Uric Acid Excretion Research Articles

Correlation of Serum Uric Acid and Urine Uric Acid in Patients with Type 2 Diabetes Mellitus and Hypertension

Aims and objectives: To estimate the proportion of Hyperuricemia in patients with type 2 Diabetes Mellitus and Hypertension patients and to assess the correlation of serum uric acid and urine uric acid. To assess the relationship between Urine Uric acid/ Creatinine ratio and subclinical Renal damage among these patients. Materials and methodology: This cross-sectional study was conducted in Sri Manakula Vinayagar Medical College and Hospital Puducherry during a period of 6 months. Adults more than or equal to 18 years of age with Type 2 Diabetes Mellitus and Hypertension were included and a total of 56 patients were recruited. Patients were randomly included based on the inclusion and exclusion criteria Results: Patients with Subclinical Renal damage were categorized and constitutes around 53.7%. Odds ratios on comparing the duration of Diabetes and Hypertension, shows inverse correlation with eGFR of both SRD and non-SRD patients (0.469,0.449 respectively) and with Urine Uric acid/ Creatinine ratio was found to have positive correlation (0.108 and 0.085). On comparing eGFR and Urine Uric acid/ Creatinine ratio of SRD and non-SRD patients, it showed positive correlation with value of 0.336. Conclusion: Lower eGFR was associated with higher levels of Serum Uric Acid and Fractional excretion of uric acid (FEUA), but lower uUA/Cr levels. Thus this study suggests that urinary Uric Acid excretion was significantly associated with the risk of Subclinical Renal Damage and Urinary Uric acid can be used as a simple, noninvasive marker for early detection of decreased renal function in otherwise healthy subjects. Keywords: Subclinical Renal Damage, Urinary Uric Acid, Fractional Excretion of Uric Acid

Research Progress on the Relationship between Dietary Patterns and Hyperuricemia.

As the final metabolite of purine metabolism, uric acid is critically associated with human health. The serum uric acid level is regulated by diet and the metabolic capacity of the human body. The impaired control of uric acid metabolism and excretion is associated with the increased level of serum uric acid, which ultimately results in hyperuricemia. Hyperuricemia is the “fourth-highest” after hypertension, hyperglycemia, and hyperlipidemia. With progress made in the relationship between diet and hyperuricemia, different dietary patterns and lifestyles have been discussed, such as exercise, the amount intake of meat, seafood, supplements with omega-3 fatty acids, sugar-sweetened soft drinks and energy drinks, and lower-fat-containing foods as well as drinking beer, wine, and spirits in the present article. This study demonstrated that a lower risk of hyperuricemia is substantially correlated with higher baseline adherence to MeDiet, and plant polyphenols can combat hyperuricemia by blocking xanthine oxidase.

Valproic-induced Fanconi syndrome: Clinical features, risk factors, diagnosis and management.

ObjectiveAlthough Fanconi syndrome (FS) induced by valproate (VPA) has occasionally been reported, the detailed clinical features of the disease remain unclear. The aim of this study was to elucidate the clinical features of patients with VPA-induced FS.MethodsWe searched Chinese and English databases for all original studies, clinical reports, and case reports on VPA-induced FS published before March 2022.ResultsA total of 29 articles including 54 patients (28 males and 24 females) were included. The patients had a median age of 7 years (range 2–34 years), had severely disabled (87.0%), tube feeding (64.8%), and received an average of 1.8 medications other than VPA. The median duration of VPA treatment was 4 years (range 0.7–15.5). Pathological fractures (25.9%), unexplained fever (11.1%), muscle weakness (9.3%), and edema (9.3%) were the most common symptoms, while 18 patients were diagnosed in incidental laboratory tests. Blood tests revealed hypokalemia (69.2%), hypophosphatemia (98.0%), and hypouricemia (93.3%). Urinalysis revealed glucosuria (96.1%), proteinuria (100.0%), generalized hyperaminoaciduria (100.0 %), β2 macroglobulin (100.0%). Decreased percent total reabsorption of phosphate (%TRP) found in 94.1% of patients, and increased fractional excretion of uric acid (FEUA) were found in 100% of patients. The median time to resolution of FS after discontinuation of drug therapy was 3 months (range 0.25–18).ConclusionsThe possibility of FS needs to be considered with long-term VPA administration, especially in young, tube-fed, severely disabled patients who are co-administered with anticonvulsants. Patients receiving VPA should have regular blood and urine tests. Abnormal laboratory values returned to normal levels after VPA discontinuation.

