Uric Acid Precipitation Research Articles

Tumour lysis syndrome.

Tumour lysis syndrome (TLS) represents a critical oncological emergency characterized by extensive tumour cell breakdown, leading to the swift release of intracellular contents into the systemic circulation, outpacing homeostatic mechanisms. This process results in hyperuricaemia (a by-product of intracellular DNA release), hyperkalaemia, hyperphosphataemia, hypocalcaemia and the accumulation of xanthine. These electrolyte and metabolic imbalances pose a significant risk of acute kidney injury, cardiac arrhythmias, seizures, multiorgan failure and, rarely, death. While TLS can occur spontaneously, it usually arises shortly after the initiation of effective treatment, particularly in patients with a large cancer cell mass (defined as ≥500 g or ≥300 g/m2 of body surface area in children). To prevent TLS, close monitoring and hydration to improve renal perfusion and urine output and to minimize uric acid or calcium phosphate precipitation in renal tubules are essential. Intervention is based on the risk of a patient of having TLS and can include rasburicase and allopurinol. Xanthine, typically enzymatically converted to uric acid, can accumulate when xanthine oxidases, such as allopurinol, are administered during TLS management. Whether measurement of xanthine is clinically useful to optimize the use of allopurinol or rasburicase remains to be determined.

Sustainable Bioconversion of Glycerine Pitch into the Novel Wickerhamomyces anomalus Bio-preservative

Background: Yeasts with high protein content are used as single-cell proteins due to their nutritional values and rare pathogenicity. However, the nucleic acid of the yeasts must be removed before consumption to avoid hazards to health. Wickerhamomyces anomalus is an authorized bio-preservative with promising antifungal activity and safety. However, its high protein content associ-ated with high nucleic acid content results in high nitrogen content that imposes additional down-stream processing costs due to the nucleic acid removal step required to prevent uric acid precipitation which leads to various health concerns. Objectives: The objectives were to (i) isolate a novel Wickerhamomyces anomalus strain with low nitrogen content and (ii) to optimize the production of W. anomalus biomass through response surface methodology (RSM). Methods: The novel Wickerhamomyces sp. USMAST-TP1 with low nitrogen content was isolated from fermented food and its biomass was optimized through RSM. Results: Wickerhamomyces sp. USMAST-TP1 showed promising tolerance to glycerine pitch with a higher composition of growth-inhibiting impurities where its biomass was not negatively affected by excessive glycerine pitch supply. Upon optimization through RSM, 11.4 g/L biomass harboring pro-tein content of 13% was achieved. Conclusion: The >17-fold lower nitrogen content of 2% indicated low nucleic acid content compared to common W. anomalus strains, thus the costly nucleic acid purification steps can be excluded, easing applications in agro-food industries.

Tumor Lysis Syndrome.

Tumor lysis syndrome (TLS) is an oncologic emergency due to massive tumor cell lysis with the release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation. Clinical presentation is characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Acute kidney injury due to tumor lysis is potentiated by the precipitation of uric acid and calcium phosphate as well as renal vasoconstriction. Early recognition of tumor lysis can help prevent cardiac arrhythmias, seizures, and death. Management includes intravenous hydration to maintain urine flow, medications targeting hyperuricemia including rasburicase and allopurinol and in severe cases renal replacement therapy may be required.

A semi-mechanistic exposure\u2013response model to assess the effects of verinurad, a potent URAT1 inhibitor, on serum and urine uric acid in patients with hyperuricemia-associated diseases

