kidney stones
Introduction
Introduction to kidney stones Calculus of kidney refers to a stone that occurs in the renal pelvis, renal pelvis, and junction of the renal pelvis and ureter. Most of them are located in the renal pelvis and renal parenchyma. The renal parenchymal stones are rare. The plain film shows that the kidney has single or multiple circular, oval or blunt triangular dense shadows. The density is high and uniform, the edges are smooth, but there are also matte mulberry . The kidney is the main part of the urinary calculi. The stones in any other part can be originated in the kidney. The ureteral stones are almost all from the kidneys, and the kidney stones are more likely to directly damage the kidneys than any other part of the stone. Therefore, early diagnosis and treatment are very important. basic knowledge The proportion of illness: 0.02% Susceptible people: no special people Mode of infection: non-infectious Complications: Bladder stones Urinary tract infections Chronic pyelonephritis
Cause
Cause of kidney stone
Too much oxalic acid accumulation (25%):
The accumulation of oxalic acid in the body is one of the factors leading to kidney urinary stones. Such things as spinach, beans, grapes, cocoa, tea, oranges, tomatoes, potatoes, plums, bamboo shoots, etc., which people generally like, are foods with higher oxalic acid. The doctor found through research that 200 grams of spinach contains 725.6 mg of oxalic acid. If one person eats 200 grams of spinach at a time. Some foods are prone to stone loss. After 8 hours of eating, the urine oxalic acid excretion is 20-25 mg, which is equivalent to the average total amount of oxalic acid discharged by normal people in 24 hours.
Metabolic disorders (20%):
Animal viscera, seafood, peanuts, beans, spinach, etc., all contain more bismuth ingredients. After entering the body, the metabolism is carried out, and the final product of its metabolism is uric acid. Uric acid promotes the precipitation of oxalate in the urine. If, too much, the food rich in sputum is consumed too much, the metabolism of sputum is abnormal, and oxalate is deposited in the urine to form urinary stones.
Too much fat intake (15%):
Meat of various animals, especially fat pork, is a fat food. Eat more body fat will increase, fat will reduce the binding of calcium in the intestine, thus causing increased absorption of oxalate, if there is a discharge function failure, such as sweating, drinking less water, less urine, kidney stones It is likely to form in this case. Therefore, doctors often say that in order to prevent stone disease, you should drink more water on hot days. When you eat more oily foods, you should drink more water to promote smooth urination and dilute the urine components. danger.
Increase in sugar (10%):
Sugar is an important nutrient for the human body. It should be supplemented regularly, but it will increase too much, especially lactose, which will also create conditions for stone formation. Experts found that regardless of normal people or stone patients, after eating 100 grams of sucrose, check their urine after 2 hours, and found that the concentration of calcium and oxalic acid in the urine increased. If lactose is used, it can promote the absorption of calcium. It may cause the accumulation of calcium oxalate in the body to form urinary stones.
Protein excess (10%):
Laboratory analysis of kidney stones found that calcium oxalate accounted for 87.5% of the stones. The source of such a large proportion of calcium oxalate is because the protein can promote the absorption of calcium by the intestinal function in addition to the raw materials containing oxalic acid, glycine and hydroxyproline. If you regularly consume high-protein foods, the calcium, oxalic acid, and uric acid in the kidneys and urine are generally increased. If the excess calcium, oxalic acid, and uric acid are not excreted through the kidney function in a timely and effective manner, the conditions for kidney stones and ureteral calculi are formed. This is the main reason why the incidence of kidney stones is increasing in today's world economy.
The main reason for the formation of kidney stones is diet. It is caused by excessive intake of related ingredients that can form stones in the diet.
Pathogenesis
1. Factors affecting the formation of stones include:
(1) Increased urinary liquid crystal substance excretion
1 high calcium urine: normal people consume 25mmol calcium and 100mmol sodium per day, daily urinary calcium discharge <7.5mmol (or 0.1mmol / kg); daily intake of 10mmol, urinary calcium displacement <5mmol, persistent high calcium urine It is the most common independent abnormal factor in patients with kidney stones. The stones caused are mostly calcium oxalate stones. Correcting high calcium urine can effectively prevent the recurrence of kidney stones. Therefore, hypercalciuria plays an important role in the pathogenesis of kidney stones. The mechanism can be divided into the following four types.
A. Absorptive hypercalciuria: the most common, seen in 20% to 40% of patients with kidney stones, the cause of which is mostly intestinal diseases (such as jejunum) cause increased intestinal calcium absorption, elevated blood calcium, inhibition of parathyroid glands Hormone (PTH) secretion, increased glomerular filtration calcium due to elevated blood calcium, decreased PTH leads to reduced renal tubular reabsorption of calcium, resulting in increased urinary calcium, normal blood calcium, increased calcium intake, VitD poisoning and knotting Increased VitD caused by joint disease can also lead to absorptive hypercalciuria. In these patients, due to increased compensatory calcium excretion, blood calcium concentration is often in the normal range.
B. Renal hypercalciuria: a type of idiopathic hypercalciuria, which accounts for about 1% to 3% of patients with kidney stones. Due to abnormal function of renal tubules, especially proximal tubules, reabsorption of calcium is reduced. Patients often develop secondary hyperparathyroidism, increased secretion of PTH; and 1,25 (OH) 2VitD3 synthesis also increased, resulting in increased bone calcium mobilization and intestinal calcium absorption, patients with blood calcium can often be normal.
C. Bone resorption hypercalciuria: mainly seen in primary hyperparathyroidism, accounting for 3% to 5% of patients with kidney stones; and 10% to 30% of patients with primary hyperparathyroidism complicated with kidney stones, It is also seen in hyperthyroidism, metastatic bone tumors, bone resorption due to prolonged bed rest and Cushing's syndrome.