Early switching of tenofovir disoproxil fumarate (TDF) in HIV-infected patients with TDF-induced nephrotoxicity: a prospective study

Background: Tenofovir disoproxil fumarate (TDF) can induce proximal renal tubulopathy (PRT) and necessitate changes in treatment regimen. This prospective study aimed to compare tubular function recovery following early switching versus late switching of TDF in human immunodeficiency virus (HIV)-infected patients with TDF-induced PRT. Methods: For this prospective study, conducted during 2017–2019, we enrolled HIV-1-infected, virologically suppressed adults undergoing TDF-containing combination antiretroviral therapy. Patients were separated into a late-switching group (LSG) and an early-switching group (ESG). The LSG included patients having an estimated glomerular filtration rate (eGFR) decrease ≥25% from the pretreatment level or Fanconi syndrome. The ESG included patients having ≥2 of the following indicators of PRT: fractional excretion of phosphate (FEUP) ≥10%, low tubular maximum reabsorption of phosphate (TmP)/GFR, or uricosuria; fractional uric acid excretion ≥10%; urine protein–creatinine index (UPCI) ≥500 mg/g creatinine, normoglycemic glycosuria, or decrease in eGFR of 15%–24%. Recovery of proximal tubular function at 6 and 12 months after TDF discontinuation was assessed. Complete recovery was defined as normalization of all abnormal tubular markers. Results: Thirty-three HIV-infected patients were enrolled (70% male). Except for tubular function markers, baseline characteristics were not significantly different between the two groups. The proportion of patients having complete recovery was significantly higher in the ESG (p = 0.007, log-rank test). FEUP improved significantly in the ESG after TDF discontinuation; improvements of eGFR and UPCI were greater in the LSG. An eGFR change of 10% from baseline was the only independent predictor of failure to achieve complete recovery after switching. After median follow-up of 2.25 years post-trial, sustained recovery of eGFR within 5% of pre-TDF eGFR was achieved only in the ESG. Conclusions: Early-switching of TDF in HIV patients with PRT may allow complete recovery of proximal renal tubular function.

The association of urinary prostaglandins with uric acid in hyperuricemia patients

PurposeTo explore the association between uric acid and urinary prostaglandins in male patients with hyperuricemia.MethodsA total of 38 male patients with hyperuricemia in outpatients of Huadong Hospital from July 2018 to January 2020 were recruited. Serum uric acid (SUA), 24 h urinary uric acid excretion and other indicators were detected respectively. 10 ml urine was taken to determine prostaglandin prostaglandin D (PGD), prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), 6-keto-PGF1α, thromboxane A2 (TXA2) and thromboxane B2 (TXB2). Fraction of uric acid excretion (FEua) and uric acid clearance rate (Cua) were calculated. According to the mean value of FEua and Cua, patients were divided into two groups, respectively. The independent-samples t test and the Mann–Whitney U test were applied for normally and non-normally distributed data, respectively.ResultsAfter adjusting confounding factors (age, BMI, eGFR, TG, TC, HDL and LDL), SUA was negatively correlated with urinary PGE1(r = -0.615, P = 0.009) and PGE2(r = -0.824, P < 0.001). Compared with SUA1 group (SUA < 482.6 mg/dl), SUA2 (SUA ge 482.6 mg/dl) had lower urinary PGE1(P = 0.022) and PGE2(P = 0.019) levels. Cua was positively correlated with PGE2 (r = 0.436, P = 0.01). The correlation persisted after adjustment for age, BMI, eGFR, TG, TC, HDL and LDL by multiple linear regression analysis. In the Cua1 group (Cua < 4.869 mL /min/1.73 m2), PGE2 were lower than that in Cua2 (Cua ge 4.869 mL /min/1.73 m2) group (P = 0.011).ConclusionsIn male patients with hyperuricemia, SUA was negatively correlated with urinary PGE2, Cua was positively correlated with urinary PGE2. Urinary PGE2 were significantly different between different SUA and Cua groups.

