Renal ureteral stones [Pathogenesis] Stones are a disease of human pathology and mineralization, and their formation is caused by certain factors that increase the concentration of crystalline material in the urine or reduce the solubility of the supersaturated state, the precipitation of crystals and the growth of local aggregation, and ultimately the formation of stones. In this process, the formation of supersaturation of urinary crystalline material and the decrease in the amount of urinary inhibitors of crystal formation are the two most important factors. First, the formation of supersaturation is seen in low urine volume and excessive absolute excretion of certain substances in the urine, such as calcium oxalate and cystine. Changes in urinary pH affect the solubility of specific substances leading to the development of specific types of stones, e.g., uric acid solubility decreases when urinary pH decreases (<5.5), whereas calcium phosphate, magnesium ammonia phosphate, and sodium urate solubility decreases when urinary pH increases. Secondly, normal urine contains certain substances that can inhibit the formation and growth of crystals, such as pyrophosphate inhibits the formation of calcium phosphate crystals, mucins and citrate inhibit the formation of calcium oxalate crystals, the urine will form stones when the decrease of these substances. In addition to the above two factors, nucleation is also an independent and important factor in stone formation, which is divided into two types: homogeneous nucleation and heterogeneous nucleation. Homogeneous nucleation refers to the crystallization of one type of crystal, calcium oxalate, for example, when there is supersaturation of the two ions to form crystals, the higher the concentration of ions, the more and larger the crystals. Heterogeneous nucleation means that if two crystals are similar in shape, one of the crystals can act as a core to promote the other crystal to aggregate on its surface. For example, sodium urate crystals can promote the formation and growth of calcium oxalate crystals. When the body occurs such as urethral stenosis, prostate hypertrophy, pelvic ureteral junction stenosis and other conditions that lead to slow flow of urine, retention, the formation of crystals in the urine stays in the local area, due to the effect of nucleation will be favorable to the growth of small crystals and conducive to the development of stones. (B) the local factors affecting the formation of stones, urinary tract obstruction, infection and foreign bodies are the main local factors inducing urinary stones. 1, urinary tract obstruction: urinary tract obstruction, the slow flow of urine, the crystalline component of urine is easy to stay in the urinary tract and deposited, resulting in the formation of stones. Urine retention is often complicated by urinary tract infections, bacterial clusters, validation of necrotic tissue and pus clots often become the core of the stone, inducing crystalline material to be deposited on their surfaces and form stones. Therefore, clinical mechanical obstruction of various urinary tracts, such as medullary sponge kidneys, polycystic kidneys, horseshoe kidneys, renal pelvic ureteral junction stenosis, prostatic hyperplasia, urethral stenosis, etc., any of these structural abnormalities and then consequently urine retention at the same time, the patient's body can make the risk of stone formation increased. In addition, changes in urodynamics such as neurogenic bladder dysfunction, prolonged bed rest in the cause of poor urinary drainage at the same time, often accompanied by bone decalcification, elevated blood and urine calcium and other conditions, they may be induced by the emergence of urinary stones. 2, urinary tract infection (infected stones): persistent or recurrent urinary tract infection can cause infected stones (also known as guano stones). Alkaline urine (pH>7.2) and the presence of ammonia are two prerequisites for the formation of infectious stones in the urine, and the presence of bacterial infections that can break down urea in the urine is an important factor in inducing urinary tract infectious stone formation. Bacteria containing urea-degrading enzymes, such as Aspergillus, certain Klebsiella, Serratia, Enterobacter aerogenes, and Escherichia coli, can break down urea in the urine to produce ammonia, which raises the urinary pH and prompts ammonium-magnesium phosphate and phosphorocarbonate to be in a supersaturated state. In addition, pus clots and necrotic tissues from infections, etc. also encourage crystals to collect on their surfaces to form stones. In some diseases with abnormal kidney structure such as ectopic kidney, polycystic kidney, horseshoe kidney, etc., kidney stones can occur due to repeated infections and poor urine flow. Infections also act as a complication of other types of kidney stones and are mutually causative. Clinically, infected stones mainly appear as staghorn-shaped stones, which can grow to completely fill the entire renal pelvis and calyces. In addition, infected stones can act as the core of the stone inducing calcium oxalate deposition on its surface. Generally speaking, women have more chances of urinary tract infection than men, therefore, there are more patients with infected stones in women than in men. 3.Foreign objects: foreign objects in the urinary tract can become the core of urinary stones, and then induce the precipitation of crystalline material on its surface and gradually form stones. For example, the long-term retention of ureteral stent tube or nephrostomy tube may induce the production of stones of medical origin. (iii) Trait analysis of mixed kidney stones Kidney stones rarely consist of a single type of crystals, but mostly have two or more types of crystals, with one of them being the main one. 90% of kidney stones contain calcium, such as calcium oxalate, calcium carbonate phosphate and magnesium ammonium phosphate. Stones that do not contain calcium form cores from uric acid and cystine. The vast majority of calcium-containing kidney stones can be visualized on X-ray. The density of the stone on X-ray and the degree of smoothness or irregularity of its surface are helpful in determining the composition of the stone. 