Polycystic kidney is a congenital genetic disorder that involves both kidneys. Unlike multiple cysts in the kidneys, its kidneys are filled with vesicles of different sizes that can communicate with each other, making the kidneys gradually increase in size and compress the renal parenchyma, causing them to atrophy and cause functional impairment until chronic renal failure. There are two types of polycystic kidney: infantile type is chromosomal recessive, often accompanied by other congenital malformations, most of them die within a few months, which is rare clinically; adult type is chromosomal dominant, most of them develop in middle age, accompanied by other organs, such as liver, spleen, pancreas, ovaries, bone and other polycystic lesions. If both parents have the disease, the incidence of children increases to 75%; children who do not have the disease do not carry the polycystic kidney gene, and their next generation (grandchildren) will not develop the disease. Adult type polycystic kidney usually has cysts at birth, but they are small and not easy to detect, and generally not easy to detect before 20 years old, but if there are cases of polycystic kidney in the family, they should be checked early and followed up regularly. 30-40 years old, the cysts grow faster, and it can be seen that both kidneys are covered with cysts of different sizes, ranging from several millimeters to several centimeters in diameter, with urine-like fluid inside the cysts. At this time patients will present with different clinical manifestations. The common ones are: persistent or paroxysmal lumbar and abdominal pain, aggravated by exertion; intermittent carnal hematuria; abdominal masses of different sizes felt; hypertension with headache and dizziness; urinary tract infection symptoms such as urinary frequency and urgency; poor appetite, nausea, vomiting and other manifestations of renal insufficiency. Urinary tract X-ray, ultrasound, CT, MRI and other examinations help in diagnosis, and renal isotope examination helps to assess the degree of kidney damage. There is no effective curative therapy, clinical treatment mainly lies in active treatment and early prevention of the occurrence and development of complications to protect the residual renal function and avoid further damage to renal function. As long as the correct and reasonable treatment can be received, the clinical symptoms and renal function of most patients can be controlled or improved, making the condition relatively stable. 1, general treatment: most patients do not need to change their lifestyle and restrict activities, but the diet needs to be controlled, such as low salt and low fat diet, reduce the consumption of animal offal, high protein foods (beans), alcoholic beverages, etc.; drink more water, eat a diet rich in vitamins and vegetable crude fiber, and keep the bowels open. Actively control hypertension, timely treatment of urinary tract infection, and in the process of medication, attention should be paid to avoid the nephrotoxic effects of drugs. 2.Cyst depanalization and decompression surgery: the surgery can reduce the compression of cyst on kidney parenchyma, so that some kidney function units can be restored and the development of the disease can be delayed. Cyst decompression must be thorough without giving up the decompression of small cysts and deep cysts. Both sides should be operated, and the interval between bilateral operations is usually more than six months. Late stage disease such as renal function impairment in azotemia, uremia stage, whether or not combined with hypertension, decompression treatment is meaningless, surgery can aggravate the condition. 3, dialysis and transplantation: when entering end-stage renal failure, should be immediately treated with dialysis, preferably hemodialysis. When the time is right, kidney transplantation can be considered.