Studies have shown that hyperuricemia is an independent risk factor affecting the prognosis of IgA nephropathy, and the risk of poor prognosis in patients with IgA nephropathy with hyperuricemia is 2.4 times higher than in those with normal blood uric acid levels. The incidence of hyperuricemia in patients with IgA nephropathy has been reported to be about 29% in all patients. Studies have shown that elevated serum creatinine, hypertriglyceridemia, hypertension, and obesity are risk factors independently associated with hyperuricemia, and reduced renal excretion of uric acid due to decreased renal function in patients with IgA nephropathy remains the main cause of hyperuricemia. /The incidence of intrarenal arteriosclerosis was also found to be 54.6% in patients with IgA nephropathy, higher than that of 26.6% in patients with non-IgA nephropathy (P<0.01)< span=""> and 46.1% in patients with membranous nephropathy (P<0.05)< span= "">. Intrarenal arteriopathy is independently associated with hyperuricemia, and intrarenal arteriopathy in patients with IgA nephropathy may be the cause of both hyperuricemia. It may also be a consequence of hyperuricemia. It has been suggested that renal ischemia not only impairs blood pressure regulation mechanisms, but also reduces urate clearance through the action of lactate due to local tissue hypoxia; therefore, renal ischemia caused by hypertension in patients with IgA nephropathy may be a cause of increased blood uric acid. It has also been shown that lowering blood triacylglycerol levels through a low-calorie diet can promote the renal uric acid excretion rate, suggesting the importance of abnormal lipid metabolism in the development of hyperuricemia in patients with IgA nephropathy. The possible mechanisms of renal damage caused by hyperuricemia are as follows: 1. Hyperuricemia causes glomerular hypertrophy: In one study, rats with hyperuricemia were found to have more pronounced glomerular hypertrophy and sclerosis and fibrosis. The main damage caused by hyperuric acid in rats with IgA nephropathy is glomerulosclerosis, tissue fibrosis and small arteriosclerosis, and the mechanism of damage seems to be related to small arteriopathy of the renal entry glomeruli. 2, blood uric acid damage to renal tubular-interstitial: blood uric acid is closely related to renal tubular atrophy in patients with IgA nephropathy. Some experiments found that rats with hyperuricemia IgA nephropathy had more severe renal interstitial lesions than the control group. It is now believed that hyperuricemia is more associated with tubular-interstitial damage in IgA nephropathy and less associated with glomerulosclerosis, and that blood uric acid levels are independently associated with tubular atrophy and interstitial fibrosis, respectively.