Kidney stone disease

　　1. Factors leading to formation:The formation process of kidney stones involves certain factors that cause the concentration of crystal substances in urine to increase and solubility to decrease, resulting in an oversaturated state. Crystals are precipitated and grow and aggregate locally, eventually forming kidney stones. In this process, the formation of an oversaturated state of crystal substances in urine and the reduction of inhibitors of crystal formation in urine are the two most important factors.

　　1. Formation of supersaturated state:It is seen in: ① insufficient urine volume; ② excessive absolute excretion of certain substances in urine, such as calcium, oxalic acid, uric acid, cysteine, and phosphates; ③ changes in urine pH. When urine pH decreases (＜5.5), the saturation of uric acid in urine increases, and when urine pH increases, the saturation of calcium phosphate, magnesium ammonium phosphate, and sodium urate increases; changes in urine pH have little effect on the saturation of calcium oxalate. Sometimes, an oversaturated state is transient and can be caused by a decrease in urine volume in a short time or an excessive increase in the excretion of certain substances after meals. Therefore, measuring 24-hour urine volume and the excretion of certain substances in urine cannot help determine the existence of a transient oversaturated state.

　　2. Formation of crystals in urine:Reduction of inhibitors: Certain substances in normal urine can inhibit the formation and growth of crystals, such as pyrophosphates inhibiting the formation of calcium phosphate crystals; mucin, citric acid, and magnesium inhibit the formation of calcium oxalate crystals. When these substances in the urine decrease, kidney stones form.

　　3. Nucleation action: Homogeneous nucleation refers to the formation of crystals from a single crystal:Taking calcium oxalate as an example, when an oversaturated state occurs, these two ions form crystals. The higher the ion concentration, the more and larger the crystals. The ions on the surface of smaller crystals continuously fall off. Research suggests that only crystals containing more than 100 ions have enough affinity to prevent the detachment of surface ions, thus achieving a state of balance and allowing the crystals to grow continuously. At this time, the required ion concentration is lower than that when the crystal just formed. Heterogeneous nucleation refers to the phenomenon where one crystal can act as a nucleus to promote the aggregation and growth of another crystal on its surface. For example, sodium urate crystals can promote the formation and growth of calcium oxalate crystals. If crystals are formed in the urine and remain locally to grow, it is beneficial for the development of kidney stones. Many crystals and small kidney stones can be flushed out of the body by urine. When certain factors such as local narrowing, obstruction, etc., lead to urinary obstruction or slow flow, it is conducive to the formation of kidney stones.

　　4. Organic matrices:Organic matrices can promote the adhesion of crystals to form stones of a certain shape. However, they do not play a key role in the process of stone formation.

　　Two, factors affecting the formation of stones

　　1. Increased excretion of urinary crystal substances

　　(1) Hypercalcemia: When a normal person consumes 25 mmol of calcium and 100 mmol of sodium per day, the daily urinary calcium excretion is less than 7.5 mmol (or 0.1 mmol/kg); when consuming 10 mmol of calcium per day, the urinary calcium excretion is less than 5 mmol. Persistent hypercalcemia is the most common independent abnormal factor in patients with kidney stones, and the stones formed are often calcium oxalate stones. Correcting hypercalcemia can effectively prevent the recurrence of kidney stones. Therefore, hypercalcemia plays a very important role in the pathogenesis of kidney stones. It can be divided into the following four types according to its pathogenesis.

　　① Absorptive hypercalcemia: The most common type, seen in 20% to 40% of patients with kidney stones. The cause is often some intestinal diseases (such as jejunitis) that cause increased intestinal calcium absorption, elevated blood calcium levels, and inhibition of parathyroid hormone (PTH) secretion. Due to increased blood calcium levels, glomerular filtration of calcium increases, and decreased PTH secretion leads to reduced calcium reabsorption in the renal tubules, causing increased urinary calcium levels. Increased calcium intake, as well as increased VitD due to sarcoidosis and increased VitD, can also lead to absorptive hypercalcemia. Such patients often have increased urinary calcium excretion as a compensatory mechanism, and blood calcium levels are often within the normal range.