D. Hunger hypercalciuria without elevated PTH: About 5% to 25% of patients with kidney stones, some factors such as increased renal phosphorus excretion caused by hypophosphatemia, resulting in increased synthesis of 1,25(OH)2VitD3 The latter inhibits PTH secretion, thereby increasing urinary calcium excretion.
2 high oxalic acid urine: normal people daily uric acid displacement is 15 ~ 60mg, oxalic acid is the second most important component of kidney stones other than calcium, but most patients with calcium oxalate kidney stones do not have abnormal oxalate metabolism, high oxalic acid urine is more common in Intestinal oxalic acid absorption abnormality, or intestinal high oxalic acid urine, accounting for 2% of patients with kidney stones, normal intestinal intestinal calcium and oxalic acid can prevent oxalic acid absorption, ileal diseases (such as ileal resection, air-ileal bypass formation Postoperative, infective small bowel disease, chronic pancreas and biliary tract disease) due to reduced fat absorption, intestinal fat and calcium, so there is not enough calcium combined with oxalic acid, resulting in increased absorption of oxalic acid in the colon; and unabsorbed fatty acids and gallbladder Salt itself can damage the colonic mucosa, causing the colon to absorb more oxalic acid. In addition, in the absorption of hypercalciuria, due to the increase of intestinal absorption of calcium, it can also cause increased absorption of oxalic acid. High oxalic acid is occasionally seen in excessive intake of oxalic acid, and VitB is lacking. Excessive intake of VitC and primary hyperoxaluria, the latter is divided into type I and type II, type I is caused by defects in alanine-glyoxylate aminotransferase (AGT) in the liver; II The liver D- glyceric acid dehydrogenase and glyoxylate reductase deficiency results in urinary oxalate excretion and glyceric acid, any cause hyperoxaluria can cause tubular injury and interstitial, cause kidney stones.
3 high uric aciduria: normal people generally have a daily uric acid output 4.5mmol, high uric aciduria is the only biochemical abnormality in patients with 10% to 20% calcium oxalate stone, some people call it "high uric acid calcium oxalate stone", and as a Independent kidney stone type, another 40% of patients with hyperuricemia have both hypercalciuria and hypocapnia, the cause of hyperuricemia is primary and myeloproliferative diseases, malignant tumors, especially after chemotherapy. Glycogen accumulation syndrome and Lesch-Nyhan syndrome, chronic diarrhea such as ulcerative colitis, focal enteritis and jejunal-ileal bypass formation, etc., on the one hand, intestinal alkali loss causes urinary pH to drop, on the other hand The amount of urine is reduced, which promotes the formation of uric acid stones.
4 homocysteine urine: a hereditary disease caused by transport defects such as cystine and lysine in proximal tubules and jejunum. Due to renal tubular transport disorder, a large amount of cystine is excreted from the urine, and cystamine in urine Acid saturation is related to pH. When the urine pH is 5, the saturation is 300 mg/L; when the urine pH is 7.5, the saturation is 500 mg/L.
5 Huangqi urine: It is a rare metabolic disease. Due to the lack of xanthine oxidase, the conversion of hypoxanthine to jaundice and jaundice to uric acid is blocked, resulting in an increase in urinary jaundice (>13mmol/24h). Urinary uric acid is reduced. In the treatment with allopurinol, jaundice oxidase activity is inhibited and urinary jaundice is increased. However, in the absence of the body's original jaundice metabolic disorder, jaundice is generally not caused.
(2) The influence of other components in urine on the formation of stones
1 Urine pH: Changes in urine pH have an important effect on the formation of kidney stones. The decrease in urine pH is conducive to the formation of uric acid stones and cystine stones. The increase in pH is beneficial to calcium phosphate stones (pH > 6.6) and magnesium ammonium phosphate stones ( pH > 7.2) formed.
2 urine volume: the amount of urine in the urine is increased, which is conducive to the formation of supersaturated state, about 26% of patients with kidney stones, and 10% of patients have no abnormalities except daily urine volume less than 1L. .
3 magnesium ion: magnesium ion can inhibit the absorption of intestinal oxalic acid and inhibit the formation of crystallization of calcium oxalate and calcium phosphate in urine.
4 citric acid: can significantly increase the solubility of calcium oxalate.
5 low bismuth uric acid: citric acid combined with calcium ions to reduce the saturation of calcium in the urine, inhibit the crystallization of calcium salts, reduce niacin in the urine, is conducive to the formation of calcium-containing stones, especially calcium oxalate stones, low Citrate is seen in any acidified state such as renal tubular acidosis, chronic diarrhea, postoperative gastrectomy, thiazide diuretics cause hypokalemia (intracellular acidosis), excessive intake of animal protein and urinary tract infections ( Bacteria decompose niacin), and some low-acid uric acid causes are unclear. Hypouric acid can be the only biochemical abnormality (10%) in patients with kidney stones or coexist with other abnormalities (50%).
(3) urinary tract infection: persistent or repeated urinary tract infection can cause infectious stones, bacteria containing urea decomposing enzymes such as Proteus, some Klebsiella, Serratia, Enterobacter aerogenes and Escherichia coli, can decompose Urea urea produces ammonia, which raises the pH of the urine, causing the ammonium magnesium phosphate and the phosphate rock to be supersaturated. In addition, the pus and necrotic tissue during infection also promotes the accumulation of crystals on the surface of the stone, in some kidney structures. Abnormal diseases such as ectopic kidney, polycystic kidney, horseshoe kidney, etc., can cause kidney stones due to repeated infection and poor urine flow, infection is still a complication of other types of kidney stones, and mutual cause and effect.