Therapeutic effects and mechanisms of N-(9,10-anthraquinone-2-ylcarbonyl) xanthine oxidase inhibitors on hyperuricemia.

Objective: To observe the antioxidative effects of N-(9,10-anthraquinone-2-ylcarbonyl) xanthine oxidase inhibitors (NAY) in vitro and in vivo models of hyperuricemia and explore the mechanism. Methods: A classical experimental method of acute toxicity and a chronic toxicity test were used to compare the toxic effects of different doses of NAY in mice. The hyperuricemia mouse model was established by gavage of potassium oxonate in vivo. After treatment with different doses of NAY (low dose: 10 mg/kg, medium dose: 20 mg/kg, and high dose: 40 mg/kg) and allopurinol (positive drug, 10 mg/kg), observe the levels of uric acid (UA), creatinine (CRE), and urea nitrogen (BUN) in urine and serum, respectively, and detect the activities of xanthine oxidase in the liver. The hyperuricemia cell model was induced by adenosine and xanthine oxidase in vitro. The cells were given different doses of NAY (50, 100, and 200 μmol/L) and allopurinol (100 μmol/L). Then the culture supernatant UA level of the medium was measured. The next step was to detect the xanthine oxidase activity in the liver and AML12 cells, and the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), and NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) inflammatory factors in the kidney and serum of mice. Western blot was used to detect xanthine oxidase protein expression in mouse liver tissue and AML12 cells, ASC, Caspase-1, NLRP3, GLUT9, OAT1, and OAT3 protein expression in mouse kidney tissue and HK-2 cells. Hematoxylin–eosin staining was used to stain the liver and kidney tissues of mice and observe the tissue lesions. Results: NAY had little effect on blood routine and biochemical indexes of mice, but significantly reduced the serum UA level. NAY significantly reduced the level of UA in hyperuricemia mice and cells by inhibiting xanthine oxidase activity and reduced the levels of TNF-α, IL-6, and other inflammatory factors in serum and kidney of mice. NAY can inhibit inflammation by inhibiting the NLRP3 pathway. In addition, NAY can downregulate GLUT9 protein expression and upregulate OAT1 and OAT3 protein expression to reduce the UA level by promoting UA excretion and inhibiting UA reabsorption. Conclusion: These findings suggested that NAY produced dual hypouricemic actions. On the one hand, it can inhibit the formation of UA by inhibiting xanthine oxidase inhibitors activity, and on the other hand, it can promote the excretion of UA by regulating the UA transporter. It provides new ideas for the development of hyperuricemia drugs in the future.

Astragalus membranaceus ultrafine powder alleviates hyperuricemia by regulating the gut microbiome and reversing bile acid and adrenal hormone biosynthesis dysregulation