　　② Renal hypercalcemia: A type of idiopathic hypercalcemia, accounting for 5% to 15% of patients with kidney stones. Due to abnormal function of renal tubules, especially the proximal tubules, calcium reabsorption is reduced. Such patients often develop secondary hyperparathyroidism, with increased PTH secretion; and increased synthesis of 1,25-(OH)2VitD2, which increases bone calcium mobilization and intestinal calcium absorption, often resulting in normal blood calcium levels.

　　③ Osteolytic hypercalcemia: Mainly seen in primary hyperparathyroidism, accounting for 3% to 5% of patients with kidney stones; while 10% to 30% of patients with primary hyperparathyroidism have concurrent kidney stones. It also occurs in hyperparathyroidism, metastatic tumors, long-term bed rest-induced bone resorption, and Cushing's syndrome.

　　④ Anorexic hypercalcemia without PTH elevation: It is approximately seen in 5% to 25% of patients with kidney stones. Certain factors, such as increased renal phosphorus excretion causing hypophosphatemia, lead to increased synthesis of 1,25-(OH)2VitD3, which inhibits PTH secretion, thereby increasing urinary calcium excretion.

　　(2) Hyperoxaluria: The normal daily excretion of oxalate in urine is 15-60mg. Oxalate is the second most important component of kidney stones after calcium, but most calcium oxalate kidney stone patients do not have abnormal oxalate metabolism. Hyperoxaluria is more common in abnormal absorption of oxalate in the intestines, also known as enterogenous hyperoxaluria, accounting for 2% of kidney stone patients. In normal intestines, the combination of calcium and oxalate can prevent the absorption of oxalate. In diseases of the ileum (such as ileal resection, postoperative bypass formation between the jejunum and ileum, infectious enteritis, chronic pancreatitis and biliary tract diseases), due to reduced fat absorption, the combination of fat in the intestinal lumen with calcium is reduced, leading to insufficient calcium to combine with oxalate stones, causing an increase in oxalate absorption in the colon; in addition, the unabsorbed fatty acids and bile salts themselves can also damage the colonic mucosa, leading to an increase in oxalate absorption in the colon. Moreover, in cases of absorptive hypercalciuria, due to increased calcium absorption in the intestines, it can also cause an increase in oxalate absorption. Hyperoxaluria occasionally occurs in excessive intake of oxalate, vitamin B6 deficiency, excessive intake of vitamin C, and primary hyperoxaluria. The latter is divided into type I and type II, with type I due to the lack of α-ketoglutarate-ε-glycerate lyase, leading to the oxidation of glycolate to oxalate; type II is due to the lack of d-glycerate dehydrogenase, causing an increase in 1-glycerate and the increase in oxalate production. Ethylene glycol poisoning and methoxyflurane can stimulate the increase in oxalate production. Any cause of hyperoxaluria can lead to tubulointerstitial damage, causing kidney stones.

　　(3) Hyperuricuria: The normal daily excretion of uric acid in urine is generally 13mmol. Hyperuricuria is the only abnormally high condition in 10% to 20% of calcium oxalate stone patients, and it is sometimes referred to as 'hyperuricotic calcium oxalate stones', and it is considered as an independent type of kidney stones. In addition, 40% of patients with hyperuricuria also have hypercalciuria and hypocitraturia. The etiology of hyperuricuria includes primary diseases and myeloproliferative diseases, malignant tumors, especially during chemotherapy, ulcerative colitis, focal enteritis, and postoperative bypass formation between the jejunum and ileum, etc. On one hand, the loss of alkalinity in the intestines leads to a decrease in urinary pH, and on the other hand, it reduces urine output, thereby promoting the formation of uric acid stones.

　　(4) Cystinuria: A genetic disease caused by transport disorders of cysteine, lysine, and other substances in the proximal renal tubules and jejunum. Due to tubular transport disorders, a large amount of cysteine is excreted in the urine. The saturation of cysteine in urine is related to pH; at a urine pH of 5, the saturation is 300mg/L; at a urine pH of 7.5, the saturation is 500mg/L.

　　(5) Xanthine Nephrolithiasis: A rare metabolic disease caused by the lack of xanthine oxidase, which leads to the inhibition of the conversion of hypoxanthine to xanthine and xanthine to uric acid, resulting in elevated urinary xanthine levels (＞13mmol/24h) and reduced urinary uric acid. When treated with allopurinol, the increase in urinary xanthine is due to the inhibition of xanthine oxidase activity, but xanthine calculi are generally not caused in the absence of a pre-existing xanthine metabolism disorder.

