In the whole process of chronic kidney disease (CKD), even if the primary disease is the same, different patients will have different rates of disease progression, and their renal function is affected by many factors, some of which are controllable in our clinical practice and are the focus of our attention in the treatment and management of chronic kidney disease. Firstly, patients with early stage chronic kidney disease should be treated aggressively according to renal pathology and clinical conditions, which is one of the main factors affecting the course of chronic kidney disease. Secondly, hypertension needs to be treated aggressively. Hypertension is prevalent in CKD stages 1-5 and is a major complication of CKD. Hypertension can both accelerate the deterioration of renal function and is a major risk factor for cardiovascular disease in CKD patients. Proper and aggressive treatment of hypertension can stop or delay the deterioration of renal function and reduce the incidence of cardiovascular and cerebrovascular complications and mortality. For patients with urine protein <1 g/day, the target value for blood pressure lowering is below 130/80 mmHg, and if urine protein >1 g/day, blood pressure should be controlled to below 125/75 mmHg. In order to control blood pressure, attention must be paid to the combination of general treatment such as low salt diet, weight control and anxiety reduction with pharmacological treatment. Clinically, one or more antihypertensive drugs should be used in combination to achieve the target blood pressure according to the etiology of CKD, concomitant diseases, renal function and the characteristics, indications and major adverse effects of various antihypertensive drugs. Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor antagonists (ARB), in addition to antihypertensive effect, also have the function of reducing urinary protein in CKD patients, delaying renal decompensation and reducing cardiovascular and cerebrovascular complications in CKD patients, and have been confirmed by many clinical studies to have good renal protective effect. These two types of drugs can be safely used in most patients with CKD, but changes in renal function and electrolytes need to be monitored, and should be used with caution or disabled when renal function is impaired to a certain extent or when hyperkalemia occurs. Lowering urine protein is also beneficial in slowing the progression of kidney disease and reducing the risk of cardiovascular disease. Depending on each patient, different treatments to lower urinary protein may be used, such as glucocorticoids, various immunosuppressants, ACEI, ARB, etc. Prevention of infection is also important for patients with CKD. Since infection can accelerate the deterioration of renal function, respiratory tract infection, acute gastroenteritis, skin pustulosis, urinary tract infection, etc. should be actively prevented. Once infection occurs, it should be controlled by choosing sensitive antibiotics in time. Avoid the use of nephrotoxic drugs. Various antipyretic and analgesic drugs, aminoglycoside antibiotics, and Chinese medicines containing aristolochic acid, such as guanxi and antifungal, may cause renal damage and should be avoided. It is important to avoid exertion, avoid over-activity and improve immunity. A low protein diet should be given to patients with CKD who develop abnormal renal function. According to the recommendations of the American Kidney Disease Foundation guidelines, low protein diet therapy should be implemented when the glomerular filtration rate (GFR) is <60 ml/min. A low-protein diet not only improves complications such as hyperphosphatemia, but also effectively delays the progression of renal function. Correction of metabolic acidosis. Patients with the presence of acidosis can be treated with 1-3 g of oral sodium bicarbonate daily in 3 divided doses. Bicarbonate below 15 mmol/L should be infused intravenously with sodium bicarbonate, depending on clinical symptoms. Correction of anemia. Anemia is a common complication of CKD. Anemia affects the supply and utilization of tissue oxygen and increases cardiac output, often manifesting fatigue and dyspnea, leading to a series of pathophysiological phenomena such as heart enlargement, ventricular hypertrophy, angina pectoris, heart failure, cerebral insufficiency of blood supply, cognitive decline, and immune function impairment, which seriously affect the prognosis and quality of survival of patients. Anemia can be effectively treated with recombinant human erythropoietin, iron and folic acid supplementation. The currently recommended target value for anemia treatment is hemoglobin 110-120 g/L. Control of hyperphosphatemia: (1) Reduce dietary phosphorus intake, daily intake should be limited to less than 800-1000 mg/d. (2) For hyperphosphatemia that cannot be controlled by dietary restriction a phosphorus binding agent, such as calcium carbonate, should be reasonably used and should be taken with meals. Treatment of secondary hyperparathyroidism (SHPT): Active vitamin D should be reasonably applied according to blood whole segment parathyroid hormone (iPTH) levels. iPTH, calcium and phosphorus levels should be closely monitored during application and drug doses should be adjusted. patients with CKD stages 3, 4 and 5 with plasma iPTH exceeding the corresponding target range (CKD stage 3 > 70 pg/ml, CKD stage 4 > 110pg/ml, CKD stage 5 > 300pg/ml), active vitamin D preparations need to be given. Abnormal calcium and phosphorus levels must be corrected before active vitamin D treatment so that Ca×P < 55 mg2/dl2. Small daily doses of continuous therapy can be used for patients with mild SHPT, and high doses of intermittent therapy (shock therapy) can be used for patients with moderate to severe SHPT. It is best to take it at bedtime.