Metabolic syndrome is closely related to the intestinal microbiota and disturbances in the host metabolome. Hyperuricemia (HUA), a manifestation of metabolic syndrome, can induce various cardiovascular diseases and gout, seriously affecting a patient’s quality of life. Astragalus membranaceus has a long history as a commonly used traditional Chinese medicine to treat kidney disease in China and East Asia. We compared the therapeutic effect of benzbromarone and two different doses Astragalus membranaceus ultrafine powder (AMUP) in rats with HUA. Ultra-performance liquid chromatography-mass spectrometer was used to analyze the AMUP metabolism in the plasma, urine, and feces. Further, 16S ribosome RNA sequencing and feces metabolomic were performed to capture the variation of the gut microbiota and metabolites changes before and after drug administration. AMUP had a notable impact on reducing blood uric acid levels while protecting the liver and kidney. Drug metabolism analysis demonstrated that effective constituent flavonoids are distributed in the blood, whereas saponins remain in the intestine. Gut microbiota analysis showed that low-dose AMUP ameliorated HUA-induced gut dysbiosis by reducing the abundance of harmful bacteria and increasing that of some beneficial bacteria with anti-inflammatory properties, such as Clostridia, Lachnospiraceae, and Muribaculaceae. In addition, HUA-induced changes in metabolite contents in bile acid and adrenal hormone biosynthesis pathways were restored after treatment with AMUP. Low-dose AMUP exerts remarkable therapeutic effects on HUA by regulating the gut microbiome and mediating gut metabolism pathways associated with uric acid excretion.

Effects of Renal Function on Urinary Excretion and Serum Concentration of Uric Acid in Patients Treated with Febuxostat for Chronic Kidney Disease.

Febuxostat is recommended for lowering serum uric acid (sUA) concentration in chronic kidney disease (CKD) patients with hyperuricemia. However, it remains uncertain how febuxostat affects associations between several laboratory variables related to glomerular filtration and renal tubular reabsorption of uric acid. We retrospectively analyzed the records of 148 patients with CKD and hyperuricemia: 122 were treated with febuxostat, and 26 were not. Clinical and laboratory variables were used to calculate estimated glomerular filtration rate (eGFR), fractional excretion of uric acid (FEUA), and estimated 24-h urinary excretion of uric acid (eEUA). We examined correlations of those variables and compared patients who did and did not receive febuxostat. eGFR and FEUA were significantly inversely regardless of febuxostat-treatment status. eGFR was significantly inversely correlated with sUA in patients who received febuxostat, but not in those who did not. Similarly, there was a significant positive correlation between FEUA and eEUA only in patients treated with febuxostat. FEUA increased as eGFR decreased in our patients. Febuxostat changed correlation patterns for clinical and laboratory variables. Additional administration of uricosuric agents might help further lower sUA by increasing FEUA and eEUA in patients treated with febuxostat.

In-silico docking, synthesis, structure analysis, DFT calculations, energy frameworks, and pharmacological intervention of [1,3,4]-thiadiazoles analogous as XO inhibitor and on multiple molecular inflammatory targets COX and LOX

Xanthine oxidase (XO) is an interesting target for the synergic treatment of several diseases such as gout, hypertension, type 2 diabetes, and kidney disease. Associated complication includes hyperuricemia, which is considered one of the most common metabolic lifestyle disorders worldwide. Overproduction and insufficient excretion of uric acid during purine metabolism results in the formation of uric acid crystals in kidneys, joints, and other tissues. Allopurinol and Febuxostat, a clinically available drug used to reduce XO activity and serum uric acid level, are demonstrated to produce adverse effects including gastrointestinal distress, hypersensitivity, and skin rash, raising safety concerns. Exploring newer and novel XO inhibitors with minimum or no side effects is the aim of the current study. [1,3,4]-Thaidiazole analogs (7a-j) scaffold plays an important role in the design of efficient and potent inhibitors. In the present work, (7a-j) were evaluated for their ability to inhibit XO and found that among the series compound (7i) is selected as the best compound for inhibition of XO. Further, cyclooxygenases (COXs) and 5-lipoxygenase (5-LOX), enzymes that generate biologically active lipid molecules termed eicosanoids, are considered inflammatory and play a vital role in inflammatory pathways in the human body. Apart from their relation with inflammation, the additional involvement of COX-2 enzyme with cancer activity was recently discovered. In some cancer types, the level of COX-2 enzyme is increased indicating that this enzyme could be a suitable target for cancer therapy. Based on these findings, we have synthesized some new novel [1,3,4]-thiadiazole analogous (7a-j) and tested them against XO, COX, and LOX. To gain insight into the activity of XO, COX, and LOX inhibition, molecular docking studies were carried out for XO, COX, and LOX enzymes utilizing the newly synthesized compounds (7a-j), and the results inferred that among the synthesized series of [1,3,4]-thiadiazoles (7a-j), the compound (7i) showed extremely good result in both In silico and evaluation studies of XO, COX, and LOX, which is in agreement with the experimental results. Furthermore, density functional theory (DFT) was applied to calculate HOMO-LUMO, energy gap, and other parameters under the hybrid exchange-correlation functional (B3LYP) with the triple split valence basis set (6-311G).