1, calcium oxalate kidney stone: the most common, accounting for 71% to 84%. Urinary monohydrate calcium oxalate crystals are often similar to erythrocytes, can be dumbbell-shaped, shape and size with birefringent. Calcium oxalate dihydrate crystals are bipyramidal and weakly birefringent. Stones are spherical, oval, rhombic or blackberry, dark brown, very hard, rough surface, so easy to damage the tissue causing hematuria, mostly seen in alkaline urine. Sometimes can form a small spherical and smooth edge stones, can be seen spherical layering, very easy to combine with ureteral obstruction. The stones can also be arranged in a tree-like manner or exist alone, X-ray features of the kidney stone has a deeper mottling, irregular edges, sometimes in the shape of the renal pelvis or calyx. Calcium phosphate and calcium carbonate kidney stones: calcium phosphate crystals are amorphous and too small to determine their refractive properties. The stone is granular, grayish-white, and can increase rapidly in alkaline urine, but simple ones are rare, and most of them are mixed with calcium oxalate or magnesium ammonium phosphate to form a stone. x-ray image is clear, and the laminar pattern is more obvious, and sometimes it fills up the whole renal pelvis and renal calyx lumens, which is in the shape of antler. 3, uric acid stones: accounting for 5% to 10%. Anhydrous uric acid crystals are very small and amorphous. Dihydrate uric acid crystals are “tear drop”-shaped or square, with birefringent. The stone is round or oval, smooth surface, orange-red, hard, radial arrangement in section, easy to occur in acidic urine, due to most of the composition of a single uric acid, the X-ray shadow is light or not. 4, cystine nephrolithiasis: about 1%, its crystals are hexagonal shape. Stones yellowish, smooth surface, soft, because of the sulfur and easy to show on the X-ray film. 5, magnesium ammonium phosphate stones: increase faster, most of the stones were “antler” shape, X-ray imaging is clear, uneven density of stones. Urine crystals are rectangular. Differential diagnosis] The vast majority of renal ureteral calculi are easy to diagnose, clinical misdiagnosis is often associated with incorrect, untimely or inexperienced examination, the following diseases need to be differentiated from renal ureteral calculi. 1, gallstones: gallstones can cause biliary colic, easily confused with right-sided renal colic. When gallstones are combined with cholecystitis, there may be persistent pain in the right upper abdomen, aggravated by paroxysms, and Murphy’s sign is positive. Sometimes, there may be an enlarged gallbladder under the right costal margin that is painful to touch and moves with breathing, or a mass wrapped by the greater omentum that has unclear boundaries, little mobility, and is painful to touch. Gallstones patient urine routine examination is generally normal, ultrasound can determine the diagnosis. 2, renal tuberculosis: renal stones combined with obstruction and infection should be identified with renal tuberculosis. Renal tuberculosis often have chronic stubborn bladder irritation symptoms, by general antibiotic treatment has no obvious effect. There are pus cells in the urine, while ordinary urine culture has no bacterial growth; sometimes it is accompanied by pulmonary tuberculosis or small tuberculous foci in the kidneys; cystoscopy reveals lesions such as congestion and edema, tuberculous nodules, tuberculous ulcers, tuberculous granulomas, and scar formations, and the lesions are especially obvious in the bladder triangle and near the ureteral opening. The ureteral opening is often cavernous, and sometimes turbid urine is seen to be discharged; calcific renal tuberculosis is seen as extensive calcification of the whole kidney on plain radiographs, and spotty calcified shadows are seen in the kidney in focal cases. Early X-ray of renal tuberculosis imaging shows that the margins of renal calyx are not neat, and there are worm-like changes, and in serious cases, it can be seen that the renal calyx is occluded, cavity is formed, and the renal calyx and renal pelvis are irregularly enlarged or fuzzy and deformed. 3.Sponge kidney: the incidence of sponge kidney is 1/5000, the patient’s renal medullary collecting ducts are cystic dilated, the general appearance of sponge-like. 70% of the cases have bilateral renal lesions, each kidney has one to several papillae involved. The disease is present at birth but asymptomatic and is usually not recognized until the age of 40 to 50 years due to the development of stones or infectious comorbidities. Dilatation of the collecting ducts causing prolonged urine retention, along with frequent combined hypercalcemia, is responsible for the development of stones and infections Renal tubular concentrating and acidifying functions are often impaired. Abdominal plain radiographs show normal-sized or mildly enlarged kidneys, and clusters of multiple stones (arranged radially in the papillary area) are seen within the renal area. Intravenous pyelography shows fan-like cystic dilatation of the medullary collecting ducts as the basis for diagnosis of the disease. Renal pelvis tumor: renal pelvis tumors are mostly papillomas with no obvious boundary between benign and malignant, and the metastatic pathway is the same as that of renal cancer; because of the thin wall of the renal pelvis and the rich surrounding lymphatic tissues, there are often early lymphatic metastases. The disease mostly occurs after 40 years old, and men are more than women. In early stage, it manifests as painless hematuria without obvious lumps; in late stage, lumps may appear when the tumor increases in size and causes obstruction. Tumor cells are sometimes seen on urine sediment examination, and blood spurting from the ureteral orifice of the affected side is seen on cystoscopy in hematuria. There are filling defects on radiographic film, which need to be differentiated from trans X-ray stone, and CT and ultrasound can assist in the differentiation. 5, biliary ascariasis: renal stone patients with renal colic, should be identified with biliary ascariasis. Biliary roundworm mainly manifested as paroxysmal “drill-like” severe colic under the raphe, which is characterized by sudden onset and rapid relief. During the attack, the patient is often restless, sweating all over the body, even pale, cold limbs, and often accompanied by nausea and vomiting, vomit may contain bile or even roundworms. In the intervals between attacks, the pain may disappear completely. Sometimes the pain may radiate to the right shoulder or back, and ultrasound can make the diagnosis clear. 6, acute appendicitis: right renