Abstract
Hyperuricemia is an important risk factor of chronic kidney disease, metabolic syndrome and cardiovascular disease. We aimed to assess the time-feature relationship of hyperuricemia mouse model on uric acid excretion and renal function. A hyperuricemia mouse model was established by potassium oxonate (PO) and adenine for 21 days. Ultra Performance Liquid Chromatography was used to determine plasma uric acid level. Hematoxylin-eosin staining was applied to observe kidney pathological changes, and Western blot was used to detect renal urate transporters’ expression. In hyperuricemia mice, plasma uric acid level increased significantly from the 3rd day, and tended to be stable from the 7th day, and the clearance rate of uric acid decreased greatly from the 3rd day. Further study found that the renal organ of hyperuricemia mice showed slight damage from the 3rd day, and significantly deteriorated renal function from the 10th day. In addition, the expression levels of GLUT9 and URAT1 were upregulated from the 3rd day, while ABCG2 and OAT1 were downregulated from the 3rd day, and NPT1 were downregulated from the 7th day in hyperuricemia mice kidney. This paper presents a method suitable for experimental hyperuricemia mouse model, and shows the time-feature of each index in a hyperuricemia mice model.
Highlights
With the improvement in people’s living standard and the change in diet structure, the incidence of hyperuricemia is increasing
Hyperuricemia can lead to uric acid deposition in renal tissue, leading to acute kidney injury (AKI)
We investigated the time-features of hyperuricemia mice which were induced by potassium oxonate (PO) combined with adenine for 21 days, especially the effects on renal injury and expression of uric acid transporter
Summary
With the improvement in people’s living standard and the change in diet structure, the incidence of hyperuricemia is increasing. A large number of clinical research results show that hyperuricemia is closely related to cardiovascular disease, immune system disorders, chronic renal failure [1,2]. Hyperuricemia can lead to uric acid deposition in renal tissue, leading to acute kidney injury (AKI). AKI is diagnosed based on a dynamic increase in serum creatinine and decreased urine output. Serum cystatin C and serum or urine neutrophil gelatinase-associated lipocalin (NGAL) have been shown to predict or diagnose AKI [4]. Urine kidney injury molecule 1 (KIM-1), urine transferrin, albuminuria, circulating angiopoietin-2, L-FABP, vanin-1, and IgG are important predictors [5,6,7,8,9,10,11]
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