Prevalences of hyperuricemia and electrolyte abnormalities in patients with chronic kidney disease in Japan: A nationwide, cross-sectional cohort study using data from the Japan Chronic Kidney Disease Database (J-CKD-DB)

Sofue, Tadashi; Nakagawa, Naoki; Kanda, Eiichiro; Nagasu, Hajime; Matsushita, Kunihiro; Nangaku, Masaomi; Maruyama, Shoichi; Wada, Takashi; Terada, Yoshio; Yamagata, Kunihiro; Narita, Ichiei; Yanagita, Motoko; Sugiyama, Hitoshi; Sügimura, Takashi; Ito, Takafumi; Tamura, Kouichi; Isaka, Yoshitaka; Okada, Hirokazu; Tsuruya, Kazuhiko; Yokoyama, Hitoshi; Nakashima, Naoki; Kataoka, Hiromi; Okada, Mihoko; Kashihara, Naoki

doi:10.1371/journal.pone.0240402

Cited by 21 publications

(13 citation statements)

References 40 publications

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“…On the other hand, in a study that examined the Japan Chronic Kidney Disease Database (J-CKD-DB) (n = 35,508), the prevalence of hyperkalemia in CKD stage G4 and G5 patients was found to be only 8.3% and 11.6%, respectively. However, though the serum potassium levels in stage G4 and G5 were significantly greater than those in G3 cases, there was little risk of rising above normal [(G3, G4, G5: 4.33 ± 0.44, 4.68 ± 0.73, 4.71 ± 0.76, respectively, (mean ± SD)] [ 22 ]. These findings support the existence of various compensatory mechanisms related to decreased renal potassium excretion.…”

Section: Epidemiological Results Showing Serum K Levels In Patients With Ckdmentioning

confidence: 99%

Potassium Metabolism and Management in Patients with CKD

Yamada

Inaba²

2021

Nutrients

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Potassium (K), the main cation inside cells, plays roles in maintaining cellular osmolarity and acid–base equilibrium, as well as nerve stimulation transmission, and regulation of cardiac and muscle functions. It has also recently been shown that K has an antihypertensive effect by promoting sodium excretion, while it is also attracting attention as an important component that can suppress hypertension associated with excessive sodium intake. Since most ingested K is excreted through the kidneys, decreased renal function is a major factor in increased serum levels, and target values for its intake according to the degree of renal dysfunction have been established. In older individuals with impaired renal function, not only hyperkalemia but also hypokalemia due to anorexia, K loss by dialysis, and effects of various drugs are likely to develop. Thus, it is necessary to pay attention to K management tailored to individual conditions. Since abnormalities in K metabolism can also cause lethal arrhythmia or sudden cardiac death, it is extremely important to monitor patients with a high risk of hyper- or hypokalemia and attempt to provide early and appropriate intervention.

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Section: Epidemiological Results Showing Serum K Levels In Patients With Ckdmentioning

confidence: 99%

Potassium Metabolism and Management in Patients with CKD

Yamada

Inaba²

2021

Nutrients

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“…The association between hyperuricemia and chronic kidney disease was also revealed by a nationwide, cross-sectional cohort study using data from the Japan Chronic Kidney Disease Database. Sofue and his colleagues had reported that the prevalence of hyperuricemia was associated with CKD stages 3b, 4, and 5 by using logistic regression analysis [ 43 ]. The animal models also supported this theory by demonstrating that hyperuricemia induced by a fructose-enriched diet, inhibiting uricase or deleting GLUT9 transporters, can result in vascular disease, metabolic syndrome, and glomerular and renal atherosclerosis [ 44 , 45 ].…”

Section: Hyperuricemia and Renal Diseasementioning

confidence: 99%

Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

Lee

Chen

et al. 2021

Diagnostics

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The relationship between hyperuricemia, gout, and renal disease has been investigated for several years. From the beginning, kidney disease has been considered a complication of gout; however, the viewpoints changed, claiming that hypertension and elevated uric acid (UA) levels are caused by decreased urate excretion in patients with renal impairment. To date, several examples of evidence support the role of hyperuricemia in cardiovascular or renal diseases. Several mechanisms have been identified that explain the relationship between hyperuricemia and chronic kidney disease, including the crystal effect, renin–angiotensin–aldosterone system activation, nitric oxide synthesis inhibition, and intracellular oxidative stress stimulation, and urate-lowering therapy (ULT) has been proven to reduce renal disease progression in the past few years. In this comprehensive review, the source and physiology of UA are introduced, and the mechanisms that explain the reciprocal relationship between hyperuricemia and kidney disease are reviewed. Lastly, current evidence supporting the use of ULT to postpone renal disease progression in patients with hyperuricemia and gout are summarized.

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“…In the current practice guideline, the information regarding whether, when and how to optimise serum UA level among patients with CKD remains undetermined. Meaningfully, the increasing evidence suggested a potential pathogenic role of serum UA in CKD progression 106 . It was reported that ULT could dramatically modify the course of renal disease in HU patients with CKD, and the risk of renal disease progression could be reduced by 69.4% with serum UA level less than 420 μmol/L 107 .…”

Section: Co‐morbidities and Management Strategiesmentioning

confidence: 99%

An update of genetics, co‐morbidities and management of hyperuricaemia

Zhu

Sun

Zhang

et al. 2021

Clin Exp Pharma Physio

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Hyperuricaemia (HU) caused by disorders of purine metabolism is a metabolic disease. A number of epidemiological reports have confirmed that HU is correlated with multiple disorders, such as chronic kidney diseases, cardiovascular disease and gout. Recent studies showed that the expression and functional changes of uric acid transporters, including URAT1, GLUT9 and ABCG2, were associated with HU. Moreover, a large number of genome‐wide association studies have shown that these transporters’ dysfunction leads to HU. In this review, we describe the recent progress of aetiology and related transporters of HU, and we also summarise the common co‐morbidities possible mechanisms, as well as the potential pharmacological and non‐pharmacological treatment methods for HU, aiming to provide new ideas for the treatment of HU.

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Prevalences of hyperuricemia and electrolyte abnormalities in patients with chronic kidney disease in Japan: A nationwide, cross-sectional cohort study using data from the Japan Chronic Kidney Disease Database (J-CKD-DB)

Abstract: Background The Japan Chronic Kidney Disease Database (J-CKD-DB) is a nationwide clinical database of patients with chronic kidney disease (CKD) based on electronic health records. The

Cited by 21 publications

References 40 publications

Potassium Metabolism and Management in Patients with CKD

Potassium Metabolism and Management in Patients with CKD

Hyperuricemia and Progression of Chronic Kidney Disease: A Review from Physiology and Pathogenesis to the Role of Urate-Lowering Therapy

An update of genetics, co‐morbidities and management of hyperuricaemia

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