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PubMed2001

Spot urine uric acid to creatinine ratio used in the estimation of uric acid excretion in primary gout.

OBJECTIVE: Uric acid overexcretion in patients with gout is frequently assessed by the measurement of 24 hour urinary uric acid excretion, which is cumbersome with ambulatory patients, and requires accurate timing and complete collection of the specimen. We assessed whether uric acid to creatinine ratio (Uua/Ucr) in spot urine is useful for the estimation of uric acid overexcretion in patients with gout. METHODS: One hundred thirty male patients with gout and 33 non-gout male control subjects were studied. Early morning urine and/or a portion of 24 h collected urine (24 h urine) were used as spot urine samples. Uric acid overexcreters were defined as those with a 24 h urinary uric acid excretion > or = 1000 mg/day, while uric acid underexcreters were defined as those with uric acid clearance < 6 ml/min. RESULTS: There was a significant relationship between 24 h urinary uric acid excretion and early morning urine Uua/Ucr in patients with gout, while no such relationship was observed in controls. No significant difference in Uua/Ucr was observed between patients with gout and controls, or in Uua/Ucr between gout uric acid overexcreters and underexcreters in early morning urine. A significant difference in this value was observed between the 2 groups in the 24 h urine specimens. Although the diagnostic accuracy of gout uric acid overexcretion was 87.2% using early morning urine and 89.6% using 24 h urine, the sensitivity of gout uric acid overexcretion was only 25.0% when using early morning urine and 25.0% when using 24 h urine, when the cutoff value of Uua/Ucr was 0.63 and 0.64, respectively. CONCLUSION: Uua/Ucr using spot urine, especially early morning urine, is not an accurate indicator of uric acid overexcretion in patients with gout.

Chemistry, Clinical↗
PubMed1994

The importance of uric acid examination.

Uric acid is the end product of purine metabolism in man. The findings of human pathological levels of uric acid in serum and urine have in most patients serious clinical implications. This paper summarizes aspects of uric acid examination in clinical biochemistry laboratory. The clinical consequences of pathological levels of uric acid are shown. Uric acid is a useful diagnostic tool as screening for most of purine metabolic disorders. The importance of uric acid measurement in plasma and urine with respect of metabolic disorders is highlighted. Not only gout and renal stones are indications to send blood to the laboratory for uric acid examination. Also familial nephritis, neurological abnormalities with mental retardation are reasons to know uric acid levels in blood and urine. The results underline the importance of urinary uric acid investigation, which is often quite overlooked, and is helpful in differential diagnosis of gout. This work is dedicated to Professor Jan Horbaczewsky and his 110th anniversary of the opening of lessons in medical chemistry at the Czech medical faculty of Charles University in Prague.

Female↗
PubMed1996

Uric acid stones.

Uric acid is the end product of purine degradation in humans. It is a weak acid with a pK of 5.35 in urine. In acidic urine the undissociated form of uric acid predominates and is poorly soluble, leading to crystalluria and stone formation. Uric acid stones account for 5% to 10% of all stones in the United States. Acidic urine, hyperuricosuria, and low urine volume are the risk factors for uric acid stone formation. Uric acid stones may be idiopathic or secondary to a systemic disease such as gout. Treatment includes alkalinization of the urine, high fluid intake, and reduction of uric acid excretion if it is abnormal.

Gout↗
PubMed2002

High-dose methylprednisolone therapy in multiple sclerosis increases serum uric acid levels.

Uric acid, which is the final product of purine nucleoside metabolism, is a strong peroxynitrite scavenger. Several studies report on lower serum uric acid levels in multiple sclerosis. In this study, we investigated serum uric acid levels before and after high-dose methylprednisolone treatment (intravenous 1 g/day/5 days) in multiple sclerosis patients. Blood samples from 25 definite multiple sclerosis patients (11 male and 14 female) before and after methylprednisolone treatment (days 0, 6 and 30) and from 20 healthy donors (9 male and 11 female) were analyzed. Serum uric acid levels were measured using a quantitative enzymatic assay (Elitech diagnostics, Sees, France) according to the manufacturer's protocol, and the results were standardized using a commercial uric acid standard solution. We observed significantly increased serum uric acid levels 1 day after the termination of the therapy (day 6). These differences were sustained for 30 days after starting treatment (during remission period). Mean serum uric acid levels were significantly higher in the control group. These results suggest that increasing the uric acid concentration may represent one of the possible mechanisms of action of methylprednisolone in multiple sclerosis.

Adult↗
PubMed1987

Interference of the chemotherapeutic agent etoposide with the direct phosphotungstic acid method for uric acid.

