The accumulation of oxalic acid in the body is one of the factors leading to kidney calculi. Such as spinach, beans, grapes, cocoa, tea, oranges, tomatoes, potatoes, plums, bamboo shoots and other things that people generally like to eat are foods with high oxalic acid content. Doctors found through research that 200 grams of spinach contains 725.6 milligrams of oxalic acid. If a person eats all 200 grams of spinach at once. Some foods are easy to cause stones to fall off. Eight hours after eating, the urine oxalic acid excretion is 20-25 mg, which is equivalent to the average total amount of oxalic acid excreted by normal people in 24 hours.
Purine metabolism disorder (20%):
Animal offal, seafood, peanuts, beans, spinach, etc. , all contain more purine components. Purine must be metabolized after entering the body, and the final product of its metabolism is uric acid. Uric acid can promote oxalate precipitation in urine. If the food rich in purine is eaten too much at one time, the purine metabolism is abnormal, and oxalate will be deposited in the urine, forming urinary calculi.
Excessive fat intake (15%);
The meat of various animals, especially fat pork, is a high-fat food. Eating too much body fat will inevitably increase, and fat will reduce the calcium that can be combined in the intestine, thus causing the absorption of oxalate to increase. If there is excretory failure, such as sweating too much, drinking too little and urinating too little, kidney calculi is likely to form in this case. Therefore, doctors often say that in order to prevent lithiasis, drink plenty of water in hot days and drink plenty of water when eating greasy food to promote smooth urination and dilute urine components, thus reducing the risk of getting stones.
Increase sugar (10%):
Sugar is an important nutrient of human body, so it should be supplemented regularly and appropriately. However, if you supplement too much at once, especially lactose, it will also create conditions for the formation of stones. Experts found that both normal people and patients with stones, after eating100g sucrose, examined their urine for 2 hours, and found that the concentration of calcium and oxalic acid in urine increased. If lactose is ingested, it can promote the absorption of calcium, which is more likely to lead to the accumulation of calcium oxalate in the body and form urinary calculi.
Protein overdose (10%):
The chemical analysis of kidney calculi showed that calcium oxalate accounted for 87.5% of the stones. The source of such a large proportion of calcium oxalate is that in protein, besides glycine and hydroxyproline, protein can also promote the absorption of calcium by intestinal function. If you often eat too much high-protein food, calcium, oxalic acid, uric acid and other components in the kidney and urine will generally increase. If the excess calcium, oxalic acid and uric acid in the body cannot be excreted through renal function in time and effectively, the conditions of kidney calculi and ureteral calculi will be formed. This is the main reason for the rising incidence in kidney calculi, a developed country in the world.
The main reason for the formation of kidney calculi is diet. It is caused by too many related ingredients that can form stones in the diet.
pathogenesis
1. Factors affecting the formation of stones include:
(1) Urine crystalline substance excretion increased.
① hypercalciuria: When normal people ingest 25mmol of calcium and 65,438+000 mmol of sodium every day, the daily urinary calcium output.
A. Absorbed hypercalciuria: the most common disease, which can be seen in 20% ~ 40% of kidney calculi patients. Its cause is that some intestinal diseases (such as jejunum) cause the increase of intestinal calcium absorption, the increase of blood calcium and the inhibition of parathyroid hormone (PTH) secretion. Due to the increase of blood calcium, glomerular filtration calcium increases, while the decrease of PTH leads to the decrease of renal tubular reabsorption calcium, which leads to the increase of urine calcium, which makes blood calcium return to normal and calcium intake increase.
B. Renal hypercalciuria: It is an idiopathic hypercalciuria, accounting for about 1% ~ 3% of kidney calculi patients. Due to the abnormal function of renal tubules, especially proximal tubules, calcium reabsorption is reduced, and such patients often have secondary hyperparathyroidism and increased PTH secretion; However, the synthesis of 1, 25 (OH) 2VitD3 also increased, which increased bone calcium mobilization and intestinal calcium absorption, and the patient's blood calcium was often normal.