Verinurad, a uric acid transporter 1 (URAT1) inhibitor, lowers serum uric acid by promoting its urinary excretion. Co-administration with a xanthine oxidase inhibitor (XOI) to simultaneously reduce uric acid production rate reduces the potential for renal tubular precipitation of uric acid, which can lead to acute kidney injury. The combination is currently in development for chronic kidney disease and heart failure. The aim of this work was to apply and extend a previously developed semi-mechanistic exposure–response model for uric acid kinetics to include between-subject variability to verinurad and its combinations with XOIs, and to provide predictions to support future treatment strategies. The model was developed using data from 12 clinical studies from a total of 434 individuals, including healthy volunteers, patients with hyperuricemia, and renally impaired subjects. The model described the data well, taking into account the impact of various patient characteristics such as renal function, baseline fractional excretion of uric acid, and race. The potencies (EC50s) of verinurad (reducing uric acid reuptake), febuxostat (reducing uric acid production), and oxypurinol (reducing uric acid production) were: 29, 128, and 13,030 ng/mL, respectively. For verinurad, symptomatic hyperuricemic (gout) subjects showed a higher EC50 compared with healthy volunteers (37 ng/mL versus 29 ng/mL); while no significant difference was found for asymptomatic hyperuricemic patients. Simulations based on the uric acid model were performed to assess dose–response of verinurad in combination with XOI, and to investigate the impact of covariates. The simulations demonstrated application of the model to support dose selection for verinurad.

SLC2A9 (GLUT9) mediates urate reabsorption in the mouse kidney

Uric acid (UA) is a metabolite of purine degradation and is involved in gout flairs and kidney stones formation. GLUT9 (SLC2A9) was previously shown to be a urate transporter in vitro. In vivo, humans carrying GLUT9 loss-of-function mutations have familial renal hypouricemia type 2, a condition characterized by hypouricemia, UA renal wasting associated with kidney stones, and an increased propensity to acute renal failure during strenuous exercise. Mice carrying a deletion of GLUT9 in the whole body are hyperuricemic and display a severe nephropathy due to intratubular uric acid precipitation. However, the precise role of GLUT9 in the kidney remains poorly characterized. We developed a mouse model in which GLUT9 was deleted specifically along the whole nephron in a tetracycline-inducible manner (subsequently called kidney-inducible KO or kiKO). The urate/creatinine ratio was increased as early as 4 days after induction of the KO and no GLUT9 protein was visible on kidney extracts. kiKO mice are morphologically identical to their wild-type littermates and had no spontaneous kidney stones. Twenty-four-hour urine collection revealed a major increase of urate urinary excretion rate and of the fractional excretion of urate, with no difference in urate concentration in the plasma. Polyuria was observed, but kiKO mice were still able to concentrate urine after water restriction. KiKO mice displayed lower blood pressure accompanied by an increased heart rate. Overall, these results indicate that GLUT9 is a crucial player in renal handling of urate in vivo and a putative target for uricosuric drugs.

Uric acid nephrolithiasis: An update.

Uric acid nephrolithiasis appears to increase in prevalence. While a relationship between uric acid stones and low urinary pH has been for long known, additional association with various metabolic conditions and pathophysiological basis has recently been elucidated. Some conditions such as diabetes and metabolic syndrome disease, excessive dietary intake, and increased endogenous uric acid production and/or defect in ammoniagenesis are associated with low urinary pH. In addition, the phenomenon of global warming could result in an increase in areas with greater climate risk for uric acid stone formation. There are three therapeutic steps to be taken for management of uric acid stones: identification of urinary pH profiles, assessment of urinary volume status, and identification of disorders leading to excessive uric acid production. However, the most important factor for uric acid stone formation is acid urinary pH, which is a prerequisite for uric acid precipitation. This article reviews recent insights into the pathophysiology of uric acid stones and their management.