　　2. The influence of other components in urine on the formation of calculi

　　(1) Urine pH: Changes in urine pH have an important impact on the formation of kidney stones. A decrease in urine pH is conducive to the formation of uric acid stones and cystine stones; while an increase in pH is conducive to the formation of calcium phosphate stones (pH > 6.6) and ammonium magnesium phosphate stones (pH > 7.2).

　　(2) Urine volume: If the urine volume is too low, the concentration of crystal substances in urine increases, which is conducive to the formation of supersaturation. About 10% of kidney stone patients have less than 1L of urine per day without any other abnormalities.

　　(3) Magnesium ions: Magnesium ions can replace the absorption of oxalic acid in the intestines and inhibit the crystallization of calcium oxalate and calcium phosphate in urine.

　　(4) Citrate: It can significantly increase the solubility of calcium oxalate.

　　(5) Hypocitraturia: Citrate combines with calcium ions to reduce the saturation of calcium salts in urine, inhibiting the crystallization of calcium salts. A decrease in citrate in urine is conducive to the formation of calcium-containing stones, especially calcium oxalate stones. Hypocitraturia is seen in any acidifying state such as renal tubular acidosis, chronic diarrhea, post-gastrectomy, hypokalemia caused by thiazide diuretics (intracellular acidosis), excessive intake of animal protein, and urinary tract infection (bacterial decomposition of citrate). There are also some unknown causes of hypocitraturia. Hypocitraturia can be the only biochemical abnormality (10%) or coexist with other abnormalities (50%) in patients with kidney stones.

　　3. Urinary tract infection

　　Persistent or recurrent urinary tract infections can cause infectious calculi. Bacteria containing urease, such as Proteus, certain Klebsiella, Serratia, Enterobacter aerogenes, and Escherichia coli, can decompose urea in urine to produce ammonia, raising the urine pH, which promotes the supersaturation of ammonium magnesium phosphate (MgNH4PO4·6H2O) and calcium carbonate [Ca10(PO4)6·CO3]. In addition, the pus and necrotic tissue during infection also promote the aggregation of crystals on their surface to form calculi. In some diseases with abnormal renal structure, such as ectopic kidney, polycystic kidney, horseshoe kidney, etc., kidney calculi can occur due to recurrent infection and poor urine flow. Infection also serves as a complication of other types of kidney calculi, and the two are mutually causal.

　　4. Diet and drugs

　　Hardening through drinking; malnutrition, lack of Vitamin A can cause the shedding of urothelial cells, forming the core of calculi; taking probenecid (as a matrix for calculi) and acetazolamide.

　　In addition, about 5% of patients with clear calculi do not have any biochemical abnormalities, and the cause of their calculi is unclear.

　　1. Infection:Infections associated with calculi are very difficult to treat before the calculi are excreted or removed. Such infections can lead to pyelonephritis, renal abscess, perinephritis, perinephric abscess, and cystitis, among others. It is worth noting that infections can accelerate the growth of calculi and damage the renal parenchyma.

　　2. Urinary tract obstruction:It usually causes hydronephrosis above the obstruction, such as lower ureteral stones can cause middle and upper ureteral and renal pelvis hydronephrosis. The obstruction of stones is usually incomplete, and if bilateral ureteral or urethral obstruction occurs, anuria will appear, and in severe cases, it can develop into uremia.

　　3. Local injury:If small stones have a high degree of mobility, the local injury is relatively light. Large and fixed stones can cause the renal papillary and renal pelvis epithelial cells to fall off, and ulcers can also cause fibrous tissue hyperplasia, leading to interstitial fibrosis. If the transitional epithelium is stimulated by stones for a long time, squamous epithelial metaplasia can occur, which can eventually lead to squamous cell carcinoma. Stones usually damage blood vessels, causing hematuria.

　　1. Asymptomatic:It is mostly calyceal stones, which can be found during physical examination with B-ultrasound, and urine tests are negative or have a small amount of red and white blood cells.

　　2. Dull lumbar pain:It is mostly large renal pelvis stones such as cast stones, and hematuria may occur after vigorous exercise.