C. Bone resorbable hypercalciuria: mainly seen in primary hyperparathyroidism, accounting for about 3% ~ 5% of kidney calculi's patients; However, 10% ~ 30% of patients with primary hyperparathyroidism complicated with kidney calculi are also seen in hyperthyroidism, metastatic bone tumors, bone resorption caused by long-term bed rest and Cushing's syndrome.
D. Hungry hypercalciuria without increased parathyroid hormone: 5% ~ 25% of kidney calculi patients were followed up. Some factors, such as hyperphosphatemia caused by increased renal phosphorus excretion, increase the synthesis of 1, 25 (OH) 2 vitd3, inhibit PTH secretion, and thus increase urinary calcium excretion.
② hyperoxaluria: The daily urinary oxalate excretion of normal people is 1.5 ~ 60mg. Oxalic acid is the second most important component in kidney calculi besides calcium, but most patients with calcium oxalate in kidney calculi have no abnormal metabolism of oxalic acid. Hyperoxaluria is more common in intestinal oxalate absorption or intestinal hyperoxaluria, accounting for 2% of kidney calculi patients. The combination of calcium and oxalic acid in the intestinal cavity of normal people can prevent the absorption of oxalate. Ileal diseases (such as ileectomy, air-ileum bypass formation, infectious small intestinal diseases and chronic pancreaticobiliary diseases) reduce fat absorption, and the fat in the intestinal cavity combines with calcium, so there is not enough calcium to combine with oxalic acid, which leads to the increase of oxalic acid absorption in the colon. However, unabsorbed fatty acids and bile salts can also damage the colon mucosa, leading to increased absorption of oxalate in the colon. In addition, in the case of absorptive hypercalciuria, the absorption of oxalate can also be increased due to the increase of calcium absorption in the intestine. Hyperoxaluria is occasionally caused by excessive oxalate intake, lack of VitB, excessive VitC intake and primary hyperoxaluria, which can be divided into type I and type II. Type I is caused by the defect of alanine-glyoxylate transaminase (AGT) in the liver. Type ⅱ is the deficiency of liver D- glycerate dehydrogenase and glyoxylate reductase, which leads to the increase of urinary oxalic acid and glycerate excretion. Hyperoxaluria caused by any cause can cause renal tubular and interstitial damage, leading to kidney calculi.
③ Hyperuricemia: The daily uric acid excretion of normal people is generally less than or equal to ≤4.5mmol. Hyperuricemia is the only biochemical abnormality in 65,438+00% ~ 20% patients with calcium oxalate stones, and some people call it "hyperuricemia calcium oxalate stones". As an independent type of kidney calculi, another 40% patients with hyperuricemia are accompanied by hypercalciuria and hypouricemia. The causes of hyperuricemia are primary and myelohyperplasia. Glycogen accumulation and Lesch-Nyhan syndrome, chronic diarrhea such as ulcerative colitis, focal enteritis and air-ileum bypass surgery, on the one hand, the loss of intestinal alkali causes the decrease of urine pH value, on the other hand, the decrease of urine volume, thus promoting the formation of uric acid stones.
④ Hypercystinuria: It is a hereditary disease caused by cystine and lysine transport disorder in proximal tubule and jejunum. Due to the obstruction of renal tubular transport, a large amount of cystine is excreted from urine, and the saturation of cystine in urine is related to pH. When the urine pH is 5, the saturation is 300 mg/L; When the pH value of urine is 7.5, the saturation is 500 mg/L. ..
⑤ Xanthine urine is a rare metabolic disease. Due to the lack of xanthine oxidase, the transformation from hypoxanthine to xanthine and from xanthine to uric acid is blocked, which leads to the increase of urinary xanthine (> 1.3 mmol/24h) and the decrease of uric acid. When allopurinol is used, urine xanthine increases due to the inhibition of xanthine oxidase activity, but in the absence of the original xanthine metabolism disorder, xanthine stones generally do not appear.
(2) The influence of other components in urine on stone formation.
① Urine pH: The change of urine pH has an important influence on the formation of kidney calculi, and the decrease of urine pH is beneficial to the formation of uric acid stones and cystine stones; The increase of pH value is beneficial to calcium phosphate stones (pH > 0.05). 6.6) and magnesium ammonium phosphate stones (pH >；; 7.2) Formation.
