bubble_chart Overview

Renal calculi (venal calculi) refers to the abnormal accumulation of crystalline substances (such as calcium, oxalate, uric acid, cystine, etc.) and organic matrix (such as matrix A, Tamm-Horsfall protein, acidic mucopolysaccharides, etc.) in the kidneys.

bubble_chart Epidemiology

The incidence is notably high in the United States, the United Kingdom, Southeast Asia, India, and other regions. In China, provinces such as Guangdong, Shandong, Jiangsu, Anhui, Hebei, Shaanxi, Zhejiang, Guangxi, Sichuan, and Guizhou report relatively high rates. The disease predominantly affects individuals aged 20 to 40, with a male-to-female ratio of 4.5:1. Kidney stones typically form in the renal pelvis or calyces and may pass into the ureter and bladder. Primary bladder stones are rare and primarily occur in males aged 1 to 10. Based on crystalline composition, 80–95% of kidney stones are calcium-containing, with the majority being mixed calcium oxalate and calcium phosphate stones or pure calcium oxalate stones. Pure calcium phosphate stones account for only 7%, while uric acid stones make up 5–8%, cystine stones 1%, and other types (such as xanthine stones, 2,8-dihydroxyadenine stones, triamterene stones, and silicate stones) less than 1%. Infection-related stones constitute approximately 5–15% of cases.

bubble_chart Pathogenesis

The formation process of kidney stones involves certain factors that lead to an increase in the concentration of crystalline substances in the urine and a decrease in solubility, resulting in a supersaturated state. Crystals precipitate, grow, and aggregate locally, eventually forming stones. In this process, the formation of a supersaturated state of urinary crystalline substances and the reduction of crystal formation inhibitors in the urine are the two most critical factors.

(1) Formation of a Supersaturated State This occurs due to: ① insufficient urine volume; ② excessive absolute excretion of certain substances in the urine, such as calcium, oxalate, uric acid, cystine, and phosphates; ③ changes in urine pH. When urine pH decreases (<5.5), the saturation of uric acid in the urine increases. When urine pH increases, the saturation of calcium phosphate, magnesium ammonium phosphate, and sodium urate rises. Changes in urine pH have little effect on the saturation of calcium oxalate. Sometimes, the supersaturated state is transient, caused by a temporary decrease in urine volume or a post-meal surge in the excretion of certain substances. Therefore, measuring 24-hour urine volume and the excretion of certain substances cannot help determine whether a transient supersaturated state exists.

(2) Reduction of Crystal Formation Inhibitors in Urine Normal urine contains substances that inhibit crystal formation and growth, such as pyrophosphate inhibiting calcium phosphate crystallization, and mucoproteins, citrate, and magnesium inhibiting calcium oxalate crystallization. When these substances decrease in the urine, stones may form.

(3) Nucleation Homogeneous nucleation refers to the formation of crystals of a single substance. Taking calcium oxalate as an example, when a supersaturated state occurs, these two ions form crystals. The higher the ion concentration, the more and larger the crystals. Smaller crystals continuously shed ions from their surfaces. Research suggests that only crystals containing more than 100 ions have sufficient affinity to prevent ion shedding from the crystal surface, achieving a balanced state that allows continuous crystal growth. At this stage, the required ion concentration is lower than when the crystals initially formed. Heterogeneous nucleation occurs when two types of crystals have similar shapes, allowing one crystal to act as a core, promoting the aggregation and growth of the other crystal on its surface. For example, sodium urate crystals can promote the formation and growth of calcium oxalate crystals. Once crystals form in the urine, their retention and local growth facilitate stone development. Many crystals and small stones can be flushed out by urine flow. However, factors such as local narrowing or obstruction that slow or block urine flow favor stone formation.

(4) Organic Matrix The organic matrix can promote crystal adhesion, forming stones of specific shapes. However, it does not play a critical role in the stone formation process.

Factors Influencing Stone Formation

(1) Increased Excretion of Crystalline Substances in Urine

1. Hypercalciuria Under normal conditions, when a person consumes 25 mmol of calcium and 100 mmol of sodium daily, the daily urinary calcium excretion is <7.5 mmol (or 0.1 mmol/kg). When consuming 10 mmol of calcium daily, urinary calcium excretion is <5 mmol. Persistent hypercalciuria is the most common independent abnormal factor in kidney stone patients, often leading to calcium oxalate stones. Correcting hypercalciuria can effectively prevent kidney stone recurrence. Therefore, hypercalciuria plays a crucial role in the pathogenesis of kidney stones. Based on its disease mechanism, it can be divided into the following four types.

(1) Absorptive Hypercalciuria: The most common type, seen in 20–40% of kidney stone patients. Its disease cause is often related to intestinal disorders (e.g., jejunal issues) that increase intestinal calcium absorption, raising blood calcium levels and suppressing parathyroid hormone (PTH) secretion. Elevated blood calcium increases glomerular filtration of calcium, while reduced PTH decreases renal tubular calcium reabsorption, leading to increased urinary calcium. Excessive calcium intake, vitamin D toxicity, and conditions like sarcoidosis that increase vitamin D levels can also cause absorptive hypercalciuria. In these patients, compensatory increases in urinary calcium excretion often keep blood calcium levels within the normal range.

(2) Renal hypercalciuria: This is a type of idiopathic hypercalciuria, accounting for approximately 5-15% of kidney stone patients. Due to dysfunction of the renal tubules, especially the proximal tubules, calcium reabsorption is reduced. Such patients often develop secondary hyperparathyroidism, leading to increased PTH secretion. Additionally, the synthesis of 1,25-(OH)₂VitD₂ also increases, resulting in enhanced bone calcium mobilization and intestinal calcium absorption. Consequently, the patient's blood calcium levels often remain normal.

(3) Resorptive hypercalciuria: Mainly seen in primary hyperparathyroidism, accounting for about 3-5% of kidney stone patients; while 10-30% of primary hyperparathyroidism patients develop kidney stones. It is also observed in hyperparathyroidism, metastatic tumors, bone resorption due to prolonged bed rest, and Cushing's syndrome.

(4) Fasting hypercalciuria without elevated PTH: Occurs in approximately 5-25% of kidney stone patients. Certain factors, such as increased renal phosphorus excretion leading to hypophosphatemia, result in increased synthesis of 1,25-(OH)₂VitD₃, which suppresses PTH secretion, thereby increasing urinary calcium excretion.

2. Hyperoxaluria: The normal daily urinary oxalate excretion is 15-60 mg. 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 often associated with abnormal intestinal oxalate absorption, also known as enteric hyperoxaluria, accounting for 2% of kidney stone patients. Normally, calcium in the intestinal lumen binds with oxalate to prevent oxalate absorption. In ileal diseases (e.g., ileal resection, jejuno-ileal bypass surgery, infectious small intestine diseases, chronic pancreatic and biliary diseases), reduced fat absorption leads to fat binding with calcium in the intestinal lumen, leaving insufficient calcium to bind with oxalate, thereby increasing colonic oxalate absorption. Additionally, unabsorbed fatty acids and bile salts can damage the colonic mucosa, further increasing oxalate absorption. In absorptive hypercalciuria, increased intestinal calcium absorption can also elevate oxalate absorption. Hyperoxaluria is occasionally seen with excessive oxalate intake, VitB₆ deficiency, excessive VitC intake, and primary hyperoxaluria. The latter is classified into type I and type II: type I is caused by a deficiency of α-ketoglutarate glyoxylate lyase, leading to glyoxylate accumulation and oxidation to oxalate; type II results from a deficiency of d-glycerate dehydrogenase, causing increased 1-glycerate and oxalate production. Ethylene glycol poisoning and methoxyflurane can also stimulate increased oxalate production. Hyperoxaluria from any cause can lead to renal tubular-interstitial damage and kidney stone formation.

3. Hyperuricosuria: The normal daily urinary uric acid excretion is 13 mmol. Hyperuricosuria is the sole biochemical abnormality in 10-20% of calcium oxalate stone patients, sometimes referred to as "hyperuricosuric calcium oxalate stones" and considered a distinct type of kidney stone. Additionally, 40% of hyperuricosuria patients also have hypercalciuria and hypocitraturia. Causes of hyperuricosuria include primary and myeloproliferative disorders, malignancies (especially during chemotherapy), ulcerative colitis, regional enteritis, and jejuno-ileal bypass surgery. These conditions lead to intestinal alkali loss, lowering urinary pH, and reducing urine volume, promoting uric acid stone formation.

