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PubMed1981

Uric acid in childhood essential hypertension.

Serum uric acid concentrations and the fractional excretion of uric acid were determined in 31 children from 3 1/2 to 18 years of age with essential hypertension. While on an unrestricted sodium intake, elevated serum values of uric acid were found in 13 of 31 (42%) of the children. After ingesting a low-sodium diet (200 mg/day) for three days, mean serum uric acid values increased by 0.7 mg/dl (P less than 0.001). There was a significant inverse correlation between the serum uric acid concentrations and fractional excretion of uric acid during the normal and low-sodium diet. This study indicates that the major factor leading to hyperuricemia in our hypertensive patients was a decrease in urate clearance. Insofar as hyperuricemia may represent a cardiovascular risk factor, this abnormality already exists in a significant fraction of hypertensive children and adolescents.

Adolescent↗
PubMed1999

Effect of amino acids on the plasma concentration and urinary excretion of uric acid and uridine.

To determine the effect of amino acids on the plasma level and urinary excretion of uric acid and uridine, 200 mL 12% amino acid solution, and 2 weeks later, 100 mL physiological saline solution containing glucagon (1.2 microg/kg weight), was infused into five healthy men. Both increased the urinary excretion of uric acid and the concentration of glucagon, insulin, and glucose in plasma and pyruvic acid in blood, whereas they decreased the concentration of uridine and inorganic phosphate in plasma. However, neither the amino acid infusion nor glucagon infusion affected the concentration of purine bases (hypoxanthine, xanthine, and uric acid), cyclic adenosine monophosphate (cAMP) in plasma, or lactic acid in blood or the urinary excretion of oxypurines (hypoxanthine and xanthine), uridine, or sodium. These results suggest that glucagon may have an important role in the amino acid-induced increase in urinary excretion of uric acid and decrease in plasma uridine.

Adult↗
PubMed2006

Nitrosation of uric acid induced by nitric oxide under aerobic conditions.

Uric acid is a well-established scavenger of reactive oxygen and nitrogen species such as hydroxyl radical and peroxynitrite. However, little attention has been paid to the relationship between uric acid and nitric oxide. This paper reports the identification and characterization of a reaction product of uric acid induced by nitric oxide. When uric acid was treated with nitric oxide gas in a neutral solution under aerobic conditions, uric acid was consumed, yielding an unknown product. The product was identified as nitrosated uric acid from mass spectrometric data, although the position of the nitroso group on the molecule was not determined. The nitrosated uric acid decomposed to several compounds including uric acid with a half-life of 2.2 min at pH 7.4 and 37 degrees C. The incubation of nitrosated uric acid with glutathione resulted in the formation of S-nitrosoglutathione. Nitrosated uric acid was also formed in the reaction with nitric oxide donors, but not with peroxynitrite. Nitrosated uric acid was detected in human serum and urine by in vitro treatment with a nitric oxide donor. In the reaction of glutathione with the nitric oxide donor, the addition of uric acid caused an increase in the yield of S-nitrosoglutathione. These results indicate that under aerobic conditions nitric oxide can convert uric acid into its nitroso derivative, which can give a nitroso group to glutathione. Uric acid may act as a vehicle of nitric oxide in humans.

Aerobiosis↗
PubMed1989

[Uric acid metabolism in patients with chronic glomerulonephritis].

Serum uric acid (SUA), creatinine clearance (Ccr), urinary excretion of uric acid (UUAV) and uric acid clearance (CUA) were determined in 357 patients with IgA nephritis (IgAN) and 81 patients with membranous nephropathy (MGN) in an attempt to clarify uric acid metabolism in patients with chronic glomerulonephritis, and UUAV/Ccr and CUA/Ccr levels were measured to investigate their correlations. As a result, hyperuricemia that could hardly be explained with a decline of Ccr alone was recognized in many cases, since the patients with hyperuricemia exceeding 7.0 mg/100 ml of SUA registered even as high as 25.5% in IgAN and 33.3% in MGN, whereas those with the Ccr levels higher than 80 ml/min registered 22.3% in IgAN and 38.0% in MGN. Although the SUA level increased and the UUAV and CUA levels decreased along with a decline of Ccr in IgAN, no similar trends were recognized in MGN. When the distribution of UUAV was studied in the patients with the Ccr levels higher than 80 ml/min, the patients whose UUAV levels higher than 800 mg/24 hrs that suggested excessive uric acid production were markedly as low as 3.9% in IgAN and 3.7% in MGN. Thus, the cause of hyperuricemia could not be attributed to an amount in the uric acid production. On the other hand, the patients whose CUA levels lower than 6.0 ml/min in the distribution of CUA that suggested a decrease of uric acid excretion registered 47.4% in IgAN and 63.0% in MGN, respectively, which equally appeared to be a type of lowered excretion in a majority of patients whose hyperuricemia was recognized in IgAN and MGN. The mechanism of the lowered excretion of uric acids from the kidney despite the normal level of Ccr has yet to be clarified.