　　3. Renal colic:It is often smaller stones, with microscopic or gross hematuria, and significant renal area tenderness. During an attack of pain, the patient may appear pale, have cold sweat, a rapid and weak pulse, or even a drop in blood pressure. Nausea, vomiting, and abdominal distension are often accompanied by gastrointestinal symptoms.

　　4. Stone passage history:During episodes of pain and hematuria, sand grains or small stones may be excreted with urine. When stones pass through the urethra, there is a feeling of urethral obstruction and stinging pain. After the stones are excreted, the urine flow immediately returns to normal, and the patient feels relaxed and comfortable.

　　5. Infection symptoms:Infection can cause pyuria, and during acute attacks, symptoms such as chills, fever, lumbar pain, frequent urination, urgency, and dysuria may occur.

　　6. Renal insufficiency:One-sided kidney stone obstruction can cause hydronephrosis on that side and progressive renal function decline; obstruction by bilateral kidney stones or solitary kidney stones can develop into uremia.

　　7. Anuria:Bilateral kidney stones can cause bilateral urinary tract obstruction, solitary kidney, or obstruction of the only functioning kidney stone, which can lead to anuria. One-sided kidney stone obstruction can cause reflexive anuria on the contralateral side.

　　8. Lumbar mass:When kidney stones cause severe hydronephrosis, a mass can be palpated in the lumbar or upper abdominal area.

　　1. Drink more water

　　One should drink at least two to three liters of plain water a day, as drinking plenty of water and urinating frequently helps dilute the toxins accumulated in the body and kidneys, and has a protective effect on the kidneys.

　　2. Consume low-salt foods

　　Salt can make the blood concentrated, thereby aggravating the functioning of the kidneys.

　　3. Do not take analgesics arbitrarily

　　According to research, many patients with kidney disease have kidney problems, mainly caused by the retention of analgesics inside the kidneys.

　　4. Appropriate exercise

　　Control blood pressure, weight, and blood sugar to reduce the burden on the kidneys.

　　The diagnosis of kidney stone disease mainly relies on clinical manifestations, such as urine routine examination, general radiography, intravenous pyelography, retrograde pyelography, renal, ureter, and bladder ultrasound examination.

　　Dietary taboos for kidney stone patients

　　Patients with kidney stones should pay special attention to their diet in daily life. Some foods can exacerbate the condition of kidney stones. The following lists the foods that kidney stone patients should pay special attention to.

　　1. Control the intake of calcium

　　About 90% of stones are formed from calcium or calcium-containing products. If your last stone was mainly composed of calcium, you should pay attention to the intake of calcium. If you are taking nutritional supplements, you should first consult a doctor to determine whether they are necessary. Next, check the daily intake of high-calcium foods, including milk, cheese, butter, and other dairy products. Milk and antacids may cause kidney stones.

　　2. Do not eat foods rich in oxalates

　　About 60% of stones are calcium oxalate stones. Therefore, it is necessary to limit the intake of foods rich in oxalates, including beans, beets, celery, chocolate, grapes, bell peppers, coriander, spinach, strawberries, and cruciferous vegetables. Also, avoid alcohol, caffeine, tea, chocolate, dried figs, lamb, nuts, bell peppers, black tea, opium poppy, etc.

　　3. Pay attention to the intake of protein

　　Kidney stones have a direct relationship with the intake of protein. Protein is prone to cause uric acid, calcium, and phosphorus to appear in urine, leading to the formation of stones. If you have had calcium stones, you should pay special attention to whether you are consuming an excessive amount of protein, especially if you have a history of hyperuricemia or cystine stones. Limit the intake of high-protein foods to 180 grams per day, including meat, cheese, chicken, and fish.

　　4. Eat less salt

　　If you have calcium stones, you should reduce the intake of salt. You should reduce your daily salt intake to 2-3 grams.

　　5. Avoid L-cysteine

　　If you have a history of kidney stones or are currently suffering from kidney stones, avoid L-cysteine. The accumulation of this amino acid can crystallize in the kidneys, forming large stones that block the internal kidney.

　　6. Limit the intake of vitamin C

　　If you are prone to form calcium oxalate stones, you should limit the intake of vitamin C. More than 3-4 grams per day may increase the production of oxalic acid, thereby increasing the likelihood of stones. Do not take high-potency vitamin C supplements.

