Hyperuricemia and chronic kidney disease: an enigma yet to be solved

Dousdampanis, Periklis; Trigka, Konstantina; Musso, Carlos G.; Fourtounas, Costas

doi:10.3109/0886022x.2014.947516

Cited by 43 publications

(53 citation statements)

References 145 publications

(170 reference statements)

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“…On the other hand, epidemiologic evidence and experimental models also have shown that hyperuricemia may impose detrimental effects as a prooxidant [89–92]. UA is often associated with other risk factors of CKD, including diabetes, hypertension, and inflammation [93], which makes it difficult to dissect the role of UA itself in the progression of CKD. However, a recent study showed an association between hyperuricemia and renal damage independently of hypertension and intrarenal renin-angiotensin system (RAS) activation [94].…”

Section: Nadph Oxidase and Hyperuricemia-related Kidney Diseasementioning

confidence: 99%

Role of NADPH Oxidase in Metabolic Disease‐Related Renal Injury: An Update

Wan

Zhang

2016

Oxidative Medicine and Cellular Longevity

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Metabolic syndrome has been linked to an increased risk of chronic kidney disease. The underlying pathogenesis of metabolic disease-related renal injury remains obscure. Accumulating evidence has shown that NADPH oxidase is a major source of intrarenal oxidative stress and is upregulated by metabolic factors leading to overproduction of ROS in podocytes, endothelial cells, and mesangial cells in glomeruli, which is closely associated with the initiation and progression of glomerular diseases. This review focuses on the role of NADPH oxidase-induced oxidative stress in the pathogenesis of metabolic disease-related renal injury. Understanding of the mechanism may help find potential therapeutic strategies.

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Section: Nadph Oxidase and Hyperuricemia-related Kidney Diseasementioning

confidence: 99%

Role of NADPH Oxidase in Metabolic Disease‐Related Renal Injury: An Update

Wan

Zhang

2016

Oxidative Medicine and Cellular Longevity

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“…This question was examined with a correlational, rather than temporally restricted design, because of circularity in associations of gout and kidney dysfunction as well as the duration of available claims data. Although CKD can lead to hyperuricemia (due to impaired uric acid excretion), more recently, it has been suggested that uric acid may, itself, contribute to the development and progression of CKD (4-7). Notably, a recent pilot study found that higher pre-donation serum uric acid was associated with larger GFR reductions at 6 months post-donation among women (15).…”

Section: Discussionmentioning

confidence: 99%

“…To complicate this association, elevated serum uric acid levels have been implicated as a risk factor for the development and progression of CKD (4-7). A recent systematic review and meta-analysis found that hyperuricemia was an independent predictor of newly diagnosed CKD in the non-CKD population (5).…”

Section: Introductionmentioning

confidence: 99%

Gout after Living Kidney Donation: Correlations with Demographic Traits and Renal Complications

et al. 2015

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Background: The demographic and clinical correlates of gout after living kidney donation are not well described. Methods: Using a unique database that integrates national registry identifiers of U.S. living kidney donors (1987-2007) with billing claims from a private health insurer (2000-2007), we identified post-donation gout based on medical diagnosis codes or pharmacy fills for gout therapies. The frequencies and demographic correlates of gout after donation were estimated by Cox regression with left- and right-censoring. We also compared the rates of renal diagnoses among donors with and without gout, matched in the ratio 1:3 by age, sex, and race. Results: The study sample of 4,650 donors included 13.1% African Americans. By seven years, African Americans were almost twice as likely to develop gout as Caucasian donors (4.4 vs. 2.4%; adjusted hazard ratio, aHR, 1.8; 95% confidence interval (CI) 1.0-3.2). Post-donation gout risk also increased with older age at donation (aHR per year 1.05) and was higher in men (aHR 2.80). Gout rates were similar in donors and age- and sex-matched general non-donors (rate ratio 0.86; 95% CI 0.66-1.13). Compared to matched donors without gout, donors with gout had more frequent renal diagnoses, reaching significance for acute kidney failure (rate ratio 12.5; 95% CI 1.5-107.0), chronic kidney disease (rate ratio 5.0; 95% CI 2.1-11.7), and other disorders of the kidney (rate ratio 2.2; 95% CI 1.2-4.2). Conclusion: Donor subgroups at increased risk of gout include African Americans, older donors, and men. Donors with gout have a higher burden of renal complications after demographic adjustment.

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“…The predictive value of UA in regard to the progression of CKD is matter of controversy [5]- [11]. Although a causal role of HU in CKD has not been estab- [35].…”

Section: Discussionmentioning

confidence: 99%

“…The impact of the serum uric acid (UA) on renal prognosis of CKD patients has recently been attracting attention [3], and our group has reported finding that the serum UA value can serve as a predictor of progression of kidney disease in biopsy-proven nephrosclerosis patients [4]. However, because the serum UA elevation due to the decreased renal UA clearance in CKD patients makes it difficult to assess the role of UA in the progression of CKD, the predictive value of UA in regard to the progression of CKD remains a matter of controversy [5]- [11].…”

Section: Introductionmentioning

confidence: 99%

Hyperuricemia as a Predictor of Progression of Chronic Kidney Disease: A Matched Cohort Analysis

Kamiyama¹,

Kataoka²,

Moriyama³

et al. 2017

IJCM

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Background: The clinical significance of uric acid (UA) in patients with chronic kidney disease (CKD) has never been elucidated in detail. Objectives: The aim of this study was to elucidate the predictive value of hyperuricemia (HU) in relation to kidney disease progression in CKD patients. Methods: We reviewed data obtained from 201 CKD patients. Renal outcome was assessed by performing the Kaplan-Meier and Cox proportional hazard regression models. The renal outcomes of CKD patients with and without HU were compared by using a propensity score-matched cohort. Results: The results of a multivariate Cox regression analysis showed that HU (UA ≥ 7.1 mg/dL) (P = 0.001), diabetes mellitus (P = 0.003), and a high urine albumin-to-creatinine ratio (P = 0.0005) were significantly associated with a ≥50% eGFR decline or ESRD. The serum UA values were positively correlated with mean blood pressure (P = 0.007), visceral fat area (P = 0.0003), and maximum carotid intima-media thickness (P = 0.0003). The Kaplan-Meier analysis in the propensity score-matched cohort indicated that the renal survival rate of the group of CKD patients with HU was significantly lower than that of the group without HU (log rank, P < 0.0001), even after complete adjustment for the eGFR.Conclusion: The results of this study suggest that the serum UA value is a predictor of CKD progression.

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Hyperuricemia and chronic kidney disease: an enigma yet to be solved

Cited by 43 publications

References 145 publications

Role of NADPH Oxidase in Metabolic Disease‐Related Renal Injury: An Update

Role of NADPH Oxidase in Metabolic Disease‐Related Renal Injury: An Update

Gout after Living Kidney Donation: Correlations with Demographic Traits and Renal Complications

Hyperuricemia as a Predictor of Progression of Chronic Kidney Disease: A Matched Cohort Analysis

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