② Urine volume: If the urine volume is too small, the concentration of crystal substance in urine will increase, which is beneficial to the formation of supersaturation. About 26% patients in kidney calculi, 65,438+00% patients have no other abnormalities except that their daily urine output is less than 65,438+0L.
③ Magnesium ion: Magnesium ion can inhibit the absorption of intestinal oxalic acid and the crystallization of calcium oxalate and calcium phosphate in urine.
④ Citric acid: It can significantly increase the solubility of calcium oxalate.
⑤ Low citrate urine: The combination of citric acid and calcium ion can reduce the saturation of calcium salt in urine, inhibit the crystallization of calcium salt and reduce the amount of citric acid in urine, which is beneficial to the formation of calcium-containing stones, especially calcium oxalate stones. Hypocitrate urine is found in any acidification state such as renal tubular acidosis and chronic diarrhea. Thiazine diuretics cause hypokalemia (intracellular acidosis), excessive animal protein intake and urinary tract infection (bacterial decomposition of citric acid) after gastrectomy. In addition, the etiology of some hypocitral urine is not clear, and hypocitral urine can be regarded as the only biochemical abnormality in kidney calculi patients (65,438+00%) or coexisting with other abnormalities (50%).
(3) Urinary tract infection: Persistent or repeated urinary tract infection can cause infectious stones. Bacteria containing urease, such as Proteus, some Klebsiella, Serratia, Enterobacter aerogenes, Escherichia coli, etc., can decompose urea in urine to generate ammonia, which will increase the pH value of urine and make magnesium ammonium phosphate and phosphate carbonate in a supersaturated state. In addition, pus and necrotic tissue during infection can also cause crystals to gather on its surface to form stones. In some diseases with abnormal renal structure, such as ectopic kidney, polycystic kidney and horseshoe kidney. Kidney calculi can be caused by repeated infection and poor urine flow. Infection is also a complication of other types of kidney calculi, which is mutually causal.
(4) Diet and medicine: drinking hardened water; Malnutrition and lack of VitA can cause urinary epithelium to fall off and form stone core; After taking triamcinolone acetonide (as a stone matrix) and acetazolamide (acetazolamide), about 5% of kidney calculi patients have no biochemical abnormalities, and the cause of stones is still unknown.
2. Composition of kidney calculi
Nephrolite is rarely composed of a single crystal, but there are mostly two or more kinds. One of them is the main body. kidney calculi contains 90% calcium, such as calcium oxalate, calcium phosphate and magnesium ammonium phosphate. A stone without calcium has a core made of uric acid and cystine. Most calcium-containing kidney calculi can be developed on X-ray films. The density of stones on X-ray films and the smoothness or irregularity of their surfaces are helpful to judge the composition of stones.
(1) kidney calculi calcium oxalate: the most common, accounting for 7 1% ~ 84%. Calcium oxalate monohydrate crystals in urine are often similar to red blood cells, and can also be dumbbell-shaped in shape and size, while calcium oxalate dihydrate crystals are biconical in weak birefringence, and stones are spherical, oval, rhombic or mulberries. Sometimes small spherical stones with smooth edges can be formed, and spherical stratification can be seen, which is easy to be complicated with ureteral obstruction. Stones can also be arranged in a tree or exist alone. X-ray shows that kidney calculi has deep internal texture, irregular edges and sometimes renal pelvis or calyx.
(2) kidney calculi of calcium phosphate and calcium carbonate: The crystal of calcium phosphate is amorphous, so it is too small to measure its refractive index. Stones are granular and grayish white, which can increase rapidly in alkaline urine, but they are simple and rare. Most of them are mixed with calcium oxalate or magnesium ammonium phosphate to form stones, which are clearly developed by X-ray and obviously layered, and sometimes fill the whole cavity of renal pelvis and calyx in the form of antlers.
(3) Uric acid calculus: 5% ~ 10%. Anhydrous uric acid crystals are very small and amorphous. Uric acid dihydrate crystals are "teardrop-shaped" or square with birefringence. Stones are round or oval, with smooth surface, orange-red, hard surface and radial arrangement, which are easy to occur in acidic urine. Because most of them are composed of single uric acid, the development under X-ray is weak.