Fufang Zhenzhu Tiaozhi capsule ameliorates hyperuricemic nephropathy by inhibition of PI3K/AKT/NF-κB pathway

Ethnopharmacological relevanceExcessive serum uric acid (SUA) causes hyperuricemic nephropathy (HN), characterized by inflammatory infiltration and tubulointerstitial fibrosis. Most recently, we demonstrated that Fufang Zhenzhu Tiaozhi (FTZ) capsule attenuated diabetic nephropathy through inhibition of renal inflammation and fibrosis. However, whether FTZ ameliorates HN is still unclear. Aim of the studyTo determine the protective roles and mechanism of FTZ in mouse renal injury and fibrosis under hyperuricemic condition. Materials and methodsHN mice, induced by potassium oxonate and hypoxanthine, were administrated with 600 and 1200 mg/kg FTZ (intragastrically) daily for three weeks. SUA levels, renal functions and histological changes were analyzed. Western blotting, quantitative real-time PCR (q-PCR) and RNA sequencing were used to identify the roles and underlying mechanism of FTZ in HN mice. ResultsWe demonstrated that FTZ treatment mitigated renal injury in mice, as evidenced by the decrease in SUA, serum creatinine (SCr) and cystatin C (Cys C) levels, as well as improved renal histology. FTZ markedly attenuates inflammasome activation, collagen deposition and the imbalance of uric acid transporters. RNA-sequencing revealed a key mechanism involved in the protective effects on HN mice was related to PI3K/AKT/NF-κB pathway. Western blot also confirmed that FTZ diminished the phosphorylation of AKT and p65 in HN mice. ConclusionsFTZ prevents renal injury, inflammation and fibrosis in HN mice via promoting uric acid excretion and inhibiting PI3K/AKT/NF-κB signaling pathway.

The antihypertensive and diuretic effect of crude root extract and saponins from Solanum sisymbriifolium Lam., in L-NAME-induced hypertension in rats

Ethnopharmacological relevanceSolanum sisymbriifolium Lam., is used in Paraguayan folk medicine claiming antihypertensive and diuretic properties. Aim of the studyThis study aimed to determine the influence of chronic oral administration of the crude root extract and saponins obtained from S. sisymbriifolium Lam., on the blood pressure of male and female rats with hypertension induced by L-NAME, and its consequences on diuresis, the body weight, blood glucose, and level of serum parameters of liver and kidney functionality. Materials and methodsWistar rats were randomly divided into seven male, and seven female groups (8 animals each), which received as 6-week pretreatment, 0.9% saline solution (two groups; 0.1mL/10 g of b.w.), L-arginine (100.0 mg/kg/day), enalapril (15.0 mg/kg/day), crude extract (CESs 100.0 mg/kg/day), and saponin purified fraction (1.0, and 10.0 mg/kg/day), and treated with L-NAME (20 mg/kg/day/i.p.) twice, 1, and 6 h after pre-treatment. The animals' body weight, glycemia, and blood pressure were recorded weekly, while serum, hepatic, renal, and histological parameters were analyzed at the end of 6-week of treatment. ResultsA protective effect of CESs (100.0 mg/kg/day), and saponins (1.0, and 10.0 mg/kg/day) against hypertension induced by L-NAME was verified in the systolic, diastolic, and mean blood pressure values, which were significantly lower than the positive L-NAME-hypertensive control group (male and female) at the end of the 6-week treatment. Also, pretreatment with enalapril (15.0 mg/kg/day) induced an efficient protective activity, which validates the method used. Likewise, the volume of urine, creatinine, uric acid, urea, and electrolyte excretion was enhanced at the end of 6-week of treatment in concordance with the reduction in serum level of the same parameters, compatible with the improvement of the diuretic activity. The glycemia, body weight, heart rate, and functional hepato-renal parameters were not modified after a 6-week of treatment, in comparison to the control group, indicating relatively acceptable harmless properties of CESs and saponins. Interestingly, the HDL level in females was increased in contrast to male rats by chronic saponins treatment when compared with the negative control group. ConclusionsIt can be concluded that either the increment in blood pressure (systolic, diastolic, and median) or cardiorenal remodeling effects in male and female rats submitted to L-NAME-induced hypertensive condition, were prevented and well-preserved without a significant variation during a period of 6-week of pretreatment with CESs and saponins pretreatments. Likewise, an important diuretic effect was revealed after this period of treatment.