A 62-year-old woman receiving chemotherapy with etoposide showed discrepant uric acid values as measured by a direct phosphotungstic acid (PTA) method (150 mg/L) compared with a uricase technique (40 mg/L). After ultrafiltration, the positive interference for the direct PTA method was retained in the protein fraction, but not in the filtrate. Adding exogenous etoposide to drug-free serum confirmed this interference for the direct PTA method, but not for the uricase procedure or a PTA technique preceded by dialysis. Decisions for aggressive patient management are often based on the magnitude of hyperuricemia. We do not recommend that the direct phosphotungstic acid method be used to measure uric acid in patients receiving etoposide.

Etoposide↗
PubMed2004

[Diagnosis and prevention of uric acid stones].

Uric acid stones occur in 10% of all kidney stones and are the second most-common cause of urinary stones after calcium oxalate and calcium phosphate calculi. The most important risk factor for uric acid crystallization and stone formation is a low urine pH (below 5.5) rather than an increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrhea or severe dehydration. Uric acid stone disease can be prevented and these are one of the few urinary tract stones that can be dissolved successfully. The treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml daily), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary alkalization with potassium citrate or sodium bicarbonate is a highly effective treatment, resulting in dissolution of existing stones. Urinary uric acid excretion can be reduced by a low-purine diet. Potassium citrate is the treatment of choice for the prevention of recurrence of uric acid calculi. Allopurinol reduces the frequency of stone formation in hyperuricosuric patients with recurrent uric acid stones and/or gout.

Adult↗
PubMed1990

Acute uric acid nephropathy in two gouty patients with moderate hyperuricemia and high urine acidity.

Acute uric acid nephropathy has been described almost uniformly in patients with massive uric acid overload (malignancies with rapid cell destruction, epileptic seizures). Severe hyperuricosuria and intratubular uric acid precipitation result. Here we present two patients with gout, normal uric acid production, and moderate hyperuricemia, both of whom developed acute uric acid nephropathy. Because of pronounced urine acidity (pH values of 4.6 and 5.0 in morning fasting urines), supersaturation with respect to undissociated uric acid exceeded solubility (0.54 mmol/l), despite basal urate secretions of less than 2.2 mmol/24 hours. Additional predisposing factors, such as uricosuric treatment, heavy beer-drinking, over-consumption of purine-rich foods, and hot environment, were superimposed in both cases.

Acute Kidney Injury↗
PubMed1993

[Value of oxypurines and uric acid in plasma, renal excretion of oxypurines and uric acid as well as plasma adenosine deaminase and AMP deaminase activity in patients with essential hypertension].

Serum uric acid and oxypurines (hypoxanthine and xanthine) renal excretion of uric acid and oxypurines as well as plasma adenosine deaminase activity and AMP deaminase activity were studied in 18 patients with essential hypertension and in 17 healthy subjects. The aim of the study was to evaluate uric acid production rate in essential hypertension. Serum uric acid was significantly higher (7.04 +/- 2.03 mg% = 370.5 +/- 106 mumol/l; p < 0.01) in essential hypertension in comparison with control group (5.2 +/- 1.0 mg% = 275.0 +/- 51.9 mumol/l) and plasma oxypurines were increased insignificantly. Impairment of fractional excretion of uric acid (p < 0.05) was found in patients with essential hypertension. Plasma adenosine deaminase activity and plasma AMP deaminase activity did not differ in the studied groups. Increased production of uric acid does not contribute the incidence of hyperuricemia in essential hypertension. The results suggest that tubular defect of oxypurines excretion similar to that of uric acid exists in patients with essential hypertension.

AMP Deaminase↗
PubMedDate not supplied

Application of intensified (+) Qi Gong energy, (-) electrical field, (S) magnetic field, electrical pulses (1-2 pulses/sec), strong Shiatsu massage or acupuncture on the accurate organ representation areas of the hands to improve circulation and enhance drug uptake in pathological organs: clinical applications with special emphasis on the "Chlamydia-(Lyme)-uric acid syndrome" and "Chlamydia-(cytomegalovirus)-uric acid syndrome".