Development of Electrochemical Sensor for Uric Acid Detection in Intestinal Closed Loop

Uric acid is a ulitimate metabolite of purine nucleotides in humans, because the uricase had been lost completely. So, the serum uric acid level is higher than other mammalians. The advantage of the higher serum uric acid levels has been suggested to be antioxidant activity of uric acid. On the other hand, hyperuricemia is an abnormally high level of uric acid in the serum that leads to uric acid precipitation in tissues and the main risk factors for the onset of gout, hypertension, chronic kidney disease, atherosclerosis, diabetes and so on. There are two important physiological mechanisms caused hyperuricemia: (a) increase production of the uric acid from dietary and endogenous substrates that raise purine levels and (b) reduced renal and extra-renal excretion of uric acid. It is commonly accepted that two thirds of the urate is excreted from the kidney into urine. The remaining one third is excreted via extra-renal excretion, mainly intestine. Recently, importance of the uric acid excretion from intestine has been gathering attention because the considerable inpact of urate transporter function in the intestine on the serum uric acid level has been revealed gradually. A novel concept in hyperuricemia was proposed as “extra renal underexcretion type”.[1] Intestinal closed loop method is one of the basic techniques to investigate the excretion of uric acid via trasporters in intestin. However, it needs troublesome procedure and time consuming process. If it is possible to detect the concentration of excreted uric acid with electrochemical sensor, dynamic analysis of urate excretion via the urate transporters will easily be available. In this study, we developed an electrode to detect uric acid sensitively. Gold beads electrode was prepared according to the literature.[2] 6-Ferrocenyl-1-hexanethiol which works as a mediator for the uric acid oxidation was used to make self -assenbled monolayers (SAMs) on gold surface. 6-Hydroxyl-1-hexananethiol, 5-Carboxyl-1-pentanethiol and 6-Amino-1-hexanethiol were also used to construct mixed SAMs. Gold beads electrodes were soaked in the ethanol solution containing these alkanethiols. The SAM-coated electrode was used as working electrode (C.E: Pt wire, R.E.: Ag/AgCl). Uric acid dissolved in phosphate buffer (pH 7.4) was added to the measurement system. Cyclic voltammograms were measeured in buffer by addition of uric acid (-0.2 to +0.5 V). Oxdation current based on the uric acid oxidation was observed with 6-Ferrocenyl-1-hexanethiol modified electrode at around +0.45 V. The oxidation current was increased with increasing of uric acid concentration. When the mixed SAMs-coated electrodes were examined, similar responses were observed regardress the component of SAMs. However, no response was observed from the SAM-coated electrode without 6-Ferrocenyl-1-hexanethiol. Responsible change was observed at oxidation current by 0.1 mg/mL change of uric acid. Furthermore, ammperometric measurement showed the step-like current change according to the added uric acid concentration.

Crystal arthritides - gout and calcium pyrophosphate arthritis : Part2: clinical features, diagnosis and differential diagnostics.

Gout develops in four stages beginning with an asymptomatic increase in blood levels of uric acid. An acute gout attack is an expression of an underlying inflammatory process, which in the course of time is self-limiting. Without therapy monosodium urate crystals remain in the synovial fluid and synovial membrane and trigger more acute attacks. In the course of the disease monosodium urate crystals form deposits (tophi) leading in severe forms to irreversible joint deformities with loss of functionality. In 20% of cases gout leads to involvement of the kidneys. Overproduction of uric acid can cause nephrolithiasis. These stones can be composed of uric acid or calcium phosphate. Another form of kidney disease caused by gout is uric acid nephropathy. This is aform of abacterial chronic inflammatory response with deposition of sodium urate crystals in the medullary interstitium. Acute obstructive nephropathy is relatively rare and characterized by renal failure due to uric acid precipitation in the tubules because of rapid cell lysis that occurs, for example, with chemotherapy. There is acausal interdependence between the occurrence of hyperuricemia and hypertension. Uric acid activates the renin-angiotensin-aldosterone (RAA) system and inhibits nitric oxide (NO) with the possible consequence of arise in systemic vascular resistance or arteriolar vasculopathy; however, uric acid is also an apparently independent risk factor for atherosclerosis. In contrast to young patients, the diagnosis of an acute gout attack in the elderly can be achallenge for the physician. Polyarticular manifestations and obscure symptoms can make it difficult to differentiate it from rheumatoid arthritis and calcium pyrophosphate deposition disease (CPPD). Aspiration of synovial fluid with visualization of urate crystals using compensated polarized light microscopy is the gold standard for diagnosis of acute gout. Moreover, analysis of synovial fluid enables a distinction from septic arthritis by Gram staining and bacterial culture. Soft tissue ultrasonography is useful to detect affected synovial tissue and monosodium urate crystals within the synovial fluid. Involvement of bone occurs relatively late in the disease so that x‑ray images are not useful in the early stages but might be helpful in differential diagnostics. Dual energy computed tomography (CT) and magnetic resonance imaging (MRI) can be used for certain indications.