Adult↗
PubMed2003

Uric acid stone disease.

The trend in uric acid stone formation appears to be on the rise again throughout much of the world. This is thought secondary to diet, body habitus, and social reasons. Uric acid stone disease has a rich and fascinating medical history and probably is the oldest known stone disease. Uric acid stone disease is strongly linked to the purine metabolic pathway, and its treatment is primarily medical. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. Surgical intervention with uric acid stone disease represents a failure of medical therapy and a whole host of modern, minimally invasive methods are available for treating patients with this disease. Finally, uric acid nephrolithiasis is associated with a variety of inborn errors of metabolism based on mutations of key enzymes in the purine metabolic pathways. This review of uric acid stone formation will start with historical consideration, review basic biochemistry, and physiology and then focus upon specific clinical scenarios. The discussions will be heavily referenced for those interested in greater details.

Animals↗
PubMed1975

The influence of the extracellular fluid volume on the tubular reabsorption of uric acid.

Changes is tubular reabsorption of uric acid in response to alterations in the extracellular fluid volume (ECFV) were examined in rats by clearance studies and by direct intratubular microinjections. Contraction of the ECFV led to a rise in the serum uric acid concentration and a 47% decrease in the clearance of uric acid. The ratio of uric acid to inulin clearance also fell, indicating an increase in the net tubular reabsorption of urate. Volume expansion resulted in an increase in the urate clearance and a 37% decrease in the net tubular reabsorption of uric acid. To localize the site in the nephron where these changes occur, microinjections of [2-14C]urate were performed. The lack of conversion of radioactive urate to allantoin after microinjections was demonstrated by thin-layer chromatography. After contraction of the ECFV, urinary recoveries of uric acid were significantly decreased after microinjections into proximal tubular sites. In contrast, recoveries were increased from these proximal sites after volume expansion. No evidence for distral reabsorption was obtained in any group of animals. These studies demonstrate that net urate reabsorption is influenced by the state of hydration of the ECFV and that these alterations are mediated by changes in the rates of reabsorption in the proximal tubule.

Allantoin↗
PubMed1999

'Pseudohypouricosuria' in alcaptonuria: homogentisic acid interference in the measurement of urinary uric acid with the uricase-peroxidase reaction.

Urinary excretion of uric acid was found to be extremely low in a 58-year-old female patient with alcaptonuria. This was due to interference with the uricase-peroxidase method used, because analysis using high-performance liquid chromatography (HPLC) showed a normal urinary concentration of uric acid. In vitro experiments demonstrated that a high concentration of homogentisic acid in the patient's urine inhibited the peroxidase reaction, possibly due to inhibition of the colour development of 3-methyl-N-ethyl-N-(beta-hydroxyethyl)aniline (MEHA) and 4-aminoantipyrine, via the peroxidase reaction. A homogentisic acid concentration equivalent to that in plasma did not affect the uricase-peroxidase reaction. This result suggests that any assay based on a peroxidase method is affected by a high urinary concentration of homogentisic acid in patients with alcaptonuria.

Alkaptonuria↗
PubMed1989

Uric acid excretion in children with urolithiasis.

Urinary uric acid excretion was assessed in 38 children to determine whether hyperuricuria was a risk factor in children with urolithiasis. Uric acid excretion (measured per deciliter glomerular filtration rate), and fractional excretion of uric acid were similar in 27 children with hypercalciuria and calcium oxalate urinary stones, in six children with idiopathic calcium oxalate urolithiasis, and in five with uric acid urolithiasis, of whom four were white boys and one was an Asian girl. One boy with a urate stone had cystinosis. Serum uric acid concentrations exceeded 6.0 mg/dl (360 mumol/L) in two children with hypercalciuria and in two patients with idiopathic calcium oxalate urolithiasis. None of the children with calcium urolithiasis had excessive urinary excretion of uric acid. In children with hypercalciuria, uric acid excretion did not change significantly when dietary sodium was increased from 1.0 to 5.0 gm/1.73 m2. We conclude that excessive urinary uric acid excretion is seldom an additional risk factor in children with calcium urolithiasis and that dietary sodium chloride does not have a strong influence on urinary excretion of uric acid in children with hypercalciuria.