4. Cystinuria: A hereditary disorder caused by impaired transport of cystine, lysine, and other amino acids in the proximal renal tubules and jejunum. Due to renal tubular transport dysfunction, large amounts of cystine are excreted in the urine. The saturation of cystine in urine depends on pH: at pH 5, saturation is 300 mg/L; at pH 7.5, it is 500 mg/L.

5. Xanthinuria: A rare metabolic disorder caused by a deficiency of xanthine oxidase, which impairs the conversion of hypoxanthine to xanthine and xanthine to uric acid, leading to elevated urinary xanthine (>13 mmol/24h) and reduced urinary uric acid. During allopurinol treatment, xanthine oxidase activity is inhibited, increasing urinary xanthine. However, in the absence of an underlying xanthine metabolism disorder, xanthine stones generally do not form.

(2) Influence of other urinary components on stone formation

1. Urine pH Changes in urine pH have a significant impact on the formation of kidney stones. A decrease in urine pH promotes the formation of uric acid stones and cystine stones, while an increase in pH favors the formation of calcium phosphate stones (pH > 6.6) and struvite stones (pH > 7.2).

2. Urine Volume Insufficient urine output leads to an increased concentration of crystalline substances in the urine, favoring the formation of a supersaturated state. Approximately 10% of kidney stone patients exhibit no other abnormalities aside from a daily urine output of less than 1 liter.

3. Magnesium Ions Magnesium ions can reduce the intestinal absorption of oxalate and inhibit the crystallization of calcium oxalate and calcium phosphate in the urine.

4. Citric Acid Citric acid can significantly increase the solubility of calcium oxalate.

5. Hypocitraturia Citrate binds with calcium ions, reducing the saturation of calcium salts in the urine and inhibiting their crystallization. A decrease in urinary citrate promotes the formation of calcium-containing stones, particularly calcium oxalate stones. Hypocitraturia occurs in any acidotic state, such as renal tubular acidosis, chronic diarrhea, post-gastrectomy, hypokalemia induced by thiazide diuretics (intracellular acidosis), excessive intake of animal protein, and urinary tract infections (bacterial breakdown of citrate). Some cases of hypocitraturia have unclear underlying causes. Hypocitraturia may be the sole biochemical abnormality in kidney stone patients (10%) or coexist with other abnormalities (50%).

(3) Urinary Tract Infection

Persistent or recurrent urinary tract infections can lead to infection-related stones. Bacteria containing urease, such as Proteus, certain Klebsiella, Serratia, Enterobacter aerogenes, and large intestine bacilli, can decompose urea in the urine to produce ammonia, raising urine pH and promoting supersaturation of magnesium ammonium phosphate (MgNH₄PO₄·6H₂O) and carbonate apatite [Ca₁₀(PO₄)₆·CO₃]. Additionally, pus and necrotic tissue during infection facilitate crystal aggregation on their surfaces, forming stones. In conditions with abnormal kidney structure, such as ectopic kidney, polycystic kidney, or horseshoe kidney, recurrent infections and poor urine flow can contribute to kidney stone formation. Infections can also complicate other types of kidney stones, with the two factors interacting causally.

(4) Diet and Medications

Hard water consumption; malnutrition and vitamin A deficiency can lead to urothelial shedding, forming the nucleus of stones; use of triamterene (as a stone matrix) and vinegar sulfonamides.

Additionally, about 5% of kidney stone patients exhibit no identifiable metabolic or structural abnormalities, and the cause of their stones remains unclear.

bubble_chart Pathological Changes

Stones are most commonly found in the renal pelvis, followed by the renal calyces, while kidney parenchymal stones are rare. Renal calyceal stones are mostly located in the lower calyx, with bilateral kidney stones accounting for less than 10%. Stones can cause injury, infection, and obstruction in the renal pelvis and calyces. These changes lead to epithelial detachment, ulcer formation, and ultimately scar formation. Obstruction caused by stones is often incomplete, as urine can flow around the stone into the ureter, but it may still result in renal pelvis dilation, thickening of the renal pelvis wall, and fibrosis. If a stone becomes impacted at the junction of the renal pelvis and ureter or within the ureter, it can lead to hydronephrosis, renal pelvis dilation, cortical atrophy and destruction, and may even result in pyonephrosis. Additionally, stones may coexist with squamous cell carcinoma of the renal pelvis.

bubble_chart Clinical Manifestations

The symptoms of kidney stones depend on the size, shape, location of the stone, and the presence of complications such as infection or obstruction.

