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At least 19 recordsLinked to original sources

Transport of p-aminohippuric acid, uric acid and glucose in highly purified rabbit renal brush border membranes.

A procedure for preparing highly purified brush border membranes from rabbit kidney cortex using differential and density gradient centrifugation is described. Brush border membranes prepared by this procedure were substantially free of basal-lateral membranes, mitochondria, endoplasmic reticulum and nuclear material as evidenced by an enrichment factor of less than 0.3 for (Na+ + K+)-ATPase, succinate dehydrogenase, NADPH-cytochrome c reductase and DNA. Alkaline phosphatase was enriched ten fold indicating that the membranes were enriched at least 30 fold with respect to other cellular organelles. The yield of brush border membranes was 20%. Transport of D-glucose by the membranes was identical to that previously reported except that the Arrhenius plot for temperature dependence of transport was curvilinear (EA = 11.3--37.6 kcal/mol) rather than biphasic. Transport of p-aminohippuric acid and uric acid were increased by the presence of NaCl, either gradient or preequilibrated. However, no overshoot was obtained in the presence of a NaCl gradient, and KCl and LiCl also produced equivalent stimulation of transport suggesting a nonspecific ionic strength effect. Uptakes of p-aminohippuric acid and uric acid were not saturable, and were increased markedly by reducing the pH from 7.5 to 5.6. Probenecid (1 mM) reduced p-aminohippuric acid and uric acid (50 muM) uptake by 49% and 21%, respectively. We conclude that the uptake of uric acid and p-aminohippuric acid by renal brush border membranes of the rabbit occurs primarily by a simple solubility-diffusion mechanism.

Aminohippuric Acids

Effect of sulphinpyrazone (Anturan) on uric acid excretion and plasma uric acid concentration in healthy volunteers.

Investigations in six healthy volunteers given single oral doses of sulphinpyrazone (Anturan) showed that the drug had a potent uricosuric effect, even if the concentration of uric acid in the plasma was normal. In the dose range tested of 50 to 800 mg the increase in uric acid excretion was dose-related. It reached a maximum within 2 h and was still detectable 6--8 h after the drug was taken. There was a corresponding dose-related reduction in the plasma concentration of uric acid, which reached its lowest level after 8--10 h. The administration of 300 mg twice daily for four days to a further five healthy volunteers reduced plasma uric acid from 5.06 to 1.8 mg%. The findings indicate that, even if plasma uric acid levels are unknown, it would be advisable to avoid the risk of formation of urinary calculi by administering sulphinpyrazone in gradually increasing doses, ensuring adequate fluid intake and alkalinizing the urine during the first few days of treatment.

Humans

Interaction of uricine with uric acid and its effect on uric acid precipitation.

Uricine is a yellow-red pigment isolated from uric acid stones where it is always found. It binds to the uric acid, as shown by gel chromatography, at constant uric acid elution. It also increases the capacity of the uric acid to form larger aggregates and therefore the capacity of the uric acid to precipitate is enhanced. The uric acid-uricine aggregates may be separated by high speed sucrose centrifugation gradients.

Binding Sites

Serotonin, folic acid, and uric acid metabolism in the diagnosis of neuropsychiatric disorders.

Metabolic compensation appears possible within the serotonergic, folate, purine system and it seems possible that clinical illness may result when the system can no longer compensate. For example, elevated serotonin, induced by stress accumulation of tryptophan, could be compensated by a lowered folate ratio, normalizing the beta-carboline index and preventing hallucinations. Conversely, deficient serotonin, induced by a psychological loss or transport deficit, could be compensated by raising the folate ratio, which would normalize the beta-carboline index and prevent further depression. Increased purine turnover would seemingly lower the folate ratio, compensating perhaps for hallucinatory activity or mania. Several genetic defects of enzymes or transport proteins could seemingly preclude normal compensations within the system.

Adolescent

Transfer and dynamics of uric acid in the pregnant rhesus monkey. I. Transplacental and renal uric acid clearances.

Data from the literature suggest that uric acid produced by the fetus could pass across the placenta and contribute to the observed increase in maternal plasma levels of uric acid in preeclamptic pregnancy. To investigate this hypothesis, fetal transplacental and renal uric acid clearances were estimated in 4 term pregnant rhesus monkeys by means of the steady infusion method using 14C-labeled uric acid. Allantoin clearances were determined in one pregnant monkey. Samples of maternal and fetal arterial blood were collected at regular intervals. The total amount of fetal urine produced during the experiment was collected at the end of the experiment. In addition, maternal endogenous renal uric acid and creatinine clearances were measured in 6 term pregnant monkeys. Fetal transplacental uric acid clearances appeared to be almost entirely limited by placental permeability and varied between 3.6 and 8.6 ml X min-1 X kg-1 of fetal weight; fetal renal clearances were between 0.11 and 0.20 ml X min-1 X kg-1. The allantoin clearances were found to be of the same magnitude. Maternal renal clearances of uric acid and creatinine were almost equal (mean 3.2 +/- 0.6 and 3.0 +/- 0.5 ml X min-1 X kg-1 of maternal weight, respectively). Extrapolation of these data to human preeclamptic pregnancy reveals that it is unlikely that fetal uric acid could significantly contribute to the maternal uric acid load.