(4) diet and drugs: drinking hardened water; malnutrition, lack of VitA can cause urinary detachment, forming a core of stone; taking triamterene (as a stone matrix) and acetazolamide (acetazolamide), another 5 There are no biochemical abnormalities in patients with % kidney stones, and the cause of stones is unclear.
2. The composition of kidney stones
Kidney stones are rarely composed of a single crystal, most of which have two or more types, and one of them is mainly composed of 90% kidney stone containing calcium, such as calcium oxalate, calcium phosphate and magnesium ammonium phosphate, excluding Calcium stones are the core formed by uric acid and cystine. Most of the calcium-containing kidney stones can be developed on X-ray films. The density of stones on the X-ray and the smoothness or irregularity of the surface can help determine the stone composition.
(1) Calcium oxalate kidney stone: the most common, accounting for 71% to 84%. Calcium monohydrate oxalate crystal in urine is often similar to red blood cells, and can also be dumbbell-shaped, with shape and size with birefringence, and calcium oxalate dihydrate crystal Double cone-shaped, weak birefringence, stone is spherical, oval, diamond or mulberry-like, dark brown, very hard, rough surface, it is easy to damage tissue caused by hematuria, more common in alkaline urine, sometimes can form small Spherical and smooth-edged stones, visible globular stratification, easy to merge with ureteral obstruction, stones can also be arranged in a tree or alone, X-ray features deeper markings in the kidney stone, irregular edges, sometimes renal pelvis or The shape of the renal pelvis.
(2) Calcium phosphate and calcium carbonate Kidney stone: Calcium phosphate crystals are amorphous, and the refractive index is too small to be determined. The stone is granular and grayish white, which can be rapidly increased in alkaline urine, but it is rare and simple. It is mixed with calcium oxalate or magnesium ammonium phosphate to form a stone. The X-ray development is clear, the layered lines are more obvious, and sometimes the cavity of the entire renal pelvis and renal pelvis is filled, which is staghorn-shaped.
(3) uric acid stones: 5% to 10%, anhydrous uric acid crystals are small, amorphous, dihydrate uric acid crystals are "teardrop" or square-like, with birefringence, stones are round or oval The surface is smooth, orange-red, hard and the cut surface is arranged radially. It is easy to occur in acidic urine. Since most of it consists of a single uric acid, the X-ray development is light or not developed.
(4) Cystine kidney stone: about 1%, its crystal has a hexagonal shape, the stone is light yellow, the surface is smooth, the quality is soft, and it is easy to develop on X-ray film due to sulfur.
(5) Magnesium ammonium phosphate stones: the increase is faster, the stones are mostly in the shape of "antlers", the X-ray development is clear, the stone density is uneven, and the urine crystals are cuboid.
Pathogenesis
1. The relevant theory of the formation of kidney stones
(1) Renal calcium plaque theory: Some scholars have repeatedly reported that calcified plaques were found in the renal papilla, accounting for 19.6% of the 1154 kidneys examined. 65 stones were grown on calcified plaques. Therefore, it is speculated that calcification is a stone occurrence. Foundation, from the current understanding, the causes of intrarenal calcification and microlithiasis can be a manifestation of supersaturation of whole body stone salt (ectopic calcification), or it can be the cause of necrosis and calcification of renal tissue by various factors, regardless of Ectopic calcification or renal damage is closely related to the formation of stones, but those with pathological damage do not necessarily form stones, and the formation of stones does not have to be based on calcification.
(2) Urine supersaturated crystallography: The theory believes that the stone is formed on the basis of the precipitation of crystalline components in the urine. Some people use the supersaturated solution for the test, without adding any matrix substances, or removing the urine with a fiber membrane. Macromolecular materials can also form artificial stones, indicating that supersaturated solutions may be one of the mechanisms of stone formation.
(3) Inhibition factors lack of theory: The concept of urinary inhibitors originated from colloidal chemistry. At present, scholars have been involved in the two systems of calcium oxalate and calcium phosphate, as well as homogenous nucleation, heterogeneous nucleation, growth and aggregation. The low-molecular and macromolecular substances of inhibition have been systematically studied, and the repeatability and comparability of the determination of urinary inhibitor activity have been significantly improved. On this basis, artificially synthesized drugs for inhibiting the formation of stones have also been studied.
(4) Free granules and fixed granules: One of the views of free granule formation calculus theory is that the saturation of urinary stone components increases, and crystals continue to grow into stones after precipitation, and free particles cannot grow up when flowing through the renal tubules. It is enough to block the extent of the collecting tube. Therefore, it is necessary to have fixed particles to grow into a stone. The crystal can grow and grow in a large amount under certain conditions, or it can be quickly aggregated into a large agglomerate, adhered to the cell wall by mucin, and Renal tubular damage is also conducive to the attachment of crystals, and the retention of particles in the urinary tract is an important factor in the growth of stones.
(5) Orientation epiphysiology: Most of the stones are mixed, calcium oxalate stones often contain hydroxyapatite (or as the core), calcium oxalate stones are not uncommon with uric acid as the core, and not clinically Urinary uric acid is also elevated in patients with calcium oxalate stones. Treatment with allopurinol can reduce the recurrence of stones. Orientation theory suggests that the crystal lattices of various crystal faces of stones often have similarities with each other. The crystal surface can be epiphytic if it has a high degree of anastomosis. The result of orientation epitaxy is obtained in a relatively simple liquid experiment in vitro. The importance of this mechanism remains to be confirmed in complex urine.
(6) Immunosuppression theory: This theory believes that the formation of stones has immunological and immunosuppressive problems. The effect of infection or environmental factors can shorten or prolong the incubation period of stone formation. Once the immune system is stimulated, lymphocytes produce antibodies. The theory that alpha-globulin transports and invades renal epithelial cells to cause kidney stones remains to be confirmed.
