Chronic kidney disease has become a global public health problem. The International Society of Nephrology predicts that one in ten people worldwide will suffer from chronic kidney disease, and about 36 million people worldwide are expected to die from chronic kidney disease and its resulting cardiovascular diseases in 2015, and chronic kidney disease has become another important disease threatening human health after cardiovascular disease, tumor and diabetes. However, chronic kidney disease is not well taken care of in the world. How to detect chronic kidney disease at an early stage and give active prevention and treatment is a difficult problem for everyone at present. The traditional indicators for monitoring kidney function impairment include serum creatinine and urea nitrogen, in addition to urine routine and other tests. However, when renal function is only mildly impaired, serum urea nitrogen may not change, and if urea nitrogen is higher than normal, it means that 60% to 70% of effective kidney units have been damaged; only when glomerular filtration function decreases to 1/3 of normal, serum creatinine rises significantly. Further clinical findings show that the determination of blood creatinine level is affected by various factors such as protein intake and body weight, and fluctuates greatly. Therefore, it is believed that the sensitivity and accuracy of blood creatinine and urea nitrogen are poor, and it is not ideal to use the measurement of blood creatinine and urea nitrogen as an indicator to determine a person’s kidney function. Cystatin C (also known as cystatin inhibitor C) is a small molecular weight protein discovered in recent years and is a member of the cysteine protease inhibitor superfamily, which can be produced by all nucleated cells in the body. The rate of cystatin C production in the body is fairly constant and is usually unaffected by changes in age, sex, body weight and diet of the subject. Furthermore, because cystatin C is a low molecular weight protein that is freely filtered by the glomerulus and is reabsorbed and degraded in the proximal tubule, the kidney is the only organ that removes cystatin C from the circulation. Serum cystatin C concentration is mainly determined by the glomerular filtration rate GFR (commonly referred to as renal function), which makes cystatin C an ideal endogenous marker of GFR changes. Elevated serum cystatin C levels are associated with reduced renal excretion, suggesting impaired renal function in the subject. In summary, circulating cystatin C is cleared only by glomerular filtration and is an ideal indicator of changes in glomerular filtration function.