Traditional Chinese herbs and natural products in hyperuricemia-induced chronic kidney disease.

Hyperuricemia is a common biochemical disorder, which resulted from both excessive uric acid (UA) production and/or absolute or relative impairment of urinary UA excretion. Growing evidence has indicated that hyperuricemia is an independent risk factor for the development and progression of chronic kidney disease (CKD), causing hyperuricemia-induced CKD (hyperuricemic nephropathy, HN). The therapeutic strategy of HN is managing hyperuricemia and protecting kidney function. Adverse effects of commercial drugs make persistent treatment of HN challenging. Traditional Chinese medicine (TCM) has exact efficacy in lowering serum UA without serious adverse effects. In addition, TCM is widely applied for the treatment of CKD. This review aimed to provide an overview of efficacy and mechanisms of traditional Chinese herbs and natural products in hyperuricemia-induced CKD.

Flavonoid extract of saffron by-product alleviates hyperuricemia via inhibiting xanthine oxidase and modulating gut microbiota.

Hyperuricemia was associated with the overproduction or inadequate excretion of uric acid, while its association with gut microbiota has emerged although few studies were focused on it. Previously, we have reported a flavonoid extract from saffron floral bio-residues lowered uric acid in potassium oxonate-induced hyperuricemic mice. In this study, the impacts of the flavonoid extract on potassium oxonate-induced hyperuricemic rats were evaluated through its effects on serum, renal, intestinal uric acid, and xanthine oxidase activity. At the same time, the microbial and metabolic features of the flavonoid extract against hyperuricemia were explored using 16S rRNA sequencing techniques and serum metabolomics, respectively. According to the results, the flavonoid extract lowered serum and intestinal uric acid levels in hyperuricemic rats without kidney damage. On the one hand, it inhibited serum and liver xanthine oxidase activities and down-regulated the expression of hepatic xanthine oxidase. On the other hand, it ameliorated the hyperuricemia-associated gut microbiota dysbiosis and alleviated the disturbance of serum metabolome, especially of lipid and amino acid metabolites. The results suggested that the flavonoid extract of saffron floral bio-residues exerts a potent antihyperuricemia effect by inhibiting xanthine oxidase to decrease uric acid production and modulating gut microbiota related to host metabolism.