(7) Multi-factor theory: There are various molecules and ions in the urine, which attract or repel each other. Because the physical and chemical environment in urine is extremely complicated, it is difficult to use a theory or a simple phenomenon to explain the formation principle of stones. So far, many basic and clinical research results have supported the multi-factor theory. At present, the comprehensive research on the formation of stones has been deepened. Robertson proposed that the six risk factors for stone formation are: 1 the pH value of urine is lowered or increased. Both may lead to stone formation; 2 increased urinary acid; 3 increased urinary calcium; 4 increased uric acid; 5 increased substances in the urine to promote stone formation, including increased urinary crystallization, TH protein, cell decomposition products, phospholipids, cells and their fragments, etc. ; 6 urinary inhibition of stone formation substances, including pyrophosphate, citrate, magnesium ions, diphosphates, etc. Recently, the role of macrophages and cell growth factors in the formation of stones has also received attention.
2. Physical and chemical processes and influencing factors of stone formation
From the point of view of physicochemistry, the formation of stones is closely related to at least three factors: 1 supersaturation of stone salt in urine; 2 reduction of inhibitor or excessive promotion; 3 urinary tract patency and abnormal mucosal surface traits.
(1) Urine liquid crystal supersaturation: Urine supersaturation is the "energy" source of stone formation. The degree of supersaturation of stone salt in urine can be determined by the activity product (AP) and solubility product. The ratio of solubility product, SP) indicates that it has the following relationship with the free energy (G) forming the solid phase, namely: G=RT/n(AP/SP), where R is the thermodynamic constant and T is absolute. Temperature, when the activity product is lower than the solubility product, the urine is in an unsaturated state; when the activity product is higher than the solubility product, the urine is in a supersaturated state, and various stone salt crystals are also common in the urine, suggesting that Although the salt of the stone is supersaturated in the urine, it does not necessarily form a stone, indicating that the supersaturation of the urine is only a prerequisite for the formation of the stone. Therefore, the kinetics of the formation of the stone and the factors affecting the process (such as inhibitors, Promoters) are more important than thermodynamic processes.
(2) The kinetic process of stone formation: Urine is a very complicated physical and chemical system, in which several kinds of stone salts can be supersaturated, and what kind of crystals are precipitated from urine, by thermodynamics and kinetics In terms of aspects, the chemical kinetics of stone formation mainly include: 1 nucleation, which refers to the process of forming a solid phase from a supersaturated solution; 2 growth, nucleation growth involves two basic processes, namely the transport of solute (by solution) There are many types of crystal growth methods, such as spiral growth and multinuclear growth; It is the growth of crystals, sometimes it is composed of small particles flocculation to form larger agglomerates; 4 solid phase conversion, there are various solid phase substances in urine, but their chemical composition is different, or the chemical composition is the same and the degree of hydration is different. Generally, the solid phase material formed under the conditions of kinetic favorable and thermodynamically unfavorable is unstable, and the combined precursor body will be sequentially transformed into a stable phase. Is not only a simple lattice transformation, it also contains other modifications, such as calcium, phosphorus ratio and the degree of hydration of chemical reactions.
During the formation of stones, once large crystals form and adhere to the wall of the urinary tract, nucleation and aggregation may be a fast dynamic process. The formation of stones in a supersaturated urine environment may be a slow dynamic process. The substance and the matrix coexist, and a series of dehydration and phase transformation processes occur during the growth process, which makes the stone structure tend to be dense and hard.
(3) Promoters and inhibitors of stone formation: Some stone salts in urine are supersaturated, but the reason why stones occur only in a few people is unknown. There may be inhibitors or enhancers in the urine of patients with stones. In addition, there are natural and synthetic inhibitors such as certain Chinese herbal medicines, artificial semi-synthetic acid mucopolysaccharides.
3. Stone matrix and stone formation
Kidney stones are composed of crystalline components and organic matter (matrix), but the significance of the matrix to the formation of stones is unknown. Most scholars believe that the matrix determines the structure of the stone and is an essential material for the formation of stones.
(1) Effect of glycosaminoglycan on stone formation:
1 glycosaminoglycan composition: glycosaminoglycans (GAG), also known as acid mucopolysaccharide, GAG molecular weight is about 2 ~ 30kD, is an important component of cell surface and connective tissue, in regulating extracellular fluid capacity, Electrolyte movement, calcium plays an important role in the balance and deposition of tissue (ossification or calcification, etc.) and tissue fibrosis. According to the different monosaccharides constituting the disaccharide unit, it can be divided into 7 types: hyaluronic acid; sulfuric acid. Chondroitin A; chondroitin sulfate B; chondroitin sulfate C; heparan sulfate; heparin; keratin sulfate.
The acidic hydroxyl group and hexosamine sulfate group of GAG have a negative charge. Except hyaluronic acid, other GAGs have a sulfate group, which is easy to combine with positively charged calcium and has antagonistic effect on negatively charged oxalic acid. Heparin and Sulfated heparin has many different structural forms and different functions. The sulfated GAG has an important role in binding to proteins. It participates in the regulation of water distribution. One GAG can bind to hundreds of water molecules. Recently reported in urine. A part of GAG is excreted in the form of proteoglycans, and GAG may participate in the reaction in the form of proteoglycans during crystallization and stone formation.
2 excretion of urinary GAG: Adults can produce 250mg of GAG in one day, about 10% of which is excreted from the urine. The GAG of normal adult serum is about 2~3mg/L, the main component is chondroitin sulfate, and the GAG in urine is mostly protein. The product of polysaccharide degrading enzyme is filtered by glomerulus or secreted into the urine by renal tubules, some of which are proteoglycans, about 60% of urinary GAG is chondroitin sulfate A, 18% is keratin sulfate, and 15% is sulfuric acid. Heparin, 4% is hyaluronic acid, 2% is chondroitin sulfate B, but no heparin.