A novel quantitative method for recovering precipitated uric acid in urine and analysis by LC-MS/MS.

Precipitation of uric acid (UA) in human urine had caused poor recovery and underestimation of UA in study samples. A UA recovery method was developed for analyzing frozen urine samples that potentially contain precipitated UA. Samples were treated with 3% v/v of a solution containing 8 M potassium hydroxide and 20% v/v of ammonium thioglycolate. The high pH enables rapid dissolution of UA crystals, while the thioglycolate protects UA from oxidation at high pH. The treated samples were diluted 20-fold with 50 mM ammonium chloride and analyzed immediately by LC-MS/MS or stored at -20°C prior to analysis. Complete recovery of UA was achieved. Thioglycolate stabilized UA at pH 13 for at least 4.5 h at room temperature. Both accuracy and precision satisfy US FDA bioanalytical method validation (BMV) guidelines.

An Open Label Efficacy Study of Amrita Guggulu and Pinda Taila in the Management of Hyperuricemia in Gout (Vatarakta) Patients

ABSTRACT Background Vatarakta vis-à-vis gout is a common condition in both primary care and specialist practice. Gout is a systemic disease characterized by manifestations of chronic under­lying hyperuricemia, resulting in the deposition of monosodium urate crystals in various tissues. Gout is the most common of the crystal induced arthritis due to disturbed uric acid metabolism and precipitation of urate crystals in extracellular space of joints, periarticular tissue, bones, and other organs. Aim and objective To explore the therapeutic efficacy and safety of Amrita Guggulu and Pinda Taila in the management of hyperuricemia in gout (Vatarakta) patients. Materials and methods A total of 100 cases (25–65 years) of primary gouty arthritis fulfilling the diagnostic criteria as recommended by the American College of Rheumatology were selected for the present study from outpatient department of the Central Ayurveda Research Institute for Respiratory Disorders Patiala and Regional Ayurveda Research Institute for Urinary Disorders, Jammu, India, irrespective of their sex, religion, and socioeconomic status. Only those patients who presented themselves with at least 6 of 12 criteria of American College of Rheumatology (1977) were selected for the clinical trial. Amrita Guggulu was given 1000 mg twice daily orally and Pinda Taila was applied locally 10 mL twice daily for 84 days. Results The trial therapy was assessed based on the improvement in clinical features, Visual Analog Scale (VAS) score, Patient's Global Assessment Scale score, Physician's Global Assessment Scale Score, SF-36 Health Survey Score for quality of life (QOL), and biochemical parameters. Each patient was subjected to routine blood test, serum uric acid, liver function tests, and renal function tests before treatment, after 28 days of treatment, and after 84 days of treatment. The trial combination showed statistically significant improvement in the clinical manifestations, QOL as well as reduction in marker of hyperuricemia, i.e., serum uric acid; the mean serum uric acid at the baseline was 7.76 mg/dL, which was reduced to 6.50 mg/dL after the trial period of 84 days. There was also decrease in the level of VAS score, Patient's Global Assessment Scale score, and Physician's Global Assessment Scale score. There were no impairment in liver function test and renal function test, indicating the good safety profile of trial therapy. Conclusion Hence, Amrita Guggulu and Pinda Taila drug combination is an effective and safe remedy for gouty arthritis (Vatarakta) patients. How to cite this article Singh H, Sannd R, Bhurke LW, Kumari K, Singh R, Vedi SK, Kumar A, Bharti, Rana R, Singhal R, Srikanth N, Padhi MM, Dhiman KS. An Open Label Efficacy Study of Amrita Guggulu and Pinda Taila in the Management of Hyperuricemia in Gout (Vatarakta) Patients. J Res Ayurvedic Sci 2017;1(1):25-33.