Adolescent↗
PubMed2002

Uric acid nephrolithiasis: current concepts and controversies.

PURPOSE: Uric acid calculi with or without a calcium component comprise a significant proportion of urinary stones. Knowledge of the pathophysiology of stone formation is important to direct medical treatment. The aim of this review is to provide an update on the epidemiology, pathophysiology and management of uric acid renal stones. MATERIALS AND METHODS: A MEDLINE search was performed on the topic of uric acid stones. Current literature was reviewed with regard to the epidemiology, pathophysiology, associated medical conditions and management of uric acid stones. RESULTS: The incidence of uric acid stones varies between countries and accounts for 5% to 40% of all urinary calculi. Hyperuricuria, low urinary output and acidic urine are well known contributing factors. However, the most important factor for uric acid stone formation is persistently acidic urine. Gout and myeloproliferative disorders are associated with uric acid stones. Why most patients with gout present with acidic urine yet only 20% have uric acid stone formation remains unclear. The pathophysiological basis for persistent urine acidity also remains unclear although various mechanisms have been proposed. Urinary alkalization with potassium citrate or sodium bicarbonate is a highly effective treatment, resulting in dissolution of existing stones and prevention of recurrence. CONCLUSIONS: Acidic urine is a prerequisite for uric acid stone formation and growth. Medical management with urinary alkalization for stone dissolution and prevention of recurrence is effective and should be the cornerstone of treatment.

Cross-Sectional Studies↗
PubMed1991

Uric acid synthesis by avian exocrine pancreas.

1. Chicken pancreas has been shown to synthesize and secrete uric acid. Uric acid synthesis from xanthine in vitro by isolated pancreatic acinii is saturable and dependent on the activity of xanthine dehydrogenase. 2. Chicken pancreas is unable to synthesize uric acid de novo but the variety of substrates which support urate synthesis suggests that it occurs by the purine degradation pathway.

Allopurinol↗
PubMed2005

Uric acid and hypertension.

Increased levels of uric acid are associated with cardiovascular disease and the metabolic syndrome. They may predict clinical outcomes and also the onset of hypertension, though it is less clear that hyperuricaemia can be regarded as an independent risk factor given its clustering with other well-recognised factors. Uric acid may increase as a result of pathophysiological processes such as impaired renal sodium handling but may also contribute to renal and vascular damage, particularly endothelial dysfunction. It is notable that the synthesis of uric acid may be associated with the generation of reactive oxygen species if the enzyme xanthine oxidorectase is converted to the oxidase, as may occur in ischaemia. It has been suggested that uric acid may play a role in the pathogenesis of early-onset hypertension but evidence for this is limited. There is also very limited data to suggest that in some circumstances lowering uric acid can lower blood pressure. In the metabolic syndrome, the presence of elevated uric acid concentrations is closely associated with raised triglyceride levels, for reasons that have not been clearly defined. It remains to be seen whether uric acid could or should be considered a specific therapeutic target in cardiovascular disease and especially in hypertension and if so what should be the optimal pharmacological approach to lowering serum urate levels.

Humans↗
PubMed2001

Potassium citrate administration ameliorates tubulointerstitial lesions in rats with uric acid nephropathy.