(4) Cystine kidney calculi: accounting for about 65,438 0%, its crystal is hexagonal, its stones are yellowish, its surface is smooth and soft, and it is easy to develop on X-ray films because of its sulfur content.
(5) Magnesium ammonium phosphate stones: they increase rapidly, and most of them are staghorn-shaped, with clear X-ray development, uneven stone density and cuboid urine crystals.
pathogenesis
1. kidney calculi's diagenetic theory.
(1) Renal calcium plaque theory: Some scholars reported that calcified plaques were found in renal papillae for many times, accounting for119.6% of 54 kidneys, and 65 stones grew on calcified plaques, suggesting that calcified plaques were the basis of stones. From the current understanding, the causes of calcification and microlithiasis in the kidney may be one of the causes of supersaturation of systemic stones. It can also be the cause of renal tissue necrosis and calcification caused by various factors. Ectopic calcification and renal damage are closely related to the formation of stones, but stones may not be formed with such pathological damage, and the formation of stones may not be based on calcification.
(2) Urine supersaturation crystallization theory: This theory holds that stones are formed on the basis of precipitation of crystalline components in urine. Some people have tried to form artificial stones by using saturated solution alone, without adding any matrix substances, or removing macromolecules in urine with fiber membrane, which shows that supersaturated solution may be one of the mechanisms of stone formation.
(3) Lack of inhibitor theory: The concept of inhibitor in urine originated from colloid chemistry. At present, scholars have systematically studied calcium oxalate and calcium phosphate, as well as low-molecular and high-molecular substances that inhibit homogeneous nucleation, heterogeneous nucleation, growth and aggregation. The repeatability and comparability of urine inhibitor activity determination have been significantly improved. On this basis, some people have studied synthetic drugs to inhibit the formation of stones.
(4) The theory of free particles and fixed particles: One of the viewpoints of the theory of free particle stone formation is that the saturation of urinary stone components increases and continues to grow into stones after crystallization. When free particles flow through the renal tubules, they cannot grow big enough to block the collecting duct. Therefore, fixed particles are necessary to grow into stones. Under certain conditions, crystals can grow in large numbers, or they can quickly gather into large blocks and attach to the cell wall with the help of mucin. In addition, renal tubular injury is also beneficial to the adhesion of crystals and particles.
(5) Directional epiphysis theory: Most stones are mixed, calcium oxalate stones often contain hydroxyapatite (or take it as the core), and it is not uncommon for calcium oxalate stones to take uric acid as the core. In addition, many patients with calcium oxalate stones have increased uric acid content in urine, and treatment with allopurinol can reduce the recurrence of stones. According to the theory of orientation epiphysis, the lattice arrangement of stones is often obviously similar to each other, if the two crystal planes are higher.
(6) Immunosuppression theory: This theory holds that there are problems of immunity and immunosuppression in stone formation, and 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, which are transported by α-globulin and invade renal epithelial cells, causing kidney calculi. This theory needs to be confirmed.
(7) Multi-factor theory: There are various molecules and ions in urine, which attract or repel each other. Because the physical and chemical environment in urine is extremely complicated, it is difficult to explain the principle of stone formation with a theory or a simple phenomenon. So far, many basic and clinical research results support the multi-factor theory. At present, the comprehensive research on stone formation has been deepened. Robertson put forward six risk factors of stone formation: ① The decrease or increase of urine pH value may lead to stone formation. ② Increased urinary oxalic acid; ③ Increased urinary calcium; ④ Uric acid increased; ⑤ The substances that promote the formation of urinary stones increase, including urinary crystals, TH proteins, cell decomposition products, phospholipids, cells and their fragments. ⑥ The substances that inhibit the formation of stones in urine are reduced, including pyrophosphate, citric acid, magnesium ion and diphosphate. Recently, the role of macrophages and cell growth factors in the formation of stones has also been concerned.
