A novel mouse model of hyperuricemia and gouty nephropathy

Guan, Jian; Huang, Xiaojun; Dong, Jiale; Lu, Huimin; Lin, Yuewei; Liu, Mei; Yi, Zhibiao; Wu, Li‐Min; Huang, Yingqi; Lan, Tian

doi:10.1097/cm9.0000000000000964

Cited by 9 publications

(5 citation statements)

References 5 publications

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“…This regimen was continued for the next seven days. 11,12 For sample collection, light anesthesia was given to rats and an intracardiac puncture was performed on day zero and also on the last day of the experiment i.e. on day seven.…”

Section: Methodsmentioning

confidence: 99%

Effect of Apium Graveolens (Celery) Seed Extract on Serum Uric Acid Level of Hyperuricemic Rats and its Comparison with Allopurinol

Karim

bhatti

Akhtar

et al. 2021

J Shalamar Med Dent Coll

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Background: Plant derived medicines are widely used in traditional culture all over the world. Objectives: To determine the effect of Celery Seed Extract (CSE) on uric acid levels in hyperuricemic rats and to compare the effect of allopurinol and CSE. Methods: It was an animal experimental research study. Group A served as negative control whereas Group B served as positive control. CSE was given orally to three groups of rats (C, D, and E). One hour prior to administration of CSE; potassium oxonate was injected intraperitoneally in all groups except negative control to induce hyperuricemia. Similarly, group F was given allopurinol one hour after injection of potassium oxonate. Blood samples were collected for uric acid estimation. Results: It was found that administration of both CSE (group C, D, E) and allopurinol (group F) significantly lowered serum uric acid levels (p<0.001) as compared to positive control (group B). Serum uric acid lowering effect of both drugs CSE and allopurinol was found to be statistically significant on day 3rd and day 7th and was almost comparable. Conclusions: Celery seed extract significantly reduces serum uric acid levels in potassium oxonate-induced hyperuricemic rats and its uric acid lowering effect was comparable with that of allopurinol.

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Section: Methodsmentioning

confidence: 99%

Effect of Apium Graveolens (Celery) Seed Extract on Serum Uric Acid Level of Hyperuricemic Rats and its Comparison with Allopurinol

Karim

bhatti

Akhtar

et al. 2021

J Shalamar Med Dent Coll

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“…At 21 days, uric acid, urea nitrogen, and creatinine concentrations increased, and renal tubular detachment and necrosis were observed in the kidneys. In the study by Guan et al ( 70 ), selected male C57BL/6J mice to establish a model of gouty nephropathy by gavage of adenine + potassium oxalate (100 + 500 mg/kg) for 3 weeks. The key manifestation was increased serum uric acid level and significant renal damage.…”

Section: In Vitro and In Vivo Models Of Gnmentioning

confidence: 99%

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

Wang,

Zhang,

Shen

et al. 2024

Front. Med.

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Gouty nephropathy (GN) is a metabolic disease with persistently elevated blood uric acid levels. The main manifestations of GN are crystalline kidney stones, chronic interstitial nephritis, and renal fibrosis. Understanding the mechanism of the occurrence and development of GN is crucial to the development of new drugs for prevention and treatment of GN. Currently, most studies exploring the pathogenesis of GN are primarily based on animal and cell models. Numerous studies have shown that inflammation, oxidative stress, and programmed cell death mediated by uric acid and sodium urate are involved in the pathogenesis of GN. In this article, we first review the mechanisms underlying the abnormal intrinsic immune activation and programmed cell death in GN and then describe the characteristics and methods used to develop animal and cell models of GN caused by elevated uric acid and deposited sodium urate crystals. Finally, we propose potential animal models for GN caused by abnormally high uric acid levels, thereby provide a reference for further investigating the methods and mechanisms of GN and developing better prevention and treatment strategies.

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“…However, after 36 and 52 weeks of hyperuricemia, the kidneys showed a predominantly interstitial mononuclear cell infiltrate around regenerated tubules, interstitial fibrosis, infrequent renal tophi and renal stones, with no evidence of glomerular or vascular abnormalities and no gross evidence of renal failure. A mouse model of intragastric administration of oxonic acid and adenosine (a precursor to uric acid) was recently used to reproduce this model of acute gouty nephropathy [53].…”

Section: Inhibition Of Xo By Oxonatementioning

confidence: 99%

The Gouty Kidney: A Reappraisal

Bardin

Letavernier

Corréas

2023

GUCDD

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This review re-examines the role of crystal deposition in the kidney in view of recent clinical and experimental findings. The involvement of the renal system in gout seems frequent. Indeed, recent studies showed that approximately 25% of patients with gout experience renal failure, defined by estimated glomerular filtration rate <60 mL/min/1.73 m2. The pathophysiology is complex and involves several factors, their respective roles being difficult to dissect. The role of crystal deposition in the kidney was the first suspected, and the concept of gouty microcrystalline nephropathy, also called gouty nephropathy, has been popular, supported by early autopsy studies demonstrating uric acid and urate crystal deposition in the renal medulla of patients with gout, together with features of tubulointerstitial nephritis. Crystal deposition was first considered an important source of renal involvement in gout. After the introduction of urate-lowering drugs and the performance of kidney biopsies, which mainly involved the renal cortex and did not reveal much crystal deposition but rather vascular changes, this concept has been criticized and even dismissed. Thereafter, kidney involvement in gout was considered mainly vascular, related to hypertension and associated comorbidities and later to hyperuricemia. The toxic effects of non-steroidal anti-inflammatory drugs is also an important factor. Modern imaging, especially renal ultrasonography, allows for atraumatic exploration of the kidney and has revealed hyperechogenicity of the renal medulla, suggesting crystalline deposits, in approximately one-third of patients with tophaceous gout. Experimental models of gouty nephropathy have recently demonstrated the pathogenic role of microcrystal deposition in the collecting ducts and parenchyma of the renal medulla. Taken together, these recent findings lead to the re-examination of the pathogenic role of crystal deposition in the renal medulla and testing the effect of urate-lowering drugs on renal features of gouty patients with evidence of renal crystal deposition.

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A novel mouse model of hyperuricemia and gouty nephropathy

Cited by 9 publications

References 5 publications

Effect of Apium Graveolens (Celery) Seed Extract on Serum Uric Acid Level of Hyperuricemic Rats and its Comparison with Allopurinol

Effect of Apium Graveolens (Celery) Seed Extract on Serum Uric Acid Level of Hyperuricemic Rats and its Comparison with Allopurinol

Models of gouty nephropathy: exploring disease mechanisms and identifying potential therapeutic targets

The Gouty Kidney: A Reappraisal

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