　　7. Do not take too much vitamin D

　　Excessive vitamin D can lead to the accumulation of calcium in various parts of the body. It is best not to exceed the RDA of 400 IU per day for vitamin D intake.

　　8. Check your stomach medicine

　　Some common antacids contain high levels of calcium. If you have calcium stones and are also taking antacids, you should check the ingredient list of this medicine to determine if it contains high calcium. If it does, you should switch to a different medication.

　　9. Reduce the intake of high-calcium foods

　　High intake of oxalic acid is prone to combine with calcium to form kidney stones. However, some reports indicate that calcium ingested through diet can combine with oxalic acid at the same time to form calcium oxalate, which is excreted from the body through feces, thereby reducing the amount of oxalic acid that may be absorbed. Therefore, it does not increase the risk of kidney stones. However, calcium supplements outside of diet do not have this effect. People with a history of kidney stones should be particularly cautious when supplementing calcium.

　　10. Pay attention to drinking more water and more exercise, drinking water

　　While paying attention to drinking more water and more exercise, knocking on the urinary tract is beneficial to the excretion of calculi.

　　11. Cod liver oil should not be taken in large doses

　　Modern medical research shows that when calcium in blood and urine increases (especially when it increases abruptly), it is most likely to form kidney stones. One of the reasons for the increase in blood calcium is the increase in vitamin D in the body, and cod liver oil contains a large amount of vitamin D.

　　12. Reduce the intake of dairy products

　　Recently, a study by the University of Washington in the United States believes that oxalate in legumes can combine with calcium in the kidneys to form calculi.

　　13. Increase the intake of black fungus

　　According to relevant reports, black fungus has the effects of litholysis and stone excretion. Black fungus contains a variety of minerals and trace elements, which can produce a strong chemical reaction with various calculi, causing the calculi to peel off, differentiate, dissolve, and finally be excreted out of the body.

　　14. Reduce beer intake

　　Some patients with kidney stones mistakenly believe that beer can diuretic, and drinking more beer can prevent and excrete calculi, but in fact, this is not the case. Beer contains a lot of calcium oxalate and uric acid, both of which can form urinary calculi.

　　Preventive and treatment measures should be formulated according to the etiology, type, size, number, location of the calculus, and whether there is concurrent infection, urinary tract obstruction, and renal function, mainly including three aspects.

　　1. Prevention and treatment of calculus formation and recurrence:Due to the high recurrence rate of kidney stones, 80% in men and 60% in women, the average time from the first recurrence to the removal or excretion of stones is 9.5 years, so in treatment, not only attention should be paid to the removal and excretion of stones, but also attention should be paid to the prevention of the recurrence of kidney stones. The preventive and treatment measures are as follows.

　　1. Eliminate the predisposing factors of kidney stones:Active treatment of the causes of calculus formation, such as the removal of parathyroid glands for primary hyperparathyroidism, the treatment of malignant tumors, the control of renal pelvis infection, and the relief of urinary tract obstruction, are all effective measures to prevent calculus formation and recurrence.

　　2. General treatment

　　(1) Ensure adequate water intake: Especially in summer and at night, to avoid excessive urine concentration at night, it is necessary to emphasize drinking water before going to bed, and drinking water again in the middle of the night. It is best to use magnetized water containing minerals to make the daily urine volume exceed 2000ml, which can dilute urine, reduce crystal precipitation, flush the urinary tract, and excrete small calculi.

　　(2) Diet: The composition of food should be determined according to the type of calculus and the acidity or alkalinity of urine. For oxalate calculi, it is necessary to avoid high-oxalate foods such as spinach, tomatoes, potatoes, beets, asparagus, nuts, tea, cocoa, chocolate, etc., as well as foods containing calcium ions such as milk and cheese. For idiopathic hypercalciuria, calcium intake should be limited to reduce urinary calcium content; for recurrent oxalate calculi without hypercalciuria, low-calcium diet is not necessary. If calculus formation occurs due to low-calcium diet causing increased excretion of urinary oxalate, low-calcium diet should also not be adopted. Controlling sodium intake, excessive sodium intake can increase urinary calcium excretion. High uric acidemia and hyperuricosuria require a purine diet, and it is necessary to avoid eating animal viscera, reducing fish and coffee intake, etc.