2. Physical and chemical processes and influencing factors of stone formation.
From the physical and chemical point of view, the formation of stones is closely related to at least three factors: ① supersaturation of stone salt in urine; (2) Inhibitors decrease or promoters increase; ③ Abnormal urinary tract patency and mucosal surface characteristics.
(1) Urine crystal supersaturation: Urine supersaturation is the source of "energy" for stone formation. The supersaturation of stone salt in urine can be expressed by the ratio of the activity product (AP) to the solubility product (SP) of stone salt, which has the following relationship with the free energy (△G) for solid phase formation, that is, △ g = RT/N. When the activity product is higher than the solubility product, Therefore, it is more important to study the dynamic process of stone formation and the factors affecting these processes (such as inhibitors and accelerators) than the thermodynamic process.
(2) Dynamic process of stone formation: Urine is a very complicated physical and chemical system, in which several kinds of stone salts can be supersaturated. What kind of crystals are precipitated from urine is determined by thermodynamics and kinetics. The chemical kinetic process of stone formation mainly includes: ① nucleation, that is, the process of supersaturated solution forming solid phase; (2) Growth: The growth of crystal nucleus includes two basic processes, namely, the transport of solute (from solution to the vicinity of crystal) and the combination of solute and crystal lattice, namely, the transport process and the surface interaction process. There are many types of crystal growth, among which the main ways are spiral growth and multi-core growth; (3) Aggregation, solid particles become larger, not only crystals grow, but also small particles flocculate to form larger lumps; ④ Solid phase transformation: There are many kinds of solid substances in urine, but their chemical compositions are different, or their chemical compositions are the same but their hydration degrees are different. Generally, the solid substances formed under favorable kinetic and unfavorable thermodynamic conditions are unstable, and the combined precursor lumps will be transformed into stable phases in turn. This transformation is not only a simple lattice transformation, but also a series of other changes, such as calcium, phosphorus ratio, hydration degree and other chemical reactions.
In the process of stone formation, once large crystals are formed and attached to the urinary tract wall, nucleation and aggregation may be a rapid dynamic process, while in supersaturated urine environment, stone formation may be a slow dynamic process, in which minerals and matrix exist, and a series of dehydration and phase transformation processes will occur during its growth, making the stone structure tend to be dense and hard.
(3) Promoter and inhibitor of stone formation: Some stone salts in urine are supersaturated, but the reason why stones only occur in a few people is unknown. Patients with stones may lack inhibitors or have too many accelerators in their urine. In addition, there are natural and synthetic inhibitors such as some Chinese herbal medicines and artificial semi-synthetic acidic mucopolysaccharides.
3. Stone matrix and stone formation
Stones in kidney calculi are composed of crystal components and organic matter (matrix), but the significance of matrix to the formation of stones is not clear. Most scholars believe that the matrix determines the structure of stones and is an essential substance for the formation of stones.
Effect of (1) glycosaminoglycan on stone formation;
① composition of glycosaminoglycan: glycosaminoglycan (GAG), also known as acidic mucopolysaccharide, has a molecular weight of about 2 ~ 30kd, is an important component of cell surface and connective tissue, and plays an important role in regulating extracellular fluid volume, electrolyte movement, calcium balance and tissue deposition (ossification or calcification, etc.). ) and tissue fibrosis. GAG can be divided into seven types according to monosaccharides that make up disaccharide units: transparent. Chondroitin sulfate a; Chondroitin sulfate b; Chondroitin sulfate c; Heparin sulfate; Heparin; Keratin sulfate.
The acidic hydroxyl group of GAG and hexosamine sulfate are negatively charged. Except hyaluronic acid, all gags have sulfate groups, which are easy to combine with positively charged calcium and antagonize negatively charged oxalic acid. Heparin and sulfated heparin have different structural forms and different functions. Sulfated gag plays an important role in binding proteins and participates in the regulation of water distribution. 1 gags can combine with hundreds of water molecules. It has recently been reported that in urine.
② Excretion of urinary GAG: Adults can produce 250 mg of GAG in 1 day, of which about 10% is excreted in urine. The GAG in normal adult serum is about 2 ~ 3 mg/L, and chondroitin sulfate is the main one. Most of GAG in urine is the product of proteoglycan decomposing enzyme, which is secreted into urine through glomerular filtration or renal tubule, and some of gag is proteoglycan, accounting for 60%. 18% is keratin sulfate, 15% is heparin sulfate, 4% is hyaluronic acid, and 2% is chondroitin sulfate b, but there is no heparin.