(1) Asymptomatic Seen in small, smooth stones that pass spontaneously without causing noticeable symptoms. Additionally, stones fixed in the renal pelvis or lower calyx without movement or infection may exist long-term without causing symptoms, or only manifest as grade I lumbar discomfort or a dull ache, and are incidentally discovered during abdominal X-ray or B-ultrasound examinations.

(2) Pain Distending pain or dull pain is caused by larger stones pressing, rubbing, or causing hydrops in the renal pelvis or calyx, often occurring in the affected costovertebral angle or upper abdomen. A few unilateral kidney stones may cause bilateral lumbago due to referred pain from the contralateral kidney. Renal colicky pain is caused by smaller stones moving within the renal pelvis or ureter, leading to ureteral spasms, occasionally triggered by blood clots. It can be induced by vigorous exercise, often suddenly starting with pain in the back, waist, or flank, radiating along the ureter to the lower abdomen, inner thigh, or external genitalia. In males, the pain may be most severe in the testicles and penis, accompanied by squatting, curling up, or restlessness, lasting from minutes to hours, until the stone stops moving or enters the bladder, when the pain suddenly stops. Physical examination may reveal tenderness in the affected kidney area, ureteral point, or bladder region. If the stone moves to the submucosal layer of the bladder, it can cause frequent, urgent, and painful urination, which should be differentiated from urinary tract infection.

(3) Hematuria Movement of the stone can scratch the mucosa of the renal pelvis and ureter, leading to microscopic or gross hematuria, often occurring simultaneously with pain. About 20–25% of patients do not experience hematuria when passing stones.

(4) Anuria Acute postrenal anuria caused by stones may occur in: ① complete obstruction by bilateral kidney or ureteral stones; ② obstruction by a stone in a solitary kidney; ③ obstruction by a stone in the affected kidney or ureter, with the contralateral diseased or normal kidney temporarily ceasing excretory function due to reflex.

(5) Urinary tract infection symptoms Refer to "Pyelonephritis."

bubble_chart Diagnosis

The diagnosis of kidney stones is divided into confirming the presence of kidney stones and determining the disease cause and pathophysiological diagnosis, the latter of which aids in guiding treatment.

(1) Establishing the diagnosis of kidney stones: Diagnosis is not difficult for those with typical clinical manifestations or those who pass stones in their urine. Plain X-ray imaging of the urinary tract is of significant importance in diagnosis. When shadows on the abdominal plain film need to be distinguished from other shadows such as gallbladder stones in the right upper abdomen, mesenteric membrane, or calcified lymph nodes, a lateral film should be taken. Kidney stones are usually located posteriorly and may overlap with the shadow of the spine, or they may be positioned slightly anterior or posterior to the spine due to hydronephrosis or calyceal dilation. Additionally, taking one film each during deep inhalation and deep exhalation in the supine position can help identify kidney stones, as their shadows will move up and down with kidney movement while maintaining a constant relative position to the kidney's edge.

Intravenous urography (counterflow of liver qi) or pyelography can clearly show the stone's position and the overall condition of the urinary tract. Sometimes, when the stone is small or has low density, diagnosis becomes challenging. In such cases, retrograde pyelography with air or oxygen contrast can be performed to confirm the stone's presence and location.

B-type ultrasonography can diagnose X-ray-negative stones, displaying them when the diameter exceeds 0.5 cm. However, its drawback is that small stones are often easily misdiagnosed (fistula disease), and it cannot be used for surgical localization.

Renal colicky pain accompanied by hematuria must also be differentiated from renal subcutaneous nodules or tumors. Additionally, renal colicky pain should be distinguished from gallstones, pancreatitis, or acute appendicitis.

Regular follow-up is necessary to monitor the stone's growth rate, changes in location, and the formation of new stones.

