzymes, or when it is due to disturbances in uric acid metabolism. Because uric acid is the main determinant of TAC of blood plasma, TAC increases in situations when the concentration of urate is increased, for example, in metabolic disorders and kidney failure. TAC is increased in urine from renal transplant recipients with delayed graft function (SI6). Ischemia of small intestine leads to an increase in TAC of rat blood serum, which is maximal (almost twofold) immediately after termination of 45-min ischemia (S22). TAC of blood plasma of rats poisoned with a high dose of carbon tetrachloride (1200 mg/kg, intraperitoneal injection, measurement 16 hr after injection) was significantly (over twofold) increased (Kl). These apparently paradoxical effects can be explained, however, by release of antioxidants from cells undergoing necrosis. Increase in TAC after intensive physical exercise also may be a marker of tissue... 

Akyilmaz E, Sezgintiirk MK, Dinfkaya E (2003) A biosensor based on urate oxidase-peroxidase coupled enzyme system for uric acid determination in urine. Talanta 61 73-79... 

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