Animals

A rapid method for the diagnosis of acute uric acid nephropathy.

Acute uric acid nephropathy is a reversible type of renal failure that results from the deposition of uric acid crystals in the collecting tubules. The present study has compared a number of laboratory tests in 5 patients with a clinical diagnosis of this disorder and 27 patients with acute renal failure of other causes. Neither the serum creatinine, BUN, serum urate concentrations, nor the ratio of serum urate:BUN differentiated between these two groups of patients. However, the ratio of uric acid to creatinine concentration on a random urine specimen did differentiate between these two patient populations. All patients with uric acid nephropathy had a ratio greater than 1.0, while all patients with other types of acute renal failure had ratios of less than 1.0.

Acute Kidney Injury

[Diagnostic value of the CSF uric acid level (author's transl)].

Uric acid is the end-product of purine metabolism, and purines are the nitrogenous bases derived from the breakdown of nucleic acids. The CSF uric acid level is thought to be the index of the turnover of the nucleic acid and the degree of the cellular destruction in the brain. CSF uric acid levels were investigated in normal controls (30 cases) and in patients with brain tumor (20 cases), microcephalus (8 cases) and craniostenosis (4 cases). The mean values and standard deviations of CSF uric acid levels in normal controls were as follows; Newborn--9 yrs 0.34 +/- 0.09 mg/dl; 10 yrs--19 yrs 0.50 +/- 0.18 mg/dl; 20 yrs--29 yrs 0.46 +/- 0.05 mg/dl; 30 yrs--39 yrs 0.35 +/- 0.10 mg/dl; 40 yrs--49 yrs 0.35 +/- 0.23 mg/dl. Thereafter 0.72 +/- 0.21 mg/dl. The increased CSF uric acid levels after the age of 50 is thought to be due to the cellular destruction in the brain. CSF uric acid levels increased in patients with highly malignant brain tumor such as grade 3 or 4 astrocytoma and sarcomatous meningioma, but were normal in patients with grade 2 astrocytoma and meningiomas of meingothelial or fibroblastic type. CSF uric acid levels decreased in patients with microcephalus, but were almost normal in patients with craniostenosis. There is a significant correlation between CSF uric acid levels and the degree of brain atrophy in infants.

Adolescent

Quantitation of renal uric acid synthesis in the chicken.

The contribution of uric acid synthesized in the kidney (nephrogenic uric acid) to the total uric acid excreted in the urine was studied in the chicken by use of the isotope-dilution technique. In the non-fasted chicken the urine-to-plasma specific activity ratio (SAR) of [14C]uric acid was 0.83, suggesting that a minimum of 17% of the uric acid excreted in the urine is synthesized in the kidney. During allopurinol infusion into the renal portal circulation of one kidney the SAR increased to 0.99, indicating that the renal synthesis of uric acid was almost completely inhibited and that the SAR is a valid indicator of the contribution of nephrogenic uric acid excreted into the urine without first entering the circulation. Chickens fasted for 18 h showed a lower rate of renal synthesis of uric acid. Hypoxanthine infusion into the systemic circulation increased the rate of renal synthesis of uric acid in both fasted and nonfasted chickens, suggesting that circulating precursor levels may in part regulate the renal synthesis of uric acid.

Animals

Serum uric acid in Jordanian Arabs.

Serum uric acid was measured in 96 male and 140 female healthy Jordanian Arabs. Values obtained for serum uric acid were slightly higher than those previously reported by workers from other parts of Arabia, but comparable to those reported from the United States and United Kingdom. The frequency histograms for serum uric acid in both males and females do not appear to be normally distributed. A hint of bimodality is evident in both sets of data, being more evident in males than in females. A significant positive correlation was seen when, uric acid was compared with ponderal index (P less than 0.05) and total body surface area in both males and females (P less than 0.001). No significant correlation was observed when, uric acid was compared with either age, height or body weight in both sexes.

Adolescent

Increased serum concentrations of lactic, pyruvic and uric acid and bilibubin after postoperative xylitol infusion.

Xylitol has been suggested as a more advantageous calory source for intravenous administration than glucose in certain clinical situation, but the general suitability of intravenous xylitol infusion has not been confirmed. Thirty-middle-aged women were infused with 100 g of xylitol as postoperative fluid therapy after gynaecological laparotomy and general anaesthesia. Another 10 women received 50 g of glucose in a similar manner and served as a reference group. Infusion of xylitol both at the rate of 0.25 g/kg/h (1000 ml 10% xylitol in approx. 8 h) and 0.5 g/kg/h (1000 ml 10% xylitol in approx. 4 h) caused a distinct increase in the serum concentrations of lactic acid, pyruvic acid, and uric acid; such an increase was not seen with glucose infusion. The faster infusion of xylitol also distinctly increased serum bilirubin concentrations. Because of the possibility of lactic acidosis and urate deposits in kidneys, infusion of 100 g or more of xylitol at a rate of 0.25 g/kg/h or faster is not safe for postoperative fluid therapy in routine clinical work.

Anesthesia, General