　　If the patient is found to have stones for the first time without underlying diseases or pathophysiological disorders, only follow-up is needed to understand the stone condition and whether new stones have formed, without the need for drug treatment.

　　3. Drug treatment

　　(1) Hypercalciuria: Patients with primary hyperparathyroidism, sarcoidosis, hyperthyroidism, multiple myeloma, and other causes should receive corresponding treatment. For other causes, the following measures can be taken.

　　① Thiazide diuretics: They can increase the reabsorption of calcium by the renal tubules and reduce the excretion of urine calcium. They are used for renal hypercalciuria and absorptive hypercalciuria. Hydrochlorothiazide 50-100mg per day or the equivalent dose of other diuretics. Long-term use may reduce its effect on reducing urine calcium, and it can cause hypocalcemia and low citrateuria, requiring the supplementation of calcium citrate.

　　② Sodium phosphate fiber resin: When taken orally, it combines with calcium in the intestines to limit calcium absorption, with a dose of 2.5-5g per time, taken with meals. Due to the reduction of calcium in the intestinal lumen, the combination with oxalate decreases, leading to increased intestinal absorption of oxalate. Moreover, the drug can combine with calcium simultaneously, preventing intestinal absorption of calcium, so it is necessary to limit the intake of oxalate and supplement calcium. It is only used for patients with hypercalciuria due to absorption, without bone disease, normal blood phosphorus levels, and ineffective for limiting calcium intake and thiazide diuretic therapy. The drug can reduce blood Ca2+ levels and increase PTH secretion.

　　③ Orthophosphates: Such as neutral or alkaline soluble sodium or potassium phosphates, which combine with calcium to form calcium phosphate salts, reducing urine calcium concentration and the saturation of calcium oxalate. Take 1.5-2.0g of phosphorus elements per day, divided into 3-4 doses. Not to be used in patients with glomerular filtration rate below 30ml/min and urinary tract infections, as it can cause metastatic soft tissue calcification and infectious calculi.

　　(2) Enterogenous hyperoxaluria: Limit the intake of oxalate and fat, supplement potassium citrate, which can significantly increase urine pH and citrate. On one hand, it acts as an inhibitor of crystal formation, and on the other hand, it combines with oxalate in the intestines to prevent its absorption, thereby reducing the excretion of urinary oxalate. Magnesium hydroxide or magnesium oxide can be used. Cholestyramine can correct malabsorption of fat in the intestines but cannot continuously inhibit the absorption of oxalate.

　　(3) Low urine citrate-containing calcium kidney stones: Potassium citrate can effectively limit the formation and recurrence of such stones. The dosage is 3-6g per day, taken in three divided doses. Some patients may have mild gastrointestinal reactions, and caution should be exercised in patients with renal insufficiency.

　　(4) Uric acid stones: Increase urine output, limit purine intake, and adjust urine pH to 6.0-6.5. Pay special attention to the urine pH at night. Use sodium citrate and sodium bicarbonate to increase urine pH, which increases the crystallization of calcium salts. Potassium citrate has no such drawback, so it is the first choice in clinical practice, with a dose of 30-60 mmol/d. If there is also an increase in blood uric acid, add allopurinol and control the blood uric acid concentration before changing to maintenance dose.

　　(5) Cystine and cystine urine: Under the condition of ensuring sufficient water intake (usually >3L/d) and alkalinization of urine (pH>7.5), when treatment is ineffective, D-penicillamine can be used, 1-2g per day, taken in divided doses. This drug combines with cystine in urine to form a highly soluble compound excreted from water, thereby reducing the content of cystine. However, it has significant side effects and can cause nephrotic syndrome, dermatitis, and pancytopenia. The mechanism of action of alpha-mercaptoacrylic acid is similar to that of D-penicillamine, but with fewer side effects. It has been reported that this drug can be infused into the renal calculus site to dissolve the calculus; taken orally, it can prevent the formation of calculi.

　　(6) Infectious calculi: Long-term and effective control of urinary tract infection can limit the formation of infectious calculi, and even dissolve some calculi that have already formed. However, due to the low concentration of antibiotics in the calculi, bacteria cannot be completely killed, so it is difficult to completely cure urinary tract infection with simple antibacterial treatment.