Although controversial, chronic uric acid nephropathy is a tubulointerstitial disease capable of developing renal function loss. On the other hand, potassium citrate (KCi) administration has demonstrated to be effective in calcium as well as uric acid nephrolithiasis therapy. Therefore, the aim of the present study was to evaluate the possible benefit of KCi treatment in the prevention or amelioration of renal interstitial damage in uric acid nephropathy. Two-month-old male Sprague-Dawley rats were divided into 3 groups: G1 hyperuricemic (HU), G2 hyperuricemic + KCi (HU+KCi), and G3 KCi. G1 and G2 were fed on oxonic acid (inhibitor of rat liver uricase), and a uric acid supplement, during 4 weeks. G2 and G3 were given 2% KCi in drinking water, and G1 regular tap water and standard rat chow. At the end of the study, renal tissue was processed for light and electron microscopy and immunostaining by alpha-smooth muscle actin (SMA). Tubulointerstitial lesions and the amount of alpha-SMA immunostaining in renal tissue were evaluated by histomorphometric quantitation. Rats belonging to the hyperuricemic groups treated with KCi (G2) showed fewer tubulointerstitial lesions as follows: % tubular atrophy: 1.7 +/- 0.3 versus 7.2 +/- 1.2, p < 0.05; inflammatory cells infiltrate (number of cells/area): 0.6 +/- 0.1 versus 2.4 +/- 0.2, p < 0.01; % interstitial fibrosis (cortex): 3.3 +/- 0.3 versus 9.3 +/- 0.5, p < 0.05; % interstitial fibrosis (medulla): 5.2 +/- 0.3 versus 21.9 +/- 1.2, p < 0.01, lower albuminuria (32.8 +/- 11.2 mg/day versus 128.5 +/- 10.4, p < 0.01), higher creatinine clearance ( 1.36 +/- 0.02 ml/min versus 0.74 +/- 0.01, p < 0.01 ) and less percentage of alpha-SMA in renal tissue (1.8 +/- 0.1 versus 10.5 +/- 1.4, p < 0.05), when compared with the hyperuricemic group not treated with KCi (G1). These data suggest that KCi administration could provide a substantial benefit in the regard to tubulointerstitial lesion and progressive renal damage.

Animals↗
PubMed1981

Renal venous portal contribution to PAH and uric acid clearance in the chicken.

The contributions of the renal venous portal and the renal arterial circulations to the renal clearance of p-aminohippuric acid (PAH) and uric acid were determined in the unanesthetized chicken by the simultaneous use of the urinary clearance technique and the Sperber preparation. The [3H]PAH apparent tubular excretion fraction (ATEF) and the clearance of inulin (CIn) were used as indicators of the renal portal and renal arterial contributions, respectively, in a planar equation for total PAH clearance. This equation accurately reflects the renal clearance of PAH as well as the renal venous portal and renal arterial contributions to the total renal clearance of PAH. The equation suggests that under normal conditions approximately 50% of the renal clearance of PAH or uric acid comes from the renal venous portal circulation, with the remaining 50% coming from the arterial circulation. An inverse hyperbolic relationship between the filtration fraction (CIn/CPAH) and the [3H]PAH ATEF was found, demonstrating that the filtration fraction in the chicken decreases from a value of 18 to approximately 6% as the renal portal plasma flow increases from zero to a maximum value. Our equation for total clearance was also used with results of experiments on inhibition of uric acid excretory transport by L- and D-dopa and by probenecid to locate the probable sites of action of those inhibitors.

Aminohippuric Acids↗
PubMed1986

Successful management of uric acid nephrolithiasis with potassium citrate.

Eighteen patients with uric acid nephrolithiasis (six with uric acid stones alone and 12 with both uric acid and calcium stones) underwent long-term treatment (1 to 5.33 years, mean of 2.78 years) with potassium citrate (30 to 80 mEq/day, usually 60 mEq/day). Urinary pH increased from low (5.30 +/- 0.31 SD) to normal (6.19 to 6.46) during treatment. Urinary content of undissociated uric acid, which was high to begin with at 204 +/- 82 mg/day, decreased to the normal range (64 to 108 mg/day) following treatment. Urinary citrate rose from 503 +/- 225 mg/day to 852 to 998 mg/day. Urinary saturation of calcium oxalate significantly declined with potassium citrate treatment. New stone formation rate declined from 1.20 +/- 1.68 stones/year to 0.01 +/- 0.04 stones/year (P less than 0.001 by chi square). Remission was experienced in 94.4% of patients, and the group stone formation rate declined by 99.2%. Detailed case reports were obtained in five patients showing different responses between sodium alkali and potassium alkali treatment. All five patients had persistently low urinary pH (typically less than 5.5) and normouricosuria, and four had hyperuricemia. Before treatment, they had stones surgically removed or spontaneously passed, which were pure uric acid in composition. When sodium alkali was give (as bicarbonate or citrate, 60 to 118 mEq/day), new stone formation continued in four patients, and a radiolucent (uric acid) calculus become "calcified" in the remaining patient. The stone analysis disclosed calcium oxalate in five patients and calcium phosphate in three patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