There are many factors that affect stone formation; age, gender, race, genetics, environmental factors, dietary habits and occupation have a strong influence on stone formation. Abnormalities in the body’s metabolism, obstruction of the urinary tract, infections, foreign bodies, and drug use are common causes of stone formation. Attention to these problems can reduce stone formation and recurrence. (A) Metabolic abnormalities 1, urine acidity and alkalinity. 2, hypercalcemia caused by hypercalcemia of common diseases including hyperparathyroidism, lacto-monobasic syndrome, nodular disease or sarcoidosis, vitamin D toxicity, malignant tumors, cortisol increase, hyperthyroidism, pheochromocytoma, adrenal insufficiency, taking thiazide diuretics, acute tubular necrosis recovery, multiple myeloma, hypothyroidism, and vitamin A toxicity, etc.. 3.Hypercalciuria primary hypercalciuria is divided into 3 types: absorptive hypercalciuria, renal hypercalciuria and resorptive hypercalciuria. In addition, some metabolic diseases with clear etiology can also cause secondary hypercalciuria and the formation of calcium-containing stones in the urinary tract, such as distal renal tubular acidosis, tuberculosis, prolonged bed-ridden, bone Page-t disease, glucocorticoid excess, hyperthyroidism, and vitamin D toxicity. Among them, about 0,5% to 3% of patients with urinary tract calcium-containing stones are accompanied by the presence of distal renal tubular acidosis. 4, hyperoxaluria primary hyperoxaluria [type I for ethanolic aciduria (glycolicaciduria), type II for glyceric aciduria (glycericaciduria)] is rare. Causes of secondary hyperoxaluria include excessive intake of VitC, excessive intake of dietary oxalic acid and its precursors, decreased intake of dietary calcium, enterogenic hyperoxaluria, and VitB6 deficiency. A common cause of increased urinary oxalate is increased absorption of enteric-derived oxalate and its precursors. On the other hand, hyperoxaluria associated with disturbances in bile acid metabolism and excessive water loss can also occur after small bowel resection or short circuit surgery, steatorrhea, or Crohn’s disease. In addition, it has been suggested that patients with hyperoxaluria have a reduced number of oxalobacteria (O, formigenes) in the intestine. 5, Hyperuricosuria. 6, Cystinuria. 7, Hypocitraturia. 8, Hypomagnesiuria. (B) Local etiology Urinary tract obstruction, infection and the presence of foreign bodies in the urinary tract are the main local factors inducing stone formation. Obstruction can lead to infection and stone formation, while stones themselves are foreign bodies in the urinary tract, the latter of which aggravate the degree of obstruction and infection. Clinical obstructive diseases that tend to cause stone formation in the urinary tract include two major categories: mechanical obstruction and kinetic obstruction. Among them, pyelo-ureteral junction stenosis, bladder neck stenosis, sponge kidney, renal ureteral malformation, bulging ureteral orifice, renal cyst, calyceal diverticulum, and horseshoe kidney are common mechanical obstructive diseases. In addition, intrarenal type of renal pelvis and calyceal neck stenosis can cause urine retention, which can induce renal stone formation. Neurogenic bladder and congenital megaureter are power obstruction diseases, the latter two can also cause urine retention and promote stone formation. (C) drug-related factors drug-induced kidney stones accounted for 1% to 2% of all stones, divided into 2 categories: a class of high concentration in the urine and the solubility of drugs is relatively low, including aminopterin (triamterene), the treatment of HIV infection (such as indinavir indinaVir), magnesium silicate and sulfonamides, etc., the drugs themselves are the components of the stone. Another group of drugs that can induce stone formation include acetazolamide, VitD, VitC, and corticosteroids, which are metabolized in a way that leads to the formation of other constituent stones.