Hyperuricemia is a metabolic disease caused by excessive production or reduced excretion of uric acid, and its incidence is increasing year by year. Hyperuricemia is closely associated with gout and renal dysfunction. Traditionally, hyperuricemia has often been regarded merely as a marker of renal function decline. Recent studies have shown that hyperuricemia plays an important role in the occurrence and progression of kidney diseases and is an independent risk factor. Animal models of uric acid nephropathy induced by hyperuricemia provide a basis for investigating the relationship between hyperuricemia and uric acid nephropathy, as well as for the screening and efficacy evaluation of uric acid-lowering drugs. At present, there are many modeling methods for inducing animal models of hyperuricemia. The modeling mechanisms generally include supplementation with exogenous uric acid and uric acid precursors (such as xanthine, hypoxanthine, adenine) or purine-rich substances (yeast), fructose, inhibition of uricase activity (oxonic acid, potassium oxonate), and inhibition of renal uric acid excretion (such as ethambutol, nicotinic acid). Establishing a rational animal model is fundamental for studying disease pathogenesis and screening and evaluating drug efficacy. Therefore, the selection of an appropriate animal model is crucial for research on related diseases.

SD rats (male, weighing 180–220 g)
Modeling method: intragastric administration of uric acid and potassium oxonate for 4 consecutive weeks.
Positive drug: allopurinol
Evaluation indicators: HE staining, Masson staining, glomerular filtration rate and serum biochemical assay

HE staining of renal tissue

Masson staining of renal tissue

Glomerular filtration rate and serum biochemical assay