(3) Gag in Stonehenge:1956. Boyce decalcified the stone with EDTA and extracted GAG (mainly in the form of mucin) from the matrix. Carbohydrate accounts for about 1/3, and protein accounts for 2/3, 1968. Amino hexose was found in the matrix, which confirmed the existence of glycosaminoglycan.
At present, it is considered that different types of stones have different GAG types. For example, heparin sulfate is the main component in calcium oxalate and uric acid stone matrix, heparin sulfate and hyaluronic acid are the main components in calcium oxalate dihydrate stone matrix, and hyaluronic acid is the main component in calcium phosphate stone.
④ The effect of ④④GAG on stone formation: The experiment proved that chondroitin sulfate A could inhibit the crystal agglutination of oxalic acid, while heparin sulfate and hyaluronic acid did not inhibit or even promote the crystal agglutination of calcium oxalate. With the increase of the concentration of heparin sulfate and hyaluronic acid, the promotion of calcium oxalate crystal agglutination is enhanced. The promotion of heparin sulfate is slightly greater than that of hyaluronic acid, but the mixture of heparin sulfate and hyaluronic acid has strong activity of promoting crystal agglutination.
(2) Effect of matrix macromolecules on stone formation:
① Tam-Horsfall protein (THP): THP is the main mucin in urine, which is synthesized by Golgi apparatus in ascending branch epithelial cells of renal medulla loop and can bind with calcium. Most scholars believe that TH protein can inhibit and promote the formation of stones.
② Renal calcineurin: Polyaspartic acid and polyglutamic acid can inhibit the growth of calcium oxalate monohydrate crystals and can be separated and extracted from human urine by chromatography. After more than 65,438+00 years of research, Nakagawa and Coe clarified the essence of this substance and named it nephrocalcin (65,438+04 KD acid glycoprotein), which is characterized by rich amino acid composition.
③ Crystal matrix protein (CMP): 199 1 year, Ryall et al. extracted a kind of protein with strong inhibitory effect on the crystallization of calcium oxalate, named CMP(3 1kD), whose N-terminal is the same as human prothrombin, and its 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 showed that CMP existed in other parts of nephron except glomerulus, and scanning electron microscope showed that CMP also existed on the surface of crystal. Because CMP exists in renal tissue and urine, it comes not only from blood, but also from renal secretions.
④ Serum protein: Dussol et al. found that serum protein can enter the stone matrix by combining with calcium oxalate crystals. In addition, the matrix also contains α -globulin and occasionally γ -globulin
⑤ Osteopontin (OPN): OPN is a glycoprotein that can connect osteoblasts with hydroxyapatite. Immunohistochemistry showed that there were scattered OPN in the distal tubule of normal kidney. When kidney calculi model was established in rats with glyoxylic acid, it was found that with the increase of glyoxylic acid, the OPN content increased, renal tubular cells became hypertrophy and vacuolar degeneration, and then calcium salt was deposited to form stone nuclei. Animal experiments show that PT.
⑥ Calcium protection: Renal calcium protection may be mainly secreted by macrophages and exists in distal renal tubules and its surrounding areas. When the kidney forms stones, the protective effect of local cal is obviously enhanced.
4. Oxalic acid metabolism and stone formation
Among the stones in kidney calculi, calcium oxalate stones are the most common (about 80%), so it is more practical to study the causes and formation process of calcium oxalate stones.
Properties of (1) oxalic acid: oxalic acid (HOOC-COOH) is a simple dihydroxy acid. Oxalic acid is the metabolic end product of many plants, animals and microorganisms. Oxalic acid exists in the form of salt in animals or plants. In nature, the most common form is calcium oxalate, which constitutes the skeleton of plants or the mycelium of fungi, but in animals (especially people), it is often a factor in the formation of stones.