(2) Disease cause and pathophysiological diagnosis: Once the diagnosis of kidney stones is confirmed, a detailed history, dietary habits, family history, and past diseases (small intestine, biliary tract, urinary tract infections, and medication history) should be reviewed. Further examinations should then be conducted to determine the disease cause and pathophysiological diagnosis, including stone X-ray formation, urine generation and transformation tests (urine pH, uric acid, urine calcium, oxalate, cystine, citrate, etc.), urine bacterial culture, and blood generation and transformation tests (blood Ca²⁺, Mg²⁺, PTH, pH, Cl^-, K⁺, etc.). When evaluating the relationship between urinary excretion and blood concentration of a substance, dietary intake of that substance should still be considered. A family history of kidney stones is commonly seen in absorptive hypercalciuria and occasionally in cystinuria, primary hyperoxaluria, and type I renal tubular acidosis. Patients with pain wind often have uric acid stones, with a few mixed with calcium oxalate stones. Those with chronic diarrhea, ileum disease, or a history of surgery should be suspected of having uric acid stones or calcium oxalate stones (enteric hyperoxaluria or hypocitraturia). X-ray-positive stones are mostly calcium-containing stones, cystine stones, and infection stones, the latter three of which may appear in a deer horn shape. X-ray-negative stones are typically pure uric acid stones, with rare cases of xanthine stones and 2,2'-dihydroxyadenine stones. A urine culture showing urea-splitting bacteria like Proteus with alkaline urine suggests infection stones (urine calcium, oxalate, uric acid, cystine, citrate, as well as blood calcium, phosphorus, PTH, and deterioration of renal tubular reabsorption and acidification functions are highly diagnostic). For patients with hypercalciuria and hyperoxaluria, further classification is needed.

In primary hyperparathyroidism, blood PTH, blood calcium, and urine calcium levels rise, while blood phosphorus decreases. Fasting urine calcium may also increase. In absorptive hypercalciuria, blood PTH is normal or low, blood calcium is normal, and fasting urine calcium is generally normal. In renal hypercalciuria, blood calcium is normal, but fasting urine calcium rises more significantly than in primary hyperparathyroidism with elevated blood PTH. Fasting hypercalciuria without elevated PTH shows a marked increase in fasting urine calcium, while blood calcium and PTH remain normal. The method for measuring fasting urine calcium involves collecting a 2-hour urine sample in the morning after fasting and measuring calcium and creatinine levels, with a normal calcium/creatinine ratio <0.11.

Patients with primary hyperoxaluria, in addition to elevated urinary oxalate, also have increased urinary glycolate and glycerate levels, often accompanied by calcium oxalate deposition in other tissues, anemia, renal impairment, and a family history of genetic inheritance. Enteric hyperoxaluria is associated with a primary disease history, decreased urinary calcium (<2.5 mmol/d), urinary oxalate >13 mmol/d, possible metabolic acidosis and decreased urinary citrate ( (3) Complications and concurrent renal abnormalities: Determine the presence of infection, obstruction, and renal function status to guide treatment.

bubble_chart Treatment Measures

Prevention and treatment measures should be formulated based on the disease cause, type, size, number, and location of the stones, as well as the presence of complications such as infection, urinary tract obstruction, and renal function. These measures mainly include three aspects.

(1) Prevention and treatment of stone formation and recurrence: Since the recurrence rate of kidney stones is very high—80% in men and 60% in women—with the average time to first recurrence after stone removal or passage being 9.5 years, treatment should not only focus on stone removal or passage but also emphasize preventing recurrence. The prevention and treatment measures are as follows.

1. Eliminating predisposing factors for stone formation: Actively treating the underlying causes of stone formation, such as removing the parathyroid glands in primary hyperparathyroidism, treating malignant tumors, controlling renal pelvis infections, and relieving urinary tract obstruction, are all effective measures to prevent stone formation and recurrence.

2. General treatment:

(1) Ensure adequate water intake: Especially during summer and at night, to avoid excessive urine concentration, it is essential to emphasize drinking water before bedtime and again in the middle of the night. It is best to drink magnetized water containing minerals, ensuring a daily urine output of over 2000 ml, which can dilute urine, reduce crystal precipitation, flush the urinary tract, and expel small stones.

