Hyperuricemia in Kidney Disease: A Major Risk Factor for Cardiovascular Events, Vascular Calcification, and Renal Damage

Ejaz, A. Ahsan; Nakagawa, Takahiko; Kanbay, Mehmet; Kuwabara, Masanari; Kumar, Ada; Arroyo, Fernando Enrique García; Roncal-Jiménez, Carlos A.; Sasai, Fumihiko; Kang, Duk‐Hee; Jensen, Thomas; Hernando, Ana Andres; Rodríguez‐Iturbe, Bernardo; García, Gabriela; Tolan, Dean R.; Sánchez‐Lozada, Laura G.; Lanaspa, Miguel A.; Johnson, Richard J.

doi:10.1016/j.semnephrol.2020.12.004

Cited by 68 publications

(46 citation statements)

References 132 publications

(155 reference statements)

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“…For recombinant and pegylated uricases, other available options for lowering serum uric acid are limited only by parenteral infusion and, presenting an addition, the possibility of producing antidrug antibodies [ 91 ].…”

Section: Available Treatment Option For Lowering Uric Acidmentioning

confidence: 99%

Uric Acid and Oxidative Stress—Relationship with Cardiovascular, Metabolic, and Renal Impairment

Gherghina

Peride

Ţigliş

et al. 2022

IJMS

179

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Background: The connection between uric acid (UA) and renal impairment is well known due to the urate capacity to precipitate within the tubules or extra-renal system. Emerging studies allege a new hypothesis concerning UA and renal impairment involving a pro-inflammatory status, endothelial dysfunction, and excessive activation of renin–angiotensin–aldosterone system (RAAS). Additionally, hyperuricemia associated with oxidative stress is incriminated in DNA damage, oxidations, inflammatory cytokine production, and even cell apoptosis. There is also increasing evidence regarding the association of hyperuricemia with chronic kidney disease (CKD), cardiovascular disease, and metabolic syndrome or diabetes mellitus. Conclusions: Important aspects need to be clarified regarding hyperuricemia predisposition to oxidative stress and its effects in order to initiate the proper treatment to determine the optimal maintenance of UA level, improving patients’ long-term prognosis and their quality of life.

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Section: Available Treatment Option For Lowering Uric Acidmentioning

confidence: 99%

Uric Acid and Oxidative Stress—Relationship with Cardiovascular, Metabolic, and Renal Impairment

Gherghina

Peride

Ţigliş

et al. 2022

IJMS

179

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“…It is well known that uric acid levels rise as kidney function decreases; however, there is controversy as to whether hyperuricemia directly worsens kidney function [ 71 , 72 ]. Although there is no consistent recommendation regarding the treatment of asymptomatic hyperuricemia in CKD patients, most Korean physicians treat asymptomatic hyperuricemia in CKD patients to prevent CKD progression and cerebrocardiovascular complications [ 73 ].…”

Section: Treatmentmentioning

confidence: 99%

Clinical and genetic characteristics of Korean autosomal dominant polycystic kidney disease patients

Park

Ryu

et al. 2021

Korean J Intern Med

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease. It is characterized by cyst growth in the kidneys, resulting in kidney enlargement and end-stage kidney disease. The polycystic kidney disease 1 (PKD1) and PKD2 have been identified as genes related to ADPKD and their significance in the molecular pathology of the disease has been studied. A disease-modifying drug has been approved; therefore, it has become important to identify patients at a high risk of kidney disease progression. Genetic tests, image analysis methods, and clinical factors for kidney disease progression prediction have been established. This review describes genetic and clinical characteristics, and discusses ongoing studies in Korean ADPKD patients.

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“…In addition, gout nephropathy, a form of chronic tubulointerstitial nephritis, induced by the deposition of urate precipitates in the distal collecting ducts and the medullary interstitium may cause progressive chronic kidney disease [4]. Furthermore, gout and hyperuricemia have been associated with a subset of comorbidities including metabolic syndrome, diabetes, hypertension as well as cardiovascular and cerebrovascular disease [5][6][7][8][9][10][11][12][13]. In most patients, the onset of gout occurs after the age of 60, with the incidence being about three times higher in men than in women [14].…”

Section: Introductionmentioning

confidence: 99%

The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update

Eckenstaler

Benndorf

2021

IJMS

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Urate homeostasis in humans is a complex and highly heritable process that involves i.e., metabolic urate biosynthesis, renal urate reabsorption, as well as renal and extrarenal urate excretion. Importantly, disturbances in urate excretion are a common cause of hyperuricemia and gout. The majority of urate is eliminated by glomerular filtration in the kidney followed by an, as yet, not fully elucidated interplay of multiple transporters involved in the reabsorption or excretion of urate in the succeeding segments of the nephron. In this context, genome-wide association studies and subsequent functional analyses have identified the ATP-binding cassette (ABC) transporter ABCG2 as an important urate transporter and have highlighted the role of single nucleotide polymorphisms (SNPs) in the pathogenesis of reduced cellular urate efflux, hyperuricemia, and early-onset gout. Recent publications also suggest that ABCG2 is particularly involved in intestinal urate elimination and thus may represent an interesting new target for pharmacotherapeutic intervention in hyperuricemia and gout. In this review, we specifically address the involvement of ABCG2 in renal and extrarenal urate elimination. In addition, we will shed light on newly identified polymorphisms in ABCG2 associated with early-onset gout.

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Hyperuricemia in Kidney Disease: A Major Risk Factor for Cardiovascular Events, Vascular Calcification, and Renal Damage

Cited by 68 publications

References 132 publications

Uric Acid and Oxidative Stress—Relationship with Cardiovascular, Metabolic, and Renal Impairment

Uric Acid and Oxidative Stress—Relationship with Cardiovascular, Metabolic, and Renal Impairment

Clinical and genetic characteristics of Korean autosomal dominant polycystic kidney disease patients

The Role of ABCG2 in the Pathogenesis of Primary Hyperuricemia and Gout—An Update

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