Various methods of improving circulation and enhancing drug uptake which were used in treating some intractable medical problems caused by infections, and two syndromes based on the co-existence of Chlamydia trachomatis infection (mixed with either Lyme Borrelia burgdorferi or Cytomegalovirus) with increased Uric acid are described. The principal author's previous studies have indicated that there are two opposite types of Qi Gong energy, positive (+) and negative (-). Positive (+) Qi Gong energy has been used clinically to enhance circulation and drug uptake in diseased areas where there is a micro-circulatory disturbance and drug uptake is markedly diminished. (-) Qi Gong energy has completely the opposite effect and therefore has not been used although there may be some as yet undiscovered application. Since the late 1980's the principal author has succeeded in storing (+) Qi Gong energy on a variety of substances including small sheets of paper, and recently has been able to intensify this energy by concentrating it as it passes through a cone-shaped, tapered glass or plastic object placed directly on the (+) Qi Gong energy stored paper. Application of (+) Qi Gong energy stored paper on the cardio-vascular representation area of the medulla oblongata at the occipital area of the skull often improved circulation and enhanced drug uptake. If the drug-uptake enhancement was still not sufficient for the drug to reach therapeutic levels in the diseased organ, direct application of (+) Qi Gong from the practitioner's hand often enhanced the drug uptake more significantly. However, this direct method often results in the practitioner developing intestinal micro-hemorrhage within 24 hours which may or may not be noticed as mild intestinal discomfort with soft, slightly tarry stool. For intensifying (+) Qi Gong energy one of the most efficient shapes is a cone with increased intensification occurring at an optimal height. However when the total mass and the total distance from base to peak is increased beyond an optimal limit, the power decreases. Clinical application of Intensified (+) Qi Gong stored energy was evaluated in this preliminary study which indicated that intensified (+) Qi Gong energy application on the heart representation area of the middle finger on the hands markedly improved circulation in the corresponding organ, and increased drug uptake and acetylcholine even more effectively than some of the previously used drug enhancement methods (Shiatsu massage of the organ representation areas and/or application of (+) Qi Gong energy stored paper to the occipital area above the cardiovascular representation area of the medulla oblongata).(ABSTRACT TRUNCATED AT 400 WORDS)

Acupuncture Therapy↗
PubMed1989

Solubility of uric acid and supersaturation of monosodium urate: why is uric acid so highly soluble in urine?

The solubility of uric acid and the stability of supersaturation of monosodium urate (NaU) were studied in buffer solutions containing 150 mM sodium in the physiological urinary pH range at 37C. The solubility of uric acid increased with the rise in pH, and the total dissolved urate (undissociated uric acid + urate anion) concentration did not change during seven-day incubation in the pH range below 6.6. In this pH range, the calculated concentration of undissociated uric acid was constant (about six mg./dl.). Consequently, the increasing solubility of uric acid with the rise in pH depended solely on the increase of urate anion. As much as 220 mg./dl. of uric acid could be dissolved for 24 hours at pH 7.0. But following seven-day incubation the total dissolved urate concentration decreased to 16 mg./dl. due to NaU crystallization. The stability of NaU supersaturation depended not only on the concentration of sodium and urate anion but also on time and pH. When monopotassium urate crystals were incubated for seven days, the total dissolved urate concentration decreased according to NaU crystallization; the higher the pH, the more marked the decrease. However, at least some 80 mg./dl. of total dissolved urate was stable up to pH 8.2 within 24 hours. These findings can well explain why NaU crystals are seldom formed in the normal urine. Urinary stasis and/or pathological high urinary pH may cause NaU crystallization.

Buffers↗
PubMed1992

Management of uric acid stone.

Uric acid stones are the most readily dissolvable of all types of urinary stones. By maintaining urinary pH between 6.2-6.8 with the use of sodium acid citrate or uralyt-U and reducing serum uric acid by allopurinol, we tried to dissolve 107 stones in 67 patients. Ninety three (86.9%) stones were dissolved and 6 (5.6%) passed spontaneously within a period of one year. Eight (7.5%) stones were removed surgically or with ESWL. Five (7.5%) patients had stone recurrence over a period of 3 years follow-up. Serum uric acid was raised in 19 (28.5%) and urinary uric acid in 12 (18%) patients while urinary pH was low in 46 (69%) patients. For uncomplicated uric acid stones oral chemolysis on an out-patient basis is the treatment of choice. It is simple, safe and inexpensive. However, it requires rigid compliance by the patient and strict follow-up by ultrasonography (JPMA 42: 153, 1992).

Adolescent↗
PubMed1987

Pharmacologic treatment of uric acid calculi.

Uric acid stone disease is dependent on three pathogenetic factors: acid urine pH, low urine volume, and hyperuricosuria. The management of nonobstructing uric acid calculi should include maintenance of an alkaline urine, an increase in urine volume, and reduction in urinary uric acid excretion. It appears that potassium alkali may avoid the complication of calcium stone formation in patients with uric acid stones. In patients with obstructing uric acid calculi, more rapid dissolution may be accomplished with intravenous alkalinization or direct irrigation of the stone with an alkaline solution.

Allopurinol↗
PubMed1978

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↗