　　Second, the treatment of calculi:The treatment of renal calculi has made great progress in recent years. Many renal calculi that required surgical treatment in the past can now be treated with extracorporeal shock wave lithotripsy or non-open surgery, or with a combination of several methods to achieve satisfactory efficacy.

　　1. Medical treatment:For smooth round calculi with a diameter less than 0.5cm, without urinary tract obstruction or infection, and with clear function, medical treatment can be adopted, methods see 'Prevention of stone formation and recurrence'. The solubilization therapy is effective for uric acid stones and cystine stones, but less effective for calcium-containing stones and infectious stones. The routes of administration include oral, intravenous, ureteral catheter, open nephrostomy catheter, and percutaneous nephrostomy catheter. During treatment, close observation of the condition changes should be made, and radioactive nuclide renal imaging and X-ray examination should be carried out regularly to understand the renal function and decide whether surgery is needed.

　　2. Extracorporeal shock wave lithotripsy:It has been widely used in clinical practice and achieved satisfactory efficacy, especially for solitary calculi with a diameter of about 1.5cm. With the maturity of extracorporeal shock wave lithotripsy experience, it is now also tried for horn-like calculi and some special calculi, such as renal papillary calculi, horseshoe kidney calculi, and multiple large calculi, for treatment. It should be noted that due to the physical effects of shock waves and their ability to cause chemical changes in water molecules, generating H2O2 and various free radicals, they can damage and cause bleeding in the surrounding tissue cells of the calculi. Shock waves can also directly and indirectly cause an increase in intrapelvic pressure by stimulating the contraction of renal pelvis smooth muscle; while post-treatment碎石的 and hematuria can increase urinary resistance, leading to an increase in intrapelvic pressure, thereby increasing the pressure in the renal tubules and renal sacs, affecting the function of the glomeruli and renal tubules. Therefore, for patients with renal urinary tract obstruction, infection, and decreased renal function, it is still necessary to weigh the pros and cons, and perform corresponding treatments such as antibacterial prophylaxis and catheterization to relieve obstruction before surgery; and postoperatively, close observation and timely control of infection, and relief of obstruction should be carried out. Care should also be taken for patients with coronary heart disease, hypertension, and incomplete cardiac function, and for those with incurable bleeding disorders and pregnant women, it is still contraindicated.

　　3. Surgical Stone Extraction:Some new non-open surgical stone extraction technologies, such as through ureterorenal pelvisoscopy, percutaneous nephroscope stone extraction, etc., are gradually widely used in clinical practice and have achieved good therapeutic effects. However, for those who are ineffective or have contraindications to the above non-open surgical stone extraction techniques, drug treatment, and extracorporeal ultrasonic lithotripsy, as well as some complex stones such as large horn-shaped stones, certain multiple stones, or stones with narrow renal pelvis and calyceal cavities, complicated with severe obstruction causing acute urinary retention and severe infection, open surgery is still recommended. The operation should be carried out as far as possible to protect renal function and ensure complete stone removal to avoid the residual core of the stone continuing to grow. Infection stones often have stone fragments left locally after surgery, which are prone to recurrence after surgery.

　　Three, Symptomatic Treatment

　　1. Treatment of renal colic:Atropine or 654-2 can be injected intramuscularly as antispasmodics, and promethazine can be used in combination to enhance efficacy. Durogesic or morphine can be used if ineffective, or other analgesics.

　　2. Treatment of urinary tract infection:See 'Urogenital Infection'.

　　3. Hematuria:When there is obvious gross hematuria, hydroxybenzamine 0.1-0.2g or tranexamic acid 0.1g can be used, administered slowly by intravenous injection, three times a day.

　　Nephrolithiasis is a common kidney disease that is prone to infection and renal function damage. In recent years, with the progress of research on its etiology and pathophysiology, some new preventive and treatment measures have emerged, reducing the recurrence rate. In addition, due to the application of extracorporeal shock wave lithotripsy and the accumulation of experience, many patients who originally needed surgical treatment can avoid the pain of surgery and receive effective treatment. However, sufficient attention should be paid to the impact of shock waves on the kidneys and the prevention and treatment of complications.