Risk and prevention strategies can help avert tumor lysis syndrome

Risk and prevention strategies can help avert tumor lysis syndrome

How neutrophil extracellular traps orchestrate the local immune response in gout.

Neutrophil granulocytes possess a large arsenal of pro-inflammatory substances and mechanisms that empower them to drive local acute immune reactions to invading microorganisms or endogenous inflammatory triggers. The use of this armory needs to be tightly controlled to avoid chronic inflammation and collateral tissue damage. In gout, inflammation arises from precipitation of uric acid in the form of needle-shaped monosodium urate crystals. Inflammasome activation by these crystals in local immune cells results in a rapid and dramatic recruitment of neutrophils. This neutrophil influx is accompanied by the infamously intense clinical symptoms of inflammation during an acute gout attack. Neutrophilic inflammation however is equipped with a built-in safeguard; activated neutrophils form neutrophil extracellular traps (NETs). At the very high neutrophil densities that occur at the site of inflammation, NETs build aggregates that densely pack the monosodium urate (MSU) crystals and trap and degrade pro-inflammatory mediators by inherent proteases. Local removal of cytokines and chemokines by aggregated NETs explains how acute inflammation can stop in the consistent presence of the inflammatory trigger. Aggregated NETs resemble early stages of the typical large MSU deposits that constitute the pathognomonic structures of gout, tophi. Although tophi contribute to muscosceletal damage and mortality in patients with chronic gout, they can therefore be considered as a payoff that is necessary to silence the intense inflammatory response during acute gout.

Elucidation of the etiology and characteristics of pink urine in young healthy subjects.

Pink urine syndrome (PUS) is attributed to the precipitation of uric acid caused by low urinary pH (U-pH). However, the reasons for the lower U-pH are unclear. To investigate the occurrence of PUS and verified the cause of U-pH reduction. Participants comprised 4,940 students who had undergone a physical examination. Data on the presence [PUS (+)] or absence [PUS (-)] of PUS, as well as age, gender, body mass index (BMI), blood pressure (BP), heart rate (HR), and U-pH were collected. Of these participants, 300 randomly selected individuals were evaluated for their waist circumference, as well as their levels of urinary C-peptide, angiotensinogen, methylglyoxal, thiobarbituric acid-reactive substances (TBARS), and Na(+) excretion. Independent risk factors of lower U-pH were decided by a multiple-regression analysis. PUS was observed in 216 students (4.4%). A greater number of men comprised the PUS (+) group compared with the PUS (-) group, and subjects in this group had high BMI, BP, and HR values, as well as low U-pH. A logistic regression analysis revealed that the BMI and U-pH were independent risk factors for PUS (+). The decrease of U-pH was closely related to the progress of chronic kidney disease (CKD). BMI value was related to PUS (+) in the CKD (-) subjects. On the other hand, low U-pH was related to PUS (+) in the CKD (+) subjects. All factors other than HR showed a significant negative correlation with U-pH. However, multiple-regression analysis revealed that TBARS and angiotensinogen were independent risk factors. Obesity and lower U-pH were each independently related to PUS, whereas increased intrarenal oxidative stress and exacerbation of the renin-angiotensin system activation were associated with the lowering of U-pH. U-pH low value is related to potential CKD.