(2) Diet: Dietary composition should be determined based on the type of stone and urine pH. For oxalate stones, avoid high-oxalate foods such as spinach, tomatoes, potatoes, beets, asparagus, nuts, tea leaves, cocoa, and chocolate, as well as calcium-rich foods like milk and cheese. For idiopathic hypercalciuria, limit calcium intake to reduce urinary calcium levels; for recurrent oxalate stones without hypercalciuria, a low-calcium diet is unnecessary. If a low-calcium diet increases urinary oxalate excretion and leads to stone formation, it should also be avoided. Control sodium intake, as excessive sodium can increase urinary calcium excretion. For hyperuricemia and hyperuricosuria, follow a low-purine diet, avoid animal organs, and reduce intake of fish and coffee beans.

If a patient is diagnosed with stones for the first time and has no underlying disease or pathophysiological disorder, only follow-up is needed to monitor the stones and check for new stone formation, without requiring medication.

3. Drug treatment:

(1) Hypercalciuria: For cases caused by primary hyperparathyroidism, sarcoidosis, hyperthyroidism, multiple myeloma, etc., corresponding treatments should be administered. For other disease causes, the following measures can be taken.

① Thiazide diuretics: These increase renal tubular calcium reabsorption and reduce urinary calcium excretion. Used for renal hypercalciuria and absorptive hypercalciuria. Hydrochlorothiazide 50–100 mg daily or an equivalent dose of other diuretics. Long-term use may reduce its hypocalciuric effect and may cause hypocalcemia and hypocitraturia, requiring calcium citrate supplementation.

② Sodium phosphate cellulose resin: Orally administered, it binds calcium in the intestines to limit calcium absorption. Take 2.5–5 g per dose with meals. Since intestinal calcium is reduced, binding with oxalate decreases, leading to increased oxalate absorption. As the drug also binds calcium, inhibiting intestinal calcium absorption, oxalate intake should be appropriately restricted while supplementing calcium. Only used for absorptive hypercalciuria without bone disease, normal blood phosphorus, and ineffective response to calcium restriction and thiazide diuretics. This drug lowers blood Ca²⁺ and increases PTH secretion. It should not be used in primary hyperparathyroidism, renal hypercalciuria, conditions with increased calcium mobilization, growing children, or postmenopausal women.

③ Orthophosphates: Such as neutral or alkaline soluble sodium or potassium phosphate salts, which bind calcium to form calcium phosphate salts, reducing urinary calcium concentration and calcium oxalate saturation. Take 1.5–2.0 g of phosphorus daily, divided into 3–4 doses. Not recommended for those with glomerular filtration rates below 30 ml/min or urinary tract infections, as it may cause metastatic soft tissue calcification and infection-related stones.

(2) Enteric hyperoxaluria: Restricting oxalate and fat intake while supplementing with potassium citrate can significantly increase urine pH and citrate levels. On one hand, citrate acts as an inhibitor of crystal formation; on the other hand, it binds with oxalate in the intestines, preventing its absorption and thereby reducing urinary oxalate excretion. Magnesium hydroxide or magnesium oxide can be used. Cholestyramine can correct intestinal fat malabsorption but cannot consistently inhibit oxalate absorption.

(3) Calcium-containing kidney stones with low urinary citrate: Potassium citrate can effectively limit the formation and recurrence of such stones. The dosage is 3–6 g per day, divided into three doses. Some patients may experience grade I gastrointestinal reactions, and caution is advised for those with renal insufficiency.

(4) Uric acid stones: Increase urine volume, restrict purine intake, and adjust urine pH to 6–6.5, especially nighttime urine pH. While sodium citrate and sodium bicarbonate can raise urine pH, they also increase calcium salt crystallization. Potassium citrate does not have this drawback and is thus the preferred clinical choice, with a dose of 30–60 mmol/day. If hyperuricemia is also present, allopurinol should be added and adjusted to a maintenance dose once uric acid levels are controlled.

(5) Cystinuria and cystine stones: Ensure adequate hydration (usually >3 L/day) and urine alkalinization (pH >7.5). If ineffective, D-penicillamine can be used at 1–2 g per day, divided into doses. The latter binds with cystine in the urine, forming a more soluble compound that is excreted, thereby reducing cystine levels. However, its side effects are significant, including nephrotic syndrome, dermatitis, and pancytopenia. α-Mercaptopropionylglycine has a similar mechanism to D-penicillamine but with fewer side effects. Reports suggest that instilling this drug at the site of kidney stones can dissolve them, while oral administration prevents stone formation.