3 GAG in the stone matrix: In 1956, Boyce decalcified the stone with EDTA, and extracted GAG from the matrix (mainly in the form of mucin). The carbohydrate content in the matrix accounted for about 1/3, and the protein accounted for 2/3. In 1968, hexosamine was found in the matrix, thereby establishing the presence of GAG.
It is currently believed that different types of stones have different types of matrix GAG. For example, the main component in the calcium oxalate and uric acid stone matrix is heparan sulfate, and the main components in the calcium oxalate stone matrix are heparan sulfate and hyaluronic acid. Calcium phosphate stones are mainly composed of hyaluronic acid.
Effect of 4GAG on stone formation: Experiments have shown that chondroitin sulfate A can inhibit oxalic acid crystal agglomeration, while heparan sulfate and hyaluronic acid have no inhibition or even promotion of agglomeration of calcium oxalate crystal, and the concentration of heparan sulfate and hyaluronic acid The increase in the promotion of calcium oxalate crystal agglomeration increases, and the promotion effect of sulfate heparin on calcium oxalate crystal agglomeration is slightly greater than that of hyaluronic acid, and the mixing of the two has an activity of strongly promoting crystal agglutination.
(2) The effect of matrix macromolecular substances on the formation of stones:
1Tamm-Horsfall protein (TH protein, THP): THP is the main mucin in the urine. It is synthesized by the Golgi apparatus in the epithelial cells of the renal pelvis. It is considered to be able to inhibit the TH protein. Can promote the formation of stones.
2 nephrocalcin: multi-day aspartic acid and polyglutamic acid can inhibit the growth of calcium oxalate crystals, can be separated from human urine by chromatographic techniques, Nakagawa and Coe for more than 10 years The study clarified the nature of this substance and named it calcitonin (14kD acid glycoprotein), its amino acid composition is characterized by the accumulation of aspartic acid and glutamic acid, while lysine, arginine, tyrosine The content of acid, phenylalanine and tryptophan is very small, and it is localized to the proximal tubule and the ascending branch of the medullary sputum by immunohistochemistry.
3 crystal matrix protein (CMP): In 1991, Ryall et al extracted a protein with strong inhibitory effect on calcium oxalate crystal from calcium oxalate crystal, and named it CMP (31kD), its N-terminus and human thrombin Originally the same, C-terminal is an active peptide (similar to human prothrombin active peptide), CMP has a strong inhibitory effect on the growth and aggregation of calcium oxalate crystals. Immunohistochemistry found that except for glomeruli, other parts of the nephron are present. CMP, immuno-scanning electron microscopy shows that CMP is also present on the crystal surface. Due to the presence of CMP in kidney tissue and urine, it is not only derived from blood but also from the secretion of the kidney.
4 serum protein: Dussol et al found that serum protein combined with calcium oxalate crystals can enter the stone matrix, in addition, the matrix still contains -globulin, and even contains -globulin.
5 Osteopontin (OPN): OPN is a glycoprotein that can connect osteoblasts with hydroxyapatite. Immunohistochemistry shows that there are scattered OPN in the distal renal tubules of normal kidneys. When the kidney was used to make a kidney stone model, it was found that as the amount of glyoxylic acid increased, the OPN content increased, and the renal tubular cells were hypertrophied, vacuolar degeneration, followed by calcium salt deposition, forming a stone core. Animal experiments showed that PTH made kidney tissue. Increased expression of OPN, hydronephrosis, urinary tract infection can also increase the expression of OPN in renal tissue, estrogen can down-regulate the expression of OPN.
6 Calprotection: Calcium prostaglandin may be mainly secreted by macrophages and present in the distal renal tubules and surrounding parts. When the kidneys form stones, the local calcium inhibitors are significantly increased.
4. Oxalic acid metabolism and stone formation
Among the kidney stones, calcium oxalate stones are the most common (about 80%), so the reason and formation process of calcium oxalate stones are more practical.
(1) Properties of oxalic acid: oxalic acid (HOOC-COOH) is a simple dihydroxy acid. oxalic acid is a metabolic end product of many plants, animals and microorganisms. Oxalic acid exists in the formation of salt in animals or plants, in nature. The most common form is calcium oxalate, which constitutes the skeleton of a plant or the hyphae of a fungus, but is often a factor in the formation of stones in animals (especially humans).
(2) Source of uric acid: About 10% of uric acid is derived from daily diet, and the rest is derived from metabolism in the body. Although oxalic acid in diet only accounts for 10% of uric acid, it is an important cause of stone formation, for example, Arab. The human diet contains more oxalic acid and less calcium, so the calcium content in the urine can be maintained at a lower level. The incidence of stones is significantly increased due to the increase in uric acid. In addition, on a low-calcium diet or on an empty stomach, Intestinal absorption of oxalic acid increased significantly; urinary oxalic acid increased after eating; due to seasonal changes, urinary oxalic acid levels fluctuated, that is, the season when vegetables were more marketed, urinary oxalic acid levels increased.
The uric acid in the urine of patients with intestinal hyperoxaluria is mainly from diet, ileal resection or jejunum-ileal anastomosis (intestinal short circuit), fat absorption is poor, fatty acid in the intestine increases, at this time, calcium in the intestine Fatty acid combines to form fecal stone, calcium combined with oxalic acid is reduced, and free oxalic acid can be absorbed. Therefore, taking calcium can reduce uric acid content in urine. However, oral calcium should not exceed 3.0g/d, otherwise urinary calcium can be mild. Increased, after drinking a lot of mineral water, due to increased calcium intake, urinary calcium increased, while urinary acid decreased.