Index of Suspicion

The reader is encouraged to write possible diagnoses for each case before turning to the discussion. We invite readers to contribute case presentations and discussions. Please inquire first by contacting Dr. Deepak Kamat at DKamat@med.wayne.edu. An 18-year-old male with a 3-year history of alcohol abuse is referred from a rehabilitation center for fever, nausea, and nonbloody diarrhea for 3 days. Six weeks ago, he enrolled in an alcohol rehabilitation program and stopped drinking alcohol. Three weeks later, he noticed yellowing of his eyes and skin, difficulty sleeping, and dyspnea. On examination, his temperature is 100.6°F (38.1°C), blood pressure is 99/62 mm Hg, pulse is 124 beats per minute, and respiratory rate is 24 breaths per minute. He is slow to answer questions. There is no asterixis. He appears thin and jaundiced with enlarged parotid glands. Decreased breath sounds are noted on the right. A tender, enlarged liver and mild abdominal distension are noted. Trace bilateral lower-extremity edema is present. No stigmata of chronic liver disease are found. Laboratory findings reveal the following: white blood cell count, 25,600/μL (25.6 × 109/L) (87% neutrophils); hemoglobin, 8.2 g/dL (82 g/L); mean corpuscular volume, 106 fL; platelets, 40 × 103/μL (40 × 109/L); sodium, 135 mEq/L (135 mmol/L); potassium, 3.5 mEq/L (3.5 mmol/L); chloride, 106 mEq/L (106 mmol/L); bicarbonate, 15 mEq/L (15 mmol/L); blood urea nitrogen, 24 mg/dL (8.6 mmol/L); creatinine, 1.01 mg/dL (89 μmol/L); glucose, 118 mg/dL (6.6 mmol/L); alkaline phosphatase, 182 U/L; aspartate aminotransferase (AST), 194 U/L; alanine aminotransferase (ALT), 71 U/L; total bilirubin, 11.8 mg/dL (201.8 μmol/L); direct bilirubin, 7.3 mg/dL (124.9 μmol/L); albumin, 2.7 g/dL (27 g/L); prothrombin time, 19.2 seconds; and international normalized ratio, 1.4. Ethanol and acetaminophen were not detected in the serum. A chest radiograph reveals a right pleural effusion …

Foudroyante Verlaufsform einer postoperativen Gicht nach Implantation einer Hüfttotalendoprothese – ein Fallbericht

The following report deals with the case of a post-surgical gout after total hip arthroplasty. Before surgery, the patient was diagnosed with hyperuricaemia. Following the procedure, the patient developed superinfected gout tophi and several joint infections. Multiple surgeries were necessary to control the illness and to finally heal the infection. This study stresses pre-surgical hyperuricaemia as a severe illness and demonstrates a positive medical history of gout as a risk for post-surgical precipitation of uric acid. We hope to increase the surgeon's awareness of post-surgical gout symptoms in order to ensure adequate patient care.

Epidemiology and clinical pathophysiology of uric acid kidney stones

There is global diversity in the prevalence of uric acid (UA) nephrolithiasis. UA nephrolithiasis comprises 8-10 % of all kidney stones in the United States. However, its prevalence is higher in patients with type 2 diabetes mellitus and those with obesity. Three significant urinary abnormalities have been described as the main etiologic factors for the development of UA nephrolithiasis; low urinary pH, hyperuricosuria and low urinary volume. However, an unduly acidic urine below the ionization constant of uric acid (pKa < 5.5) increases the urinary content of undissociated uric acid and thereby uric acid precipitation. Previous studies have shown the two major pathogenic mechanisms for unduly urinary pH are increased net acid excretion (NAE) and reduced renal ammonium (NH4 (+)), with a combination resulting in overly acidic urine. The impaired ammonium excretion has been demonstrated in a steady state in 24-hour urine and also following an oral ammonium chloride (NH4Cl) challenge to amplify ammoniogenic defects in this population. Similar abnormalities have been disclosed in normal populations and also in T2DM populations without kidney stones. To date, the underlying mechanism of increased acid production, source and nature of putative organic acid anions have not been fully elucidated. One plausible mechanism is the production of organic acid by intestinal and aerobic metabolism. This may occur in obese, diabetic and uric acid stone formers due to the differences in gut microflora.

