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[Uric acid and arterial hypertension. IV. Relation between serum uric acid level, the extent of vascular changes and heart enlargement in primary arterial hypertension].

In forty patients with essential hypertension correlation between serum uric acid and some clinical features of hypertensive disease i.e. severity and time of duration of arterial hypertension, the extent of vascular, retinal changes and left ventricular wall thickness was evaluated. Results showed that diastolic arterial pressure and the extent of retinal changes are significantly higher in hypertensive patients with concomitant hyperuricemia in comparison with normal uricemia patients with essential hypertension. Positive correlation was found between serum uric acid and diastolic as well as mean arterial pressure. Moreover, patients with essential hypertension and hyperuricemia demonstrated left ventricular hypertrophy in comparison with normal uricemia in hypertensive patients. Elevated serum uric acid in essential hypertension should be regarded as an early "harbinger" of disposition to the quick progress of vascular changes.

Adult↗

Lack of effect of warfarin on uric acid concentration.

Uric acid concentrations reportedly are increased in patients being treated with warfarin. We measured uric acid in 40 patients before and during warfarin administration. The mean pre- and post-warfarin uric acid concentrations for our patients were 0.39 mmol/L and 0.40 mmol/L, respectively, not a significant difference. Further observations of hyperuricemic patients started on warfarin are needed to prove that their risk of gout is not increased.

Adult↗

Urinary calculi associated with purine metabolism. Uric acid nephrolithiasis.

Uric acid stones are the consequences of abnormalities in purine metabolism, urate/uric acid renal handling, or excess dietary protein. Treatment is aimed at preventing additional formation by decreasing the degree of urate and uric acid supersaturation in urine, by altering diet, fluid intake, and the urine pH, and by blocking steps in uric acid production.

Adenine Phosphoribosyltransferase↗

Enhanced renal clearance of uric acid in hepatic cirrhosis.

Serum and urinary acid were measured in 10 patients with chronic hepatitis, in 22 patients with hepatic cirrhosis, and in 11 control subjects. Significant differences were found in urinary acid excretion, uric acid clearance, and uric acid:creatinine clearance ratio between patients with hepatic cirrhosis and control subjects. Two patients with hepatic cirrhosis were found to have hypouricemia. They showed a two- to threefold increase in uric acid clearance and in the uric acid:creatinine clearance ratio compared with control subjects, but their 24-h uric acid excretion was normal. In patients with hepatic cirrhosis, a significant negative correlation was found between plasma testosterone level and either uric acid clearance or uric acid:creatinine clearance ratio. These results indicate that uric acid clearance may be increased in patients with hepatic cirrhosis and that hypouricemia may result from a change in renal handling of uric acid. Moreover, changes in plasma testosterone levels may play an important part in affecting the renal handling of uric acid in these patients.

Adult↗

[The uric acid lowering effect of protein-rich diets. Behavior of human uric acid metabolism under reducing diet forms with varied protein content].

The effect of a 60 g protein diet was compared to a 120 g protein diet. Under nutrition with 60 g protein/day the uric acid clearance dropped from 6.3 +/- 2.2 ml/min to 4.9 +/- 1.6 ml/min. During application of 120 g protein/day uric acid clearance was not reduced. Therefore serum uric acid concentration dropped from 7.7 +/- 0.5 mg/dl to 6.4 +/- 0.5 mg/dl. The supply of 120 g protein/day has such a strong uricosuric action that the otherwise occurring inhibition of uric acid clearance during weight reduction can be balanced.

Diet, Reducing↗

[Physiology and biochemistry of uric acid].

In humans, uric acid is the final breakdown product of unwanted purine nucleotides. Uric acid is the last stage in purine degradation, because humans lack the enzyme uricase which converts uric acid into allantoin. Uric acid has profound beneficial effects since it scavenges potential harmful radicals in our body. However, in conjunction with genetic or environmental factors, uric acid can cause significant health problems, leading to kidney stones when it builds up in the kidneys and to gout when crystals accumulate in the joints. The levels of uric acid in the blood must be tightly controlled to minimize these detrimental effects. Normally, the body eliminates enough uric acid in the kidney, and in part also through the intestines, to keep its concentration at a healthy level in the blood (approximately 300 microM). In patients with gout or kidney stone disease, however, the body either produces excessive amounts of uric acid or its ability to eliminate uric acid is disturbed in some way. In the kidney, uric acid is reabsorbed via the uric acid transporter URAT1. This transporter is the major mechanism for regulating blood uric acid levels and therefore may prove an interesting target for future drug development.

Animals↗

Sex differences in the effect of uric acid on the survival of analbuminemic rats exposed to cold: effects of gonadal hormones and uric acid.

When female analbuminemic rats were injected with 0.8 mg uric acid every 3 h, their survival time at 5 degrees C increased from 14 h to 28 h, but uric acid had no effect on analbuminemic male rats. When female rats were oophorectomized 1 week before cold exposure, the injection of uric acid had no effect on their survival. Furthermore, uric acid did not increase the survival of the female rats that were administered a pellet containing 5 mg testosterone 1 week before the cold exposure. When the male rats were castrated 1 week before cold exposure, their survival time decreased from 20 h to 14 h, and administrations of 5 mg estradiol pellet at the time of castration and 0.8 mg uric acid every 3 h during cold exposure increased their survival time to 23 h.

Animals↗

The effects of amphetamine and pilocarpine on the release of ascorbic and uric acid in several rat brain areas.

Linear sweep voltammetry was used to investigate the effects of amphetamine (which enhances the release of dopamine) and/or pilocarpine (a cholinergic agonist) on the release of ascorbic acid and uric acid in brain areas differing in dopamine and acetylcholine concentrations. In caudate, nucleus accumbens, and hippocampus, the magnitude of the amphetamine-induced increase in ascorbic acid was roughly correlated with dopamine content of the brain area tested. Cingulate cortex was a notable exception; the increase in ascorbic acid was greater than that in nucleus accumbens. Pilocarpine produced the greatest increase in ascorbic acid in cingulate cortex, even though cingulate cortex has the lowest acetylcholine concentration of the brain areas tested. Except for cingulate cortex, the ascorbic acid data were consistent with the hypothesis that amphetamine and pilocarpine release different pools of ascorbic acid. The uric acid data were consistent with the hypothesis that amphetamine and pilocarpine release the same pool of uric acid. The unexpected findings in cingulate cortex may point to an important role of ascorbic acid in this brain area.

Amphetamine↗