With the improvement of people’s living standard, the number of patients with diabetes combined with hyperuricemia has been increasing in recent years, people’s awareness of diabetes is increasing, and people are increasingly alert to the hazards of diabetes, but diabetes is still far from reaching a better control goal, which leads to chronic complications of diabetes also quietly arising in subtle ways. If combined with hyperuricemia, many patients have not paid enough attention to the control of diet and the application of uric acid-lowering drugs, and once kidney failure occurs, they still attribute the culprit to diabetes, but in fact, hyperuricemia is more harmful to kidney function than diabetes. Uric acid is mainly deposited in the renal interstitium and tubules. The tubular epithelium atrophies and degenerates and impairs tubular function, and patients often have increased nocturia, polyuria, and decreased specific gravity of urine. The interstitial kidney may develop edema and inflammatory reaction, and even fibrosis, which is clinically called interstitial nephritis. Small amounts of proteinuria, microscopic or meatus hematuria, swelling, and moderate hypertension may be seen clinically. Renal damage caused by hyperuricemia is quite common, and uric acid-induced renal damage can manifest itself in three types, namely chronic uric acid nephropathy, uric acid nephrolithiasis and acute uric acid nephropathy, which may overlap with each other. Under microscopic observation, 100% of gout patients have chronic kidney damage, which is mainly caused by the deposition of urate crystals in the kidney tissue and obstruction of the renal tubules by urate crystals. Excessive uric acid crystals blocking the renal tubules can lead to acute renal failure, so we can lower uric acid and blood sugar at the same time, a two-pronged approach.