Natural bioactives in the management of hyperuricemia

Hyperuricemia, also known as gout, has been identified as a well-known metabolic disorder associated with an elevated uric acid level in serum. Gout is commonly associated with various chronic disorders like hypertension, obesity, hyperlipidemia, cardiovascular disorders, and diabetes. Drugs, like nonsteroidal anti-inflammatory medications [NSAIDs] and glucocorticoids, are shown to exhibit serious side effects, when used in this therapy, although they are the first-line of treatment options available to date. Bioactive compounds have been explored for the management of hyperuricemia for their effectiveness and ability to minimize complications. Related research have reported the use of plant-based bioactives on hyperuricemia. The objective of the present review is to highlight the therapeutic effect of the naturally occurring phytochemicals and the pharmacology of the compounds involved in the same. These phytochemicals are categorized into five classes, namely alkaloids, flavonoids, saponins, and phenolic acids, that describe their anti-gout activity. Additionally, the mechanism of action by which these bioactive compounds display the hypouricemic consequences has been divided into three parts, namely, the inhibition of the production of uric acid, lowering of intestinal uric acid secretion, and enhancement of elimination of renal uric acid.

Folic acid and zinc improve hyperuricemia by altering the gut microbiota of rats with high-purine diet-induced hyperuricemia.

A high-purine diet can cause hyperuricemia and destroy the microbial composition of the gut microbiota. Both folic acid and zinc significantly reduce uric acid levels and alleviate hyperuricemia. However, whether the underlying mechanisms are associated with the regulation of the gut microbiota remain unknown. To explore alterations of the gut microbiota related to folic acid and zinc treatment in rats with hyperuricemia in our study. A hyperuricemic rat model was established with a high-purine diet. The effects of folic acid and zinc on uric acid levels were evaluated. Alterations of the gut microbiota related to hyperuricemia and the treatments were evaluated by sequencing using the Illumina MiSeq system. The results demonstrated that uric acid levels dropped observably, and the activities of adenosine deaminase (ADA) and xanthine oxidase (XOD) were downregulated after folic acid or zinc intervention. 16S rRNA gene sequencing-based gut microbiota analysis revealed that folic acid and zinc enhanced the abundance of probiotic bacteria and reduced that of pathogenic bacteria, thus improving intestinal barrier function. PICRUST analysis indicated that folic acid and zinc restored gut microbiota metabolism. These findings indicate that folic acid and zinc ameliorate hyperuricemia by inhibiting uric acid biosynthesis and stimulating uric acid excretion by modulating the gut microbiota. Thus, folic acid and zinc may be new and safe therapeutic agents to improve hyperuricemia.

KARAKTERISTIK DEMOGRAFI DAN OBESITAS SEBAGAI FAKTOR RISIKO TERJADINYA GOUT ARTHRITIS

Obesity is often associated with an increase in uric acid. This occurs through the process of decreasing the excretion of uric acid so that there is a buildup in the blood. This situation will trigger the occurrence of gout arthritis. This quantitative descriptive research aims to determine the characteristic picture of demography and obesity as risk factors for gout arthritis in students. Sampling was carried out with a total sampling so that 68 respondents were involved in this study. Data collection was carried out using metering tools and scales to obtain the respondent's body mass index. The collected data were analyzed using frequency distributions. Results; there were 3 respondents who were obese (4.4%), all aged 10-20 years, female 2 respondents (2.9%) and 1 person male (1.5%). Conclusion: based on the description of demographic characteristics and obesity, there are 4.4% of respondents who have a risk of gout arthritis in students

Treatment for hyperuricemia and gout in Japan: Aspect of prescription and duration.

Treatment for hyperuricemia and gout in Japan: Aspect of prescription and duration.

Effect of High-altitude Hypoxia Environment on Uric Acid Excretion, Desmin Protein Level in Podocytes, and Na+-K+- ATPase Activity.