(3) Factors affecting urinary acid excretion:
1 Calcium uptake: Due to the regulation of 1,25-(OH)2D3 and PTH, even if the calcium intake is increased, the calcium absorbed by the intestine will not increase excessively. The absorption of oxalic acid in the intestine lacks this feedback regulation mechanism. If the oxalic acid content in the diet increases, the free oxalic acid that can be absorbed in the intestine also increases. The amount of oxalic acid in the diet can directly determine the amount of oxalic acid absorbed by the intestine. If the intake of calcium increases, the absorption of oxalic acid decreases, generally, oxalic acid is considered. From glomerular filtration, secretion or reabsorption in the proximal tubules, endogenous oxalic acid and oxalic acid absorbed by the intestine are almost excreted by the kidneys, while taking calcium lactate and citrate preparations can reduce the excretion of oxalic acid in the urine. Therefore, the frequent intake of calcium-containing diet may have important implications for reducing the incidence of stones in China.
2 high-protein diet: In recent years, the sharp increase in the incidence of urinary calculi is mainly related to the high-protein diet (especially the excessive intake of animal protein), so excessive intake of protein increases uric acid in the urine, promotes stone formation, and high protein. Diet may promote the formation of stones may be: after eating a high-protein diet, the urine uric acid increased, the urine pH decreased, easily lead to the formation of calcium oxalate stones; increased uric acid in the urine to increase the formation of uric acid crystals, resulting in epiphytic effects In the formation of mixed stones of uric acid and calcium oxalate.
3 high-fat diet: Ito Haruka used multivariate analysis of the relationship between nutrients and uric acid, and found that calcium can reduce uric acid, while fat can increase uric acid level, because the intake of fat is not completely absorbed, the intestine The fatty acid remaining in the tract is combined with calcium, so the calcium which should be combined with oxalic acid is reduced, resulting in an increase in free oxalic acid and absorption by the intestine, resulting in an increase in uric acid.
4 Intestinal oxalic acid-decomposing bacteria: bacteria that can decompose oxalic acid (bifidobacterium bifidum-sine and propionibacterium of the genus Propionibacterium) are isolated from the intestinal tract, and these intestinal bacteria can be used to prevent kidney stones. A new way of formation.
(4) Calcium oxalate stone: The vast majority of kidney stone stones are calcium oxalate stones. Studies have shown that calcium oxalate stones are closely related to the following factors: 1 high oxalic acid environment at the site of stone formation; 2 calcium-binding protein involved in calcium oxalate crystal core The formation of 3 macrophages and cytokines involved in the formation of calcium oxalate stones; 4 stone matrix and calcium oxalate stone inhibitors present in the urine.
The general process of calcium oxalate stone formation is as follows: under the pathogenic factors of the stone (such as high oxalic aciduria, infection and hydronephrosis), crystals are formed in the distal renal tubule or in the renal tubular cells, and the renal tissue is partially oxalic acid. The concentration is also increased, the former allows the crystallization to continue to grow, agglutinate, adhere, and stay in the renal tubular epithelial cells and form stone particles, which induce macrophage aggregation, phagocytosis of oxalic acid and calcium oxalate crystal, while releasing osteopontin and calcium Inhibition, with the participation of cytokines, forms the core of the stone and falls off the lumen to form stones.
Prevention
Kidney stone prevention
The main measures to prevent the recurrence of urolithiasis are:
1. According to the results of urinary component analysis and the shape of the stones on the flat sheet, the composition of the stone is judged, and the preventive measures are formulated.
2. For pediatric bladder stones, the main problem is to increase nutrition (dairy products), here we especially emphasize the importance of breastfeeding.
3. Drink plenty of water, drinking water is very effective in preventing urinary recurrence. Drinking more water can increase urine output (the daily urine volume should be kept at 2000-3000m1), which significantly reduces the saturation of urinary components (especially calcium oxalate). Statistics, an increase of 50% of urine can reduce the incidence of urinary stones by 86%, 3h after meals is the peak of excretion, but also to maintain sufficient urine output, drinking water before going to sleep, so that the relative density (weight) of nighttime urine is lower than 1.015, drinking more water can produce a certain pressure in the proximal urinary tract of the stone, which promotes the discharge of small stones; it can dilute the excrement and some substances related to the formation of stones (such as TH protein), but some people think that a lot of drinking water is also diluted. The concentration of inhibitors in urine is unfavorable for the prevention of stone formation. In fact, in the influence of urinary formation, the supersaturation of urine plays an important role. In contrast, the effect of large amount of drinking water on the concentration of inhibitors is Much smaller, Itoh et al believe that green tea can prevent the formation of calcium oxalate stones. Green tea contains 13% catechin, which has anti-oxidation effect, can reduce the excretion of oxalic acid in the urine and the formation of calcium oxalate precipitate. Tea therapy can increase the activity of superoxide dismutase (superoxide dismutase, SOD) of.
4. Patients with stones should limit excess nutrients according to the needs of calories, and maintain a daily intake of 75-90 g of protein to maintain energy balance, reduce the risk of urinary stones, and have familial hyperuric acid or gout. Patients should limit the intake of protein to 1g / kg body weight, control the intake of refined sugar, eat spinach, animal viscera and other foods.
5. Magnetized water has a certain anti-rock effect: ordinary water becomes magnetized water after passing through a magnetic field with a strong magnetic field strength. In 1973, it was found that the dissolution of the stone in a container containing magnetized water occurred. Research has found that the charge of various ions in the water changes after the water is magnetized, and the tendency to form crystals is significantly reduced, which can prevent the formation of urinary stones.
6. Treatment of diseases that cause stone formation: such as primary hyperparathyroidism, urinary tract obstruction, urinary tract infections, etc.
