The increase of blood creatinine and urea nitrogen in renal function does not necessarily mean renal insufficiency, which is affected by many factors. The amount of muscle tissue and metabolic status are the main extra-renal factors affecting blood creatinine; muscle metabolism is reduced in patients with muscular dystrophy disease, protein synthesis is increased in pregnant women, creatinine production is reduced, and blood creatinine may be slightly lower; fever, etc. may cause enhanced catabolism, resulting in increased blood creatinine; a high-protein diet may cause transient increases in blood creatinine. The amount of dietary protein, gastrointestinal bleeding, high catabolism, prerenal factors, and cardiac insufficiency are the main extrarenal factors affecting the blood urea nitrogen level. Under normal conditions, renal tubular reabsorption of urea nitrogen is about 30%-40%, and a small amount of urea nitrogen is excreted. When dehydration, blood volume deficiency, or heart failure occurs, renal blood flow decreases, renal tubular reabsorption is enhanced, urea nitrogen reabsorption increases, and blood urea nitrogen concentration rises, which is prerenal azotemia; high protein diet, gastrointestinal bleeding, and high catabolism such as fever increase urea nitrogen production in the body, and blood urea nitrogen The blood urea nitrogen is elevated. Therefore, elevated blood urea nitrogen and creatinine do not necessarily indicate impaired glomerular function, but should be combined with the clinical situation.