(6) Infection stones: Long-term, effective control of urinary tract infections can limit the formation of infection stones and even dissolve some existing ones. However, due to low antibiotic concentrations within the stones, bacteria may not be completely eradicated, making it difficult to fully cure the infection with antibiotics alone.

(B) Management of Stones: Treatment for kidney stones has advanced significantly in recent years. Many cases that previously required surgery can now be managed with extracorporeal shock wave lithotripsy (ESWL) or minimally invasive procedures, or a combination of methods, achieving satisfactory results.

1. Medical Treatment: For smooth, round stones smaller than 0.5 cm in diameter, without urinary obstruction or infection, and with good renal function, medical treatment is appropriate (see the "Prevention of Stone Formation and Recurrence" section). Dissolution therapy is more effective for uric acid and cystine stones but less so for calcium-containing and infection stones. Administration routes include oral, intravenous, ureteral catheterization, open nephrostomy, and percutaneous nephrostomy. During treatment, monitor the condition closely, perform regular renal isotope scans and X-rays to assess renal function, and decide whether surgery is necessary.

2. Extracorporeal Shock Wave Lithotripsy (ESWL): This method is now widely used clinically with satisfactory results, especially for single stones around 1.5 cm in diameter. With growing experience, ESWL is also being tested for staghorn stones and other special cases, such as calyceal stones, horseshoe kidney stones, and large multiple stones. However, it should be noted that the physical effects of shockwaves and the generation of H₂O₂ and various free radicals from water molecule transformation can cause injury and bleeding in surrounding tissues. Shockwaves can also directly or indirectly increase renal pelvic pressure by stimulating ureteral smooth muscle contraction, while post-treatment stone fragments and hematuria may increase urinary resistance, raising intratubular and capsular pressure and affecting glomerular and tubular function. Therefore, for patients with urinary obstruction, infection, or impaired renal function, the risks and benefits should be weighed. Preoperative measures such as antibiotics and catheterization to relieve obstruction may be necessary, and postoperative monitoring, infection control, and obstruction relief are crucial. Caution is advised for patients with coronary heart disease, hypertension, or cardiac insufficiency, while uncorrectable bleeding disorders and pregnancy remain contraindications.

3. Surgical Stone Removal Some new minimally invasive surgical techniques for stone removal, such as ureteroscopic and percutaneous nephrolithotomy, have gradually gained widespread clinical use and achieved good therapeutic outcomes. However, for cases where the above-mentioned minimally invasive stone removal procedures, drug therapy, and extracorporeal shockwave lithotripsy are ineffective or contraindicated, as well as for complex stones such as large staghorn calculi, certain multiple stones, or stones with narrowing of the renal pelvis and calyces, accompanied by severe obstruction causing acute urinary retention or severe infection, open surgery remains the preferred treatment. The principle of surgery should prioritize the preservation of renal function as much as possible, and complete stone removal is required to avoid residual stone fragments that could lead to regrowth. Infectious stones often leave residual debris at the surgical site, making postoperative recurrence highly likely.

（III）Symptomatic Treatment

1. Treatment of renal colicky pain: Administer antispasmodics such as atropine or 654-2 via intramuscular injection. Combining with promethazine can enhance efficacy. If ineffective, use pethidine or morphine as needed.

2. Treatment of urinary tract infection: Refer to "Urinary Tract Infection."

3. Hematuria: For significant gross hematuria, administer tranexamic acid 0.1-0.2g or aminomethylbenzoic acid 0.1g via slow intravenous injection, three times daily.

Kidney stone disease is a common renal condition that can easily lead to infections and renal function impairment. In recent years, advancements in understanding its disease causes and pathophysiological research have led to new preventive and therapeutic measures, reducing recurrence rates. Additionally, the application and accumulated experience of extracorporeal shock wave lithotripsy have enabled many patients who previously required surgical intervention to receive effective treatment without the pain of surgery. However, sufficient attention should be paid to the impact of shock waves on the kidneys and the prevention and management of related complications.