7. Drugs: According to the abnormal metabolism in the body, appropriate oral administration of some drugs, such as thiazide drugs, allopurinol, orthophosphate, etc., patients with recurrent calcium oxalate stones should avoid excessive intake of vitamin C.
8. Regular review: urinary stones patients must be reviewed regularly after the stones are discharged. This is mainly because: 1 For most patients with stones, after the stones are discharged, the factors that cause the formation of stones are not solved, and the stones may recur. 2 In addition to clear stones during surgery, no matter what method is used, there may be some stone fragments of different sizes in the body. These stone fragments may become the core of future stone recurrence.
Complication
Kidney stone complications Complications, bladder stones, urinary tract infection, chronic pyelonephritis
Urinary obstruction
Kidney stones caused by urinary tract occlusion can cause water accumulation above the obstruction site, stone obstruction is often incomplete obstruction, some stones have small grooves on the surface, urine can pass along the small groove; sometimes the stone is larger Even the cast stone, but the urine can still flow around the stone, it may not cause water accumulation for a long time, the fibrous tissue of the renal pelvis wall becomes thicker and thicker, the expansion performance is not obvious.
Obstruction of kidney stones is different due to the rapid onset of the disease. Although the clinical manifestations are very different, although it can eventually cause hydronephrosis, the clinical manifestations of hydronephrosis are not necessarily the case. The hydronephrosis sometimes has no clinical symptoms, some cases until The hydronephrosis reaches a serious degree, and the abdomen has a mass and renal insufficiency, even when there is no urine.
2. Local damage
Small and active stones, the damage to local tissue is very light, large and fixed staghorn stones can cause renal pelvis, renal epithelial cells to fall off, ulcers, fibrous tissue hyperplasia, neutrophils and lymphocytes infiltration, resulting in Fibrosis, after transitional epithelial cells are stimulated by stones for a long time, squamous epithelial cell metaplasia can occur, and even squamous cell carcinoma can be caused. Therefore, urine exfoliative cytology should be performed, although abnormalities of exfoliated cells may not be diagnosed. However, it is suggested that abnormal changes of urothelial cells can be obtained. For long-term renal pelvis or bladder stones, the possibility of epithelial cell carcinogenesis should be considered. The frozen tissue should be taken for rapid frozen biopsy.
3. Infection
The presence or absence of infection is of great significance for the treatment and prevention of kidney stones. Patients with urinary tract infections have clinical manifestations of fever, low back pain, pus cells in the urine, and urinary culture with bacteria.
When stones are combined with infection, the growth of stones and the damage of renal parenchyma can be accelerated. Before the stones are discharged or taken out, the infection is difficult to cure, and pyelonephritis, renal empyema, peri-renal inflammation, and even kidneys can be developed. Peripheral abscess; after adhesion to the peritoneum, can be broken into the intestine, microscopically visible renal interstitial inflammation, cell infiltration and fibrosis, neutrophils and epithelial cells in the renal tubules, tubular atrophy and glomerulosclerosis later .
4. Renal insufficiency
Kidney stones in patients with urinary tract obstruction, especially bilateral urinary tract obstruction or on the basis of serious infection, patients may have renal insufficiency, when obstruction and / or infection is effectively controlled, some patients, renal function can be Better or return to normal.
In addition to the detection of serum urea nitrogen, creatinine and endogenous creatinine, the method of judging renal function can also be performed by intravenous pyelography and based on the time and concentration of contrast agent. B-ultrasound can understand urinary dilatation and renal parenchyma. Thickness, but it is difficult to judge renal function. Static or dynamic radionuclide scanning or imaging can provide valuable clues, because kidney block is caused by obstruction and renal damage with changes in the moving parts of the stones, as well as different stages of treatment. Patients need to be followed up, especially dynamic scans to understand the condition of the renal parenchyma. When the stones are discharged, or after drainage, this test can provide a basis for prognosis or further treatment.
5. Renal calcareosis
Calcium in the kidney tissue, mostly in patients with hypercalcemia, primary hyperparathyroidism, renal tubular acidosis and chronic pyelonephritis patients, may have renal calcium deposits, calcium mainly precipitated in the medulla Inside, when the lesion is severe, all renal parenchyma may have calcium deposition, leading to interstitial fibrosis, glomerular sclerosis and tubular atrophy.
6. Kidney tissue is replaced by adipose tissue
Kidney stones, pyelonephritis, kidney tissue can be replaced by adipose tissue, the kidney maintains its original shape but generally shrinks, the kidney capsule and the surface of the kidney are closely adhered, the kidney tissue is atrophied and hardened, and the kidney tissue is scarce in severe cases, even Completely disappeared, filled with grayish yellow adipose tissue between the renal parenchyma and the renal pelvis and renal pelvis.
7. Gastrointestinal symptoms, anemia, etc.
Symptom
Kidney stones symptoms Common symptoms Men's abdominal pain, urinary distress, kidney crystal, high oxalic acid, abdominal muscles, tension, urine, waiting for stones, kidney area, snoring, dull pain
Clinical manifestation
1. Asymptomatic: Most of them are renal pelvis stones. When the physical examination is performed by B-ultrasound, the urine test is negative or there is a small amount of red and white blood cells.
2. Lumbar pain in the waist: Most of the kidneys are larger stones such as cast stones, and there may be hematuria after strenuous exercise.
3. Renal colic: often small stones, microscopic or gross hematuria, obvious pain in the kidney area, pale face, painful cold sweat, rapid pulse and even blood pressure drop, often accompanied by nausea, vomiting and bloating And other gastrointestinal symptoms.
4. History of row of stones: In the case of pain and hematuria, sand or small stones may be excreted in the urine. When the stones pass through the urethra, there is urinary flow obstruction and tingling in the urethra. After the stones are discharged, the urine flow immediately recovers smoothly. Feel relaxed and comfortable.