Urine processing impacts uric acid level in HIV-infected adults

Urine specimens are valuable to investigate kidney disease and antiretroviral nephrotoxicity. We observed large rust-colored pellets in some urine specimens after overnight storage at 4°C. Testing of supernatant under varying conditions demonstrated that this phenomenon reflects supersaturation and precipitation of uric acid in samples with high uric acid concentration. Delays in processing, even with refrigeration, may decrease the sensitivity of urine uric acid testing, with implications for the evaluation of proximal tubulopathy related to tenofovir.

Virtual and In Vitro Bioassay Screening of Phytochemical Inhibitors from Flavonoids and Isoflavones Against Xanthine Oxidase and Cyclooxygenase‐2 for Gout Treatment

Synthetic drugs such as allopurinol and benzbromarone are commonly used to treat the complex pathogenesis of gout, a metabolic disease that results from an inflammation of the joints caused by precipitation of uric acid. We seek to discover novel phytochemicals that could treat gout, by targeting the xanthine oxidase and cyclooxygenase-2 enzymes. In this study, we report the screening of nine compounds of flavonoids from the ZINC and PubChem databases (containing 2092 flavonoids) using the IGEMDOCK software tool against the xanthine oxidase and cyclooxygenase-2 3D protein structures. Each compound was also evaluated by an in vitro bioassay testing the inhibition of xanthine oxidase and cyclooxygenase-2. Myricetin and luteolin were found to be the potential dual inhibitors of xanthine oxidase and cyclooxygenase-2 as demonstrated by IC(50): 62.7 and 3.29 μg/mL (xanthine oxidase)/70.8 and 16.38 μg/mL (cyclooxygenase-2), respectively. In addition, structure-activity relationships and other important factors of the flavonoids binding to the active site of xanthine oxidase and cyclooxygenase-2 were discussed, which is expected for further rational drug design.

Preliminary Study on Factors that Enhanced the Production of Uricase by Aspergillus Flavus

Urate oxidase or uricase is an enzyme that catalyses the oxidation of uric acid to allantoin and plays important rule in purine metabolism. The first important application discovered for uricase was in clinical biochemistry as diagnosis reagent for measurement of uric acid in blood. The precipitation of uric acid can leading to gout symptom. The main purpose of this research is to optimize the culture condition for maximum uricase production by Aspergillus flavus. The parameters studied were pH (ranged pH4 to pH8),the sucrose concentration (10g/l to 50 g/l) and the agitation rate(100 to 300 rpm). The Aspergillus flavus were inoculated in yeast extract with sucrose and incubated for 24 hours at 200 rpm and 30oC. The maximum enzyme activity obtained from the experiment is 0.03974 U/ml at pH 6, 200 rpm and 30 g/l sucrose concentration.

Metabolic syndrome and bariatric surgery in stone disease etiology

To review the prevalence and mechanisms of stone formation in patients with metabolic syndrome and in those submitted to bariatric surgery. MetS is associated with urinary stone disease, which appears to be sustained by dietetic factors and insulin resistance. The latter represented in obesity and diabetes favors uric acid precipitation in urine via a more acidic urinary load. Patients submitted to modern bariatric surgery are at risk of nephrolithiasis and nephropathy as a consequence of malabsorption and hyperoxaluria, which are more consistent after Roux-en-Y gastric bypass than after gastric banding. Other stone risk factors such as hypocitraturia may also be present. Patients with metabolic syndrome and those submitted to modern bariatric surgery are both at risk of nephrolithiasis and nephropathy. Accurate stone screening careful monitoring of renal function and diet counseling are strongly encouraged in these patients.