Distribution of serum uric acid levels and prevalence of hyper- and hypouricemia in a Korean general population of 172,970

Koo, Bon San; Jeong, Hye-­Jin; Son, Chang-Nam; Kim, Sang-Hyon; Kim, Hyun Jung; Kim, Gheun-Ho; Jun, Jae‐Bum

doi:10.3904/kjim.2020.116

Cited by 22 publications

(20 citation statements)

References 33 publications

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“…The prevalence of hyperuricemia in the general population of Korea has been reported in different ways. Koo et al [29] reported that the prevalence of hyperuricemia was 133.25 per 1,000 persons in men and 8.17 per 1,000 persons in women (2004)(2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013). In another study [13], the proportion of hyperuricemia was 11.4% (17.0% in men and 5.9% in women).…”

Section: Discussionmentioning

confidence: 99%

Metabolic risks in living kidney donors in South Korea

Kang

Park

Kim

et al. 2021

Kidney Res Clin Pract

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Background: Considering the growing prevalence of Western lifestyles and related chronic diseases occurring in South Korea, this study aimed to explore the progression of metabolic risk factors in living kidney donors. Methods: This study enrolled living kidney donors from seven hospitals from 1982 to 2016. The controls were individuals that voluntarily received health check-ups from 1995 to 2016 that were matched with donors according to age, sex, diabetes status, baseline estimated glomerular filtration rate, and date of the medical record. Data on hyperuricemia, hypertension, hypercholesterolemia, and overweight/obesity were collected to determine metabolic risks. Logistic regressions with interaction terms between the medical record date and donor status were used to compare the trends in metabolic risks over time in the two groups. Results: A total of 2,018 living kidney donors and matched non-donors were included. The median age was 44.0 years and 54.0% were women. The living kidney donors showed a lower absolute prevalence for all metabolic risk factors, except for those that were overweight/obese, than the non-donors. The proportion of subjects that were overweight/obese was consistently higher over time in the donor group. The changes over time in the prevalence of each metabolic risk were not significantly different between groups, except for a lower prevalence of metabolic risk factors ≥ 3 in donors.

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Section: Discussionmentioning

confidence: 99%

Metabolic risks in living kidney donors in South Korea

Kang

Park

Kim

et al. 2021

Kidney Res Clin Pract

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“…Serum uric acid levels are different between men and women, and the prevalence of hyperuricemia in adult males is higher than in females 51) . Sex hormones may play a role in regulating the expression or activity of urate transporters because SLC2A9 may have a stronger association with lower serum uric acid levels in females, whereas ABCG2 may have a stronger association with higher serum uric acid levels in males 52) .…”

Section: Regulation Of Urate Transporters In the Gut And Kidneymentioning

confidence: 97%

Urate Transporters in the Kidney: What Clinicians Need to Know

Chung

Kim

2021

Electrolyte Blood Press

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Urate is produced in the liver by the degradation of purines from the diet and nucleotide turnover and excreted by the kidney and gut. The kidney is the major route of urate removal and has a pivotal role in the regulation of urate homeostasis. Approximately 10% of the glomerular filtered urate is excreted in the urine, and the remainder is reabsorbed by the proximal tubule. However, the transport of urate in the proximal tubule is bidirectional: reabsorption and secretion. Thus, an increase in reabsorption or a decrease in secretion may induce hyperuricemia. In contrast, a decrease in reabsorption or an increase in secretion may result in hyperuricosuria. In the proximal tubule, urate reabsorption is mainly mediated by apical URAT1 ( SLC22A12 ) and basolateral GLUT9 ( SLC2A9 ) transporter. OAT4 ( SLC22A11 ) also acts in urate reabsorption in the apical membrane, and its polymorphism is associated with the risk of hyperuricemia. Renal hypouricemia is caused by SLC22A12 or SLC2A9 loss-of-function mutations, and it may be complicated by exercise-induced acute kidney injury. URAT1 and GLUT9 are also drug targets for uricosuric agents. Sodium-glucose cotransporter inhibitors may induce hyperuricosuria by inhibiting GLUT9b located in the apical plasma membrane. Urate secretion is mediated by basolateral OAT1 ( SLC22A6 ) and OAT3 ( SLC22A8 ) and apical ATP-binding cassette super-family G member 2 ( ABCG2 ), NPT1 ( SLC17A1 ), and NPT4 ( SLC17A3 ) transporter in the proximal tubule. NPT1 and NPT4 may be key players in renal urate secretion in humans, and deletion of SLC22A6 and SLC22A8 in mice leads to decreased urate excretion. Dysfunctional variants of ABCG2 inhibit urate secretion from the gut and kidney and may cause gout. In summary, the net result of urate transport in the proximal tubule is determined by the dominance of transporters between reabsorption (URAT1, OAT4, and GLUT9) and secretion (ABCG2, NPT1, NPT4, OAT1, and OAT3).

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“…Hypouricemia is frequently defined using an SUA concentration of ≤2.0 mg/dL [ 5 ]. Using this reference value, the prevalence of hypouricemia in the general population was reported for Japan [ 8 , 9 , 10 , 11 ] and Korea [ 12 ]. These two countries have similar prevalences of hypouricemia at between 0.2 and 0.4%.…”

Section: Prevalence Of Hypouricemiamentioning

confidence: 99%

Genetic Basis of the Epidemiological Features and Clinical Significance of Renal Hypouricemia

Hakoda

Ichida

2022

Biomedicines

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A genetic defect in urate transporter 1 (URAT1) is the major cause of renal hypouricemia (RHUC). Although RHUC is detected using a serum uric acid (UA) concentration <2.0 mg/dL, the relationship between the genetic state of URAT1 and serum UA concentration is not clear. Homozygosity and compound heterozygosity with respect to mutant URAT1 alleles are associated with a serum UA concentration of <1.0 mg/dL and are present at a prevalence of ~0.1% in Japan. In heterozygous individuals, the prevalence of a serum UA of 1.1–2.0 mg/dL is much higher in women than in men. The frequency of mutant URAT1 alleles is as high as 3% in the general Japanese population. The expansion of a specific mutant URAT1 allele derived from a single mutant gene that occurred in ancient times is reflected in modern Japan at a high frequency. Similar findings were reported in Roma populations in Europe. These phenomena are thought to reflect the ancient migration history of each ethnic group (founder effects). Exercise-induced acute kidney injury (EI-AKI) is mostly observed in individuals with homozygous/compound heterozygous URAT1 mutation, and laboratory experiments suggested that a high UA load on the renal tubules is a plausible mechanism for EI-AKI.

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Distribution of serum uric acid levels and prevalence of hyper- and hypouricemia in a Korean general population of 172,970

Cited by 22 publications

References 33 publications

Metabolic risks in living kidney donors in South Korea

Metabolic risks in living kidney donors in South Korea

Urate Transporters in the Kidney: What Clinicians Need to Know

Genetic Basis of the Epidemiological Features and Clinical Significance of Renal Hypouricemia

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