5. Symptoms of infection: pyuria can occur when the infection is combined, and there may be chills, fever, low back pain, frequent urination, urgency, and painful urination during an acute attack.
6. Renal insufficiency: obstruction caused by one side of kidney stones, can cause hydronephrosis and progressive renal dysfunction on the side; bilateral renal stones or isolated kidney stones cause obstruction, which can develop into uremia.
7. Urine closure: bilateral renal calculi cause bilateral urinary tract obstruction, isolated kidney or only functional renal stone obstruction may occur urinary closure, one side of kidney stone obstruction, contralateral side may have reflex urine closure.
8. Waist mass: When the stone obstruction causes severe hydronephrosis, it can be rubbed and covered in the waist or upper abdomen.
Examine
Kidney stone examination
Laboratory inspection:
1. Urine test can be divided into general inspection and special inspection:
(1) The general examination is mainly urine: it includes pH, relative density (specific gravity), red blood cells, pus cells, proteins, sugar, crystals, etc. Hematuria, crystal urine and pus cells can be found in the urine of patients with uroliths. The pH value often indicates certain types of stones: calcium phosphate, the pH value of patients with carbonate apatite stones is often higher than 7.0; while the urine pH of patients with uric acid, cystine and calcium oxalate stones is often less than 5.5, visible Microscopic hematuria or gross hematuria, but 15% of patients have no hematuria. In non-infectious stones, there may be mild pyuria.
(2) Special inspections include:
1 urine crystallization check: fresh urine should be retained, if you see benzene-like cystine crystals suggest that there may be cystine stones; such as urine found in uric acid crystals, often suggest uric acid stones; found that the envelope-like crystal may be two Calcium oxalate stone; coffin cover crystal is magnesium ammonium phosphate crystal; sulfonamide crystals are found in the urine of patients suspected of having sulfa drug stones.
2 urinary bacterial culture: colonies > 105 / ml are positive, susceptibility test can understand the most effective antibiotics, urine culture, such as bacteria that produce urea, there is the possibility of infected stones.
324h urine test: 24 hours of urine must be collected correctly, urine measurement should be accurate, the test content includes: 24h urinary calcium, phosphorus, magnesium, tannic acid, uric acid, oxalic acid, cystine and so on.
2. Blood biochemical examination:
(1) Normal adult serum calcium is 2.13 ~ 2.6mmol / L (8.5 ~ 10.4mg / dl), inorganic phosphorus is 0.87 ~ 1.45mmol / L (2.7 ~ 4.5mg / dl), primary hyperparathyroidism The patient's serum calcium is higher than the normal value, often above 2.75mmol / L (11mg / dl), and accompanied by a decrease in serum inorganic phosphorus.
(2) Normal adult male serum uric acid does not exceed z416.36mmol / L (7mg / dl), female does not exceed 386.62mmoL / L (6.5mg / dl), when this value is exceeded, hyperuricemia, gout patients Blood uric acid increased.
(3) Kidney stones often have acidosis when accompanied by renal dysfunction. At this time, serum electrolyte changes, serum sodium and carbon dioxide binding capacity decreases, blood potassium levels increase, and hypokalemia and hyperclonality may occur in renal tubular acidosis. Acidosis.
(4) Determination of urea nitrogen and creatinine can understand the renal function of patients, when the renal function is impaired, the blood urea nitrogen, creatinine can be increased to varying degrees.
In short, blood and urine tests in patients with urinary stones can help to understand the renal function of patients with urinary stones, whether there are concurrent infections of stones, the possible types of stones and the causes of stones, and play a role in guiding the treatment and prevention of stones.
Film degree exam:
1. X-ray inspection:
X-ray examination is the most important method for diagnosing urinary calculi, including abdominal plain film, excretory urography, retrograde pyelography, or percutaneous nephrography.
(1) urinary tract film:
The urinary tract X-ray film is the most basic method for diagnosing urinary calculi. According to the impervious X-ray shadow of the kidney, ureter, bladder and urethra, it is possible to preliminarily diagnose the presence or absence of stones. The calcium content in the stones is different. The degree of transmission to the X-ray is also different. About 40% of the stones can be judged according to the dense shadow displayed on the X-ray film. The calcium oxalate stone is the most impervious to the X-ray; the magnesium ammonium phosphate is the second; the uric acid stone is The most common X-ray permeable stones, cystine stones are slightly impervious to X-rays due to sulfur, but indinavir stones and some matrix stones can be developed in plain CT slices, and renal calcification is common in medulla. Sponge kidneys (close to the dilated collecting tube) can also be compared with the density of the lumbar vertebrae and diagnosed, and 10% of the calcium-free stones are not easily found by X-ray films.
The calcified shadow of the abdomen can be confused with urinary calculi. The main shadows of these calcifications are:
1 dirt and gas in the intestines,
2 mesenteric lymph node calcification shadow,
3 bone island formation in the skeletal part (such as the ankle joint area), calcification of the 11th and 12th costal cartilage,
4 "venous stone" shadow formed by venous calcification in the pelvic region,
5 foreign body interference in vitro (such as buttons, knots on the belt, etc.),
6 After the digestive tract tincture was checked, there was no sputum.
(2) Excretory urography:
Excretory urography can further confirm the relationship between the impervious X-ray shadow and the urinary tract on the X-ray film. It can also be seen that the development of the upper urinary tract is delayed; the renal shadow is enlarged; the ureteral dilatation above the renal pelvis and obstruction is distorted. Such changes, and according to this to understand the function of the kidney, if necessary, need to extend the time of angiography in order to achieve satisfactory development of the affected side, the stones in the ureteral wall, filling the bladder shadow can cover the image of the stone, at this time, the patient can urinate after urinatingXIVUIVUIVU(1)
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