(2) Sources of urinary oxalic acid: About 65,438+00% of urinary oxalic acid comes from daily diet, and the rest comes from internal metabolism. Although oxalic acid in diet only accounts for 65,438+00% of urinary oxalic acid, it is an important cause of stone formation. For example, the Arab diet contains more oxalic acid and less calcium, so the urinary calcium content can be maintained at a low level. Due to the increase of urinary oxalic acid, urinary oxalic acid generally increases after eating; Due to seasonal changes, the urinary oxalic acid level fluctuates, that is, the urinary oxalic acid level rises in the season when vegetables are on the market.
Oxalic acid in urine of patients with enterogenous hyperoxaluria mainly comes from diet. After ileectomy or empty ileum anastomosis (intestinal short circuit), fat malabsorption and fatty acids increase in the intestine. At this time, calcium in the intestine combines with fatty acids to form fecal stones, while calcium combined with oxalic acid decreases and absorbable free oxalic acid increases. Therefore, calcium supplementation can reduce the content of oxalic acid in urine. However, oral calcium should not exceed 3.0g/d, otherwise urine output will be low.
(3) Influencing factors of urinary oxalic acid excretion:
① Calcium intake: 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, and the intestinal absorption of oxalic acid lacks this feedback regulation mechanism. If the content of oxalic acid in the diet increases, the free oxalic acid absorbed by the intestine will also increase, which can directly determine the amount of oxalic acid absorbed by the intestine. If the intake of calcium increases, the absorption of oxalic acid will decrease. Oxalic acid is filtered out of the glomerulus and secreted or reabsorbed in the proximal renal tubule. Both endogenous oxalic acid and oxalic acid absorbed by the intestine are excreted by the kidney. Taking calcium lactate and citric acid at the same time can reduce the excretion of oxalic acid in urine. Therefore, it may be of great significance to eat more calcium-containing diet in peacetime to reduce the incidence of stones in China.
② High protein diet: The reason for the rapid increase of urinary calculi in recent years is mainly related to high protein diet (especially excessive intake of animal protein). Therefore, excessive intake of protein increases oxalic acid in urine and promotes the formation of stones. The reasons why high-protein diet promotes the formation of stones may be as follows: after eating high-protein diet, uric acid in urine increases and pH value in urine decreases, which easily leads to the formation of calcium oxalate stones; The increase of uric acid in urine increases the formation of uric acid crystals and helps to form mixed stones of uric acid and calcium oxalate.
③ High-fat diet: Haruko Ito used multivariate analysis to analyze the relationship between intake of nutrients and urinary oxalic acid. The results show that calcium can reduce urinary oxalic acid, while fat can increase urinary oxalic acid level. Because the ingested fat is not completely absorbed, the residual fatty acids in the intestine combine with calcium, so the calcium that should be combined with oxalic acid decreases, which leads to the increase of free oxalic acid absorbed by the intestine and the increase of urinary oxalic acid.
④ Oxalic acid decomposing bacteria in intestine: Oxalic acid decomposing bacteria (Bifidobacterium of lactic acid bacteria, Propionibacterium of propionibacterium, etc.). ) isolated from the intestine, using these intestinal bacteria can explore new ways to prevent the formation of kidney calculi.
(4) Calcium oxalate stones: Most of the stones in kidney calculi are calcium oxalate stones. The study shows that calcium oxalate stone is closely related to the following factors: ① high oxalic acid environment at the site where the stone is formed; ② Calcium binding protein participates in the formation of calcium oxalate crystal nucleus; ③ Macrophages and cytokines are involved in the formation of calcium oxalate stones; ④ Calcium oxalate stone inhibitor in stone matrix and urine.
The general process of calcium oxalate stone formation is as follows: under the condition of stone pathogenic factors (such as excessive urinary oxalate, infection and hydronephrosis), crystals form in the distal renal tubular cavity or renal tubular cells, and the local oxalic acid concentration in renal tissue also increases. The former makes the crystals continue to grow, agglutinate and adhere, and stay in the epithelial cells in the renal tubular cavity to form stone particles, while the latter induces macrophage aggregation, devours oxalic acid and calcium oxalate crystals, and releases osteopontin and calcin at the same time.