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Identification of three distinct cell populations for urate excretion in human kidneys.
J Physiol Sci
January 2025
Department of Future Basic Medicine, Nara Medical University, Kashihara, Nara, Japan; V-iCliniX Laboratory, Nara Medical University, Kashihara, Nara, Japan. Electronic address:
In humans, uric acid is an end-product of purine metabolism. Urate excretion from the human kidney is tightly regulated by reabsorption and secretion. At least eleven genes have been identified as human renal urate transporters.
View Article and Find Full Text PDFThe Gut Microbiome in Hyperuricemia and Gout.
Arthritis Rheumatol
January 2025
Assistant Professor of Pathology and of Microbiology and Microbiology and Immunology, Stanford University, Stanford, CA, 94305.
Humans develop hyperuricemia via decreased urate elimination and excess urate production, consequently promoting monosodium urate crystal deposition and incident gout. Normally, approximately two thirds of urate elimination is renal. However, chronic kidney disease (CKD) and other causes of decreased renal urate elimination drive hyperuricemia in most with gout.
View Article and Find Full Text PDFSpatiotemporal landscape of kidney in a mouse model of hyperuricemia at single-cell level.
FASEB J
January 2025
Department of Internal Medicine, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Serum uric acid is an end-product of purine metabolism. Uric acid concentrations in excess of the physiological range may lead to diseases such as gout, cardiovascular disease, and kidney injury. The kidney includes a variety of cell types with specialized functions such as fluid and electrolyte homeostasis, detoxification, and endocrine functions.
View Article and Find Full Text PDFInpatient management of gout: we are still failing.
J Rheumatol
January 2025
LKS: Rheumatologist, MBChB, FRACP, PhD, Department of Rheumatology, Immunology and Allergy, Rheumatology Registrar Te Whatu Ora Waitaha, New Zealand and Department of Medicine, University of Otago Christchurch, Christchurch, New Zealand.
Objective: Despite effective treatment, gout is poorly managed. The aim of this study was to determine rates of serum urate (SU) testing and allopurinol dose adjustment in patients on allopurinol admitted to Christchurch based hospitals.
Methods: The hospital electronic prescribing and administration (ePA) system was used to identify patients on allopurinol during hospital admissions from March 2016-March 2023.
Association between urate-lowering therapy and kidney failure in patients with chronic kidney disease.
J Nephrol
January 2025
Pharmacoepidemiology Unit, Department of Clinical Pharmacology, Amiens-Picardie University Medical Center, CHU Amiens-Picardie, Rond-Point du Professeur Christian Cabrol, 80054, Amiens Cedex, France.
Background: Hyperuricemia is a hallmark of gout and a suspected risk factor for the progression of chronic kidney disease (CKD). However, the impact of urate-lowering therapy on CKD progression is subject to debate. The objective of the present study was to describe the prevalence of inappropriate urate-lowering therapy prescriptions and evaluate the association between urate-lowering therapy prescription and the progression of kidney disease in patients with CKD.
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