To investigate the oxidative stress and adaptive compensation of kidneys in rats in high-altitude hypoxia environments, 20 Wistar rats (3 months) were randomly and equally grouped. The rats in the test group were fed in a low-pressure oxygen chamber, and those in the control group (controls) were fed in a normal environment. On the 5th, 10th, 20th, and 30th day, the excretion of uric acid in rats was detected by a biochemical analyzer, the level of desmin protein in rat podocytes was detected by immunohistochemistry, and the activity of Na+-K+- ATPase in rat proximal tubular epithelial cells was measured by liquid scintillation method. The results showed that with the increased time, the level of uric acid in the blood of rats in the test group increased dramatically (P<0.05). On the 30th day, the blood uric acid content of the test group was 52.33μmol/L, and that of the control group was 38.43μmol/L. The blood uric acid content in the test group was dramatically increased relative to the control group. Immunohistochemistry showed that the desmin protein in podocytes of the test group (0.14) was considerably higher than that in the control group (P<0.05). The Na+-K+- ATPase activity of proximal renal tubular epithelial cells in the test group was 611.2 pmol pi/mg protein/h, which was considerably lower than the versus control group (P<0.05). In summary, in high altitude hypoxia environment, uric acid accumulated in the body, and renal filtration and excretion ability was limited.

Effect of sodium-glucose co-transporter inhibitors on blood pressure values. A new class of diuretic drugs?

New sodium-glucose co-transporter (SGLT 2) inhibitors are already widely used in patients with diabetes mellitus and in patients with heart failure. From the beginning of their use, it has been noticed that they slightly but statistically significantly lower both systolic blood pressure (SBP) and diastolic blood pressure (DBP). The antidiabetic activity of these drugs is based on the inhibition of the reabsorption of glucose and partially sodium in the renal tubules, which leads to an increase in the amount of urine excreted. Most likely, increased diuresis is responsible for the drop in blood pressure (BP). So far, numerous meta-analyses confirming the reduction of BP in diabetic patients have already been published, for both office BP and home BP, twenty-four hour BP and ambulatory central blood pressure. The action of SGLT 2 inhibitors, after a single administration, extends over 24 hours and there are already the first successful attempts to use them in hypertension in the course of diabetes mellitus with obstructive sleep apnea. The action of SGLT 2 inhibitors is pleiotropic and, apart from the diuretic effect, they slightly reduce the patient’s weight, reduce the activity of the sympathetic nervous system, restore the normal function of the endothelium, increase uric acid excretion, and reduce blood vessel stiffness. All these factors are responsible for the drop in BP. These favorable properties of SGLT 2 inhibitors indicate that these drugs will be increasingly used, probably not only in diabetes.

Katsuwonus pelamis Peptide and its Complexes Protect Zebrafish and Mice From Hyperuricemia Through Promoting Kidney Excretion of Uric Acid and Inhibiting Liver Xanthine Oxidase Activity.

Katsuwonus pelamis peptide and its complexes have the effect of lowering uric acid (UA)-levels. To identify the effect and possible mechanisms, different concentrations of Katsuwonus pelamis peptide and its complexes were administered to the zebrafish and mice hyperuricemia models, and the UA level was measured. Meanwhile, the hyperuricemic mice were treated orally at 0.83, 1.67, and 5.00 mg/g body weight for 7 days with Katsuwonus pelamis peptide and the complexes groups, separately. The levels of serum UA (SUA), urinary UA (UUA), serum creatinine (SCR), blood urine nitrogen (BUN), and xanthine oxidase (XOD) activities were detected in each group. The results showed that the Katsuwonus pelamis peptide (125 μg/ml) and its complexes (83.3 and 250 μg/ml) effectively reduced UA level in zebrafish with hyperuricemia (p < 0.05). The Katsuwonus pelamis peptide at high concentration (5.00 mg/g) decreased the SUA level, SCR level, BUN level, and hepatic XOD activity, and the complexes (1.67 and 5.00 mg/g) significantly reduced the SUA level and hepatic XOD activity (p < 0.05) in the hyperuricemic mice. In addition, in a hyperuricemic mouse model, the UUA level was increased after treatment with Katsuwonus pelamis peptide and its complexes at high concentrations (p < 0.05). The total therapeutic effects in the Katsuwonus pelamis peptide complex group were better than those in the Katsuwonus pelamis peptide group. Thus, Katsuwonus pelamis peptide and its complexes may possibly be used to prevent hyperuricemia via promoting urate secretion and inhibiting XOD activity production.