Serum uric acid levels among physical examination populations in Balikun County / 预防医学

Objective@#To investigate the serum uric acid levels among residents living in Balikun County, Xinjiang Uygur Autonomous Region from 2018 to 2021, so as to provide insights into local hyperuricemia control.@*Methods@#The residents at ages of 20 to 69 years undergoing physical examinations in Balikun County Hospital during the period from 2018 to 2021 were enrolled. Their age, gender, and history of medication and disease were collected, and serum uric acid levels were measured. The gender- and age-specific prevalence of hyperuricemia and hypouricemia was descriptively analyzed.@*Results@#A total of 3 097 subjects were enrolled, which included 1 210 males ( 39.07% ) and 1 887 females ( 60.93% ) and had a mean age of ( 46.12±12.84 ) years. The overall mean serum uric acid was ( 260.41±71.99 ) μmol/L, and the mean serum uric acid was ( 298.22±69.57 ) μmol/L in men and ( 236.17±62.44 ) μmol/L in women. The serum uric acid level appeared a tendency towards a rise with ages both in whole study subjects and in women ( P<0.05 ). The overall prevalence of hyperuricemia was 4.26%, with 4.63% prevalence in men and 4.03% in women. The prevalence of hyperuricemia appeared a tendency towards a rise with ages both in whole study subjects and in women ( P<0.05 ). The overall prevalence of hypouricemia was 0.71%, with 0.25% prevalence in men and 1.01% in women; the prevalence of moderate hypouricemia was 11.11%, with 2.56% prevalence in men and 16.59% in women.@*Conclusions@#Low level of serum uric acid and prevalence of hyperuricemia is detected among residents living in Balikun County. Monitoring of serum uric acid is recommended to be intensified among men.

The adverse effects of low serum uric acid on patients with cardiovascular and cerebrovascular diseases / 中华内分泌代谢杂志

In recent years, it is noted clinically that the low level of serum uric acid is closely related to the adverse outcomes of cardiovascular and cerebrovascular diseases. Recent studies have shown that low uric acid levels not only boost the incidence of arrhythmia and cardiovascular events, but also increase mortality. It also has adverse effects on the development and prognosis of cerebrovascular diseases, including intracerebral hemorrhage and stroke. This article reviews research advances in the adverse effects of low uric acid on cardiovascular diseases andcerebrovascular diseases.

The Association between Serum Uric Acid Level and Dementia in Geriatric Population – A Case–Control Study

Importance: The increasing prevalence of dementia worldwide has reduced the quality of life in geriatric patients, therebyincreasing the burden on the caregivers. As dementia evolves gradually, diagnosis of the disease is often delayed. Thus, theneed for a sensitive biomarker for early diagnosis is instrumental.Objective: The objective of the study was to study the association between serum uric acid levels and dementia in geriatric patients.Design: This is a case–control study comparing the age-matched geriatric patients with and without dementia (cases – 50and controls – 50).Setting and Participants: A total of 100 geriatric patients from Government Villupuram Medical College and Hospital wereincluded in this study for a study period of 4 months. Out of this, 50 were cases (with dementia) and 50 were controls (withoutdementia). Mini-mental state examination test was done to categorize the cases into mild, moderate, and severe subgroups(24–30 out of 30 as normal; 20–23 out of 30 as mild; 10–19 out of 30 as moderate; and score lesser than 10 out of 30 as severe).Serum uric acid levels were measured in the study population and compared between the cases and controls.Results: The correlation of serum uric acid levels with cases and controls revealed 16% of the cases had hypouricemia,whereas none in the control group had hypouricemia. When serum uric acid levels were compared, it was found that 44% ofthe control group had normal serum uric acid levels and 82% of the cases had normal serum uric acid levels. Based on minimental state examination score, 10% of mild group and 21% of moderate group had hypouricemia and 4% of moderate grouphad hyperuricemia while the others had normal serum uric acid levels. All the data were statistically significant with “P” < 0.001.Conclusion: The study identified the prevalence of hypouricemia in the study population. This study can pave the path forfurther multicentric research to delineate the role of uric acid level as potential biomarker for dementia.Relevance: The information gained from this study will enable us to diagnose dementia in the early stages and improve thequality of life of the patients.

Prevalence and possible causes of hypouricemia at a tertiary care hospital

BACKGROUND/AIMS: We aimed to investigate the prevalence and possible causes of hypouricemia in the Korean population and to compare our findings with published results of other populations. METHODS: We examined the serum uric acid levels of 30,757 subjects who had their uric acid values measured at least once during a 1-year period. All individuals with hypouricemia (serum uric acid < 2.0 mg/dL, n = 424) were reviewed with respect to medical drug history and concomitant diseases previously identified as being associated with hypouricemia. RESULTS: The prevalence of hypouricemia was 4.14% (299/7,223) among inpatients and 0.53% (125/23,534) among outpatients, for an overall prevalence of 1.39% (424/30,757). Possible causes associated with hypouricemia were found to be solid or hematologic malignancies (n = 86), diabetes mellitus (n = 56), and therapeutic drugs (n = 29). The medications were allopurinol (n = 11), angiotensin II receptor blockers (n = 10), salicylates (n = 6), febuxostat (n = 1), and warfarin (n = 1). In the remaining 226 individuals, the cause of hypouricemia was not identified. CONCLUSIONS: Hypouricemia is relatively common in the Korean population compared to those of other countries. The possible causes associated with hypouricemia are related to underlying diseases and medications.

A Case Report of Familial Renal Hypouricemia Confirmed by Genotyping of SLC22A12, and a Literature Review

A 24-year-old male visited our hospital because of pain in both flanks. His biochemistry profile showed an elevated serum creatinine level and low serum uric acid level. History taking revealed that he had undertaken exercise prior to the acute kidney injury (AKI) event, and he stated that family members had a history of urolithiasis. His renal profile improved after hydration and supportive care during hospitalization. Although the patient was subsequently admitted again due to AKI, his status recovered with similar treatment. Since the diagnosis of the patient was familial renal hypouricemia with exercise-induced AKI, we performed genotyping of SLC22A12, which encodes human urate transporter 1. The diagnosis was confirmed by the detection of a homozygous mutation of W258X. We herein, report a case of familial renal hypouricemia confirmed by genotyping of SLC22A12, and review the relevant literature.

A Case of Recurrent Exercise-Induced Acute Renal Failure and Renal Hypouricemia with R90H Mutation in a SCL22A12 Gene / 영남의대학술지

Acute renal failure with severe loin pain and patch renal ischemia after anaerobic exercise (ALPE) is a rare cause of exercise-induced acute kidney injury. Some ALPE patients also have renal hypouricemia. Mutations in the SCL22A12 gene are among the major factors of hypouricemia. Education for the prevention of relapse and genetic counseling should be recommended to ALPE patients with renal hypouricemia. This paper reports a 25-year-old man who showed recurrent exercise-induced ARF and renal hypouricemia with R90H mutation in his SCL22A12 gene.

Clinical characteristics of acute renal failure with severe loin pain and patchy renal vasoconstriction

BACKGROUND: Acute renal failure (ARF) with severe loin pain and patchy renal vasoconstriction (PRV) is a syndrome presenting with sudden loin pain after anaerobic exercise. We aimed to investigate the clinical characteristics and the efficacy of diagnostic imaging studies of patients with this syndrome. METHODS: We retrospectively selected 17 patients with ARF accompanied by loin or abdominal pain who showed multiple patchy wedge-shaped delayed contrast enhancements on a computerized tomography scan. Information about the clinical characteristics, including the nature of pain and combined symptoms, suspected causes, such as exercise, drug or alcohol intake, and renal hypouricemia, and the results of laboratory and imaging tests were gathered. RESULTS: The mean age of patients with episodes of ARF accompanied by loin pain was 23.0+/-6.5 (range 16-35) years old. Pain was mainly located in the loin (70.6%) or abdominal area (76.5%) and continued for approximately 3.5+/-4.0 days. Exercise was suspected as a primary cause of disease in 12 (70.6%) patients. Maximal serum creatinine was 5.42+/-3.16 (1.4-12.1) mg/dL 3.1+/-1.8 (1-7) days after the onset of pain. The peak level of serum uric acid was 9.41+/-2.91 (6.0-15.8) mg/dL. All of the patients recovered to near-normal renal function, and one patient showed hypouricemia after recovery. CONCLUSION: ARF with severe loin pain and PRV can present with loin or abdominal pain, even without a history of anaerobic exercise. Careful history taking and appropriate imaging studies are critical in the diagnosis and management of this syndrome.

A Case of Exercise-induced Acute Renal Failure with G774A Mutation in SCL22A12 Causing Renal Hypouricemia

Acute renal failure with severe loin pain which develops after anaerobic exercise is rare. One of predisposing factors of exercise-induced acute renal failure is renal hypouricemia. Idiopathic renal hypouricemia is a genetic disorder characterized by hypouricemia with abnormally high renal tubular uric acid excretion. The mutation in SCL22A12 gene which encodes renal uric acid transporter, URAT1, is the known major cause of this disorder. We here described a 25-yr-old man showing idiopathic renal hypouricemia with G774A mutation in SCL22A12 who presented exercise-induced acute renal failure. There have been a few reports of mutational analysis in Korean idiopathic renal hypouricemia without acute renal failure. This is the first report of genetically diagnosed idiopathic renal hypouricemia with exercise-induced acute renal failure in Korea.

Hyponatremia in visceral leishmaniasis / Hiponatremia no calazar

There are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100 percent of kala-azar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H2O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H2O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8 percent of patients and increased fractional urinary uric acid excretion was detected in 74.5 percent of them. Increased glomerular filtration rate was present in 25.4 percent of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

Existem poucos relatos relacionando hiponatremia com a leshmaniose visceral (calazar). Este é um estudo de 55 pacientes portadores de calazar e um grupo controle de 20 indivíduos normais. Hiponatremia e hipo-osmolalidade sérica foram detectados em 100 por cento dos pacientes portadores de calazar. A presença de alta osmolalidade da primeira urina da manhã (750,0 ± 52,0 vs. 894,5 ± 30 mOsm/Kg H2O, p < 0,05) e da urina de 24h (426,0 ± 167,0 vs. 514,6 ± 132,0 mOsm/Kg H2O, p < 0,05), demonstraram a presença de persistente secreção de hormônio antidiurético. A concentração de sódio urinário foi elevada (82,3 ± 44,2 vs. 110,3 ± 34,7 mEq/L, p < 0,05). Hipouricemia ocorreu em 61,8 por cento dos pacientes e aumento da fração de excreção urinária de ácido úrico foi detectada em 74,5 por cento dos casos. Aumento da velocidade de filtração glomerular estava presente em 25,4 por cento dos pacientes. Não havia evidência clínica de depleção de volume extracelular. Valores normais de ADH plasmático foram observados nos pacientes com calazar. Não foi detectada disfunção renal ou endócrina. É provável, que a maioria dos pacientes com calazar apresente uma síndrome de secreção inapropriada de hormônio antidiurético.

A case of idiopathic renal hypouricemia / 소아과

Idiopathic renal hypouricemia is a disorder characterized by impaired urate handling in the renal tubules. This disease usually produces no symptoms, but hematuria, uric acid nephrolithiasis or acute renal failure may develop. A defect in the SLC22A12 gene, which encodes the human urate transporter, is the known major cause of this disorder. We describe a 10-month-old boy with idiopathic renal hypouricemia. He was diagnosed with transient pseudohypoaldosteronism at admission, but hypouricemia was accidentally found through follow-up study. By gene analysis, his diagnosis was confirmed to idiopathic renal hypouricemia. In addition, we report a mutation in the human urate transporter 1 (hURAT1) gene identified in his family.

Clinical and etiological analysis of 177 patients with hypouricemia / 中国基层医药

0.05).Conclusion There are hapatic and renal disease,craniocerebral disease,wound,toxicaion with hypouricemia,the clinical assay should be paid more attention.

A Case of Idiopathic Renal Hypouricemia with URAT1 Gene Mutation who Showed Persistent Orange-colored Urine

Idiopathic renal hypouricemia is a disorder characterized by impaired urate handling in the renal tubules. Most patients with hypouricemia are asymptomatic and are found incidentally, but the condition is known to be at high risk for exercise-induced acute renal failure or urolithiasis. URAT1 protein encoded by SLC22A12 gene has been identified recently as a urate/anion exchanger in the human kidney. Inactivation mutations in SLC22A12 gene have been shown to cause renal idiopathic hypouricemia. We experienced a 3-year-old boy who presented with persistent orange-colored urine since infancy. His urine contained many uric acid crystals, while the serum showed hypouricemia(0.7 mg/dL). The fractional excretion of uric acid was increased to 41.7%. SLC22a12 gene analysis revealed W258X homozygote alleles. Renal hypouricemia must be included in the differential diagnosis of red-urine and SLC22A12 gene analysis is recommended in idiopathic renal hypouricemia.

Patient with Renal Hypouricemia and Exercise Induced Acute Renal Failure / 대한신장학회잡지

We have described a male patient with a episode of acute renal failure after strenuous exercise. He was found to have low serum uric acid(0.6 mg/dL, after recovery) and normal 24 hour urinary excretion in the steady state. The possibility of other diseases that cause hypouricemia could be excluded, acute renal failure associated with idiopathic renal hypouricemia was diagnosed in this case. A renal computed tomography showed the delayed wedge shaped contrast enhancement, these findings suggested that the cause of acute renal failure could be renal vasoconstriction rather than obstruction by uric acid crystals. Hypouricemia appear to play a crucial role in this reperfusion oxygen free radical induced acute renal failure. We have suggested that the renal hypouricemia should be suspected in the case of acute renal failure associated with exercise when the patient's uric acid level was within or slight alone normal range at the time of acute renal failure.

Exercise-induced Acute Renal Failure in a Patient with Renal Hypouricemia / 대한신장학회잡지

We report a case of exercise-induced acute renal failure associated with renal hypouricemia in a 35- year-old man who complained of oliguria and back pain after swimming. Laboratory tests revealed that serum blood urea nitrogen and creatinine level were elevated, the serum uric acid concentration was subnormal(2.1 mg/dL). After conservative treatment, renal function was recovered. But, uric acid level decreased to 0.4 mg/dL. In addition, there was no supression of urate clearance to creatinine clearnace ratio(CUA/CCr) following the administration of pyrazinamide, and no increase of CUA/CCr after benzbromarone. Therefore, we think the cause of renal hypouricemia in this patient may be the subtotal defect in the urate transport.

Syndrome of Inappropriate Antidiuresis-report of 40 cases / 中国实用内科杂志

Objective We have summarized the clinical characteristics of inappropriate antidiuresis(SIAD).Methods We adopted retrospective analysis to analyze the clinical and lab data of 40 cases.Results The most common causes of SIAD were malignant tumor,lung disease,and central nervous system disease.The five major abnormal lab data were:hypochloraemia,hypouricemia,hyponitremia,hypocalcemia,and low hematocrit.Conclusion It is important to diagnose SIAD as soon as possible,and patient presented hyponatremia combined with hypouricemia must be suspected to have SIAD.

A Case of Renal Hypouricemia and Hypercalciuria / 대한신장학회잡지

We encountered a case of renal hypouricemia and absorptive hypercalciuria. Although renal hypouricemia is asymptomatic as usual, it is rarely complicated with acute renal failure and urolithiasis. A 43-year-old man had hypouricemia (serum uric acid, 0.6-1.0mg/dl) with an increased renal uric acid clearance (69.4ml/min), hypercalciuria (367.2mg/day). In present case, there was no response of uric acid excretion to either pyrazinamide or probenecid and hypercalciuria disappeared after calcium restriction diet. These results suggest that the present case had the defect of both pre-and postsecretory reabsorption of uric acid and absorptive hypercalciuria.

Recurrent Hematuria due to Renal Hypouricemia

A marked low concentration of serum uric acid(0.7-1.2mg/dl) was detected in a 14-year-old boy with recurrent episodes of gross hematuria. The hypouricemia accompanied with a markedly increased urinary clearance of uric acid (32.6-56.0ml/min), which was only minimally changed after both the administration of pyrazinamide, and inhibitor of the renal tubular secretion of uric acid, and the administration of probenecid, and inhibitor of the renal tubular reabsorption of uric acid. Other renal tubular functions were normal. There were no other family members with hypouricemia. Thies is the first case report of isolated renal hypouricemia due to presecretory reabsorption defect of uric acid in the renal proximal tubule in Korea. And renal hypouricemia should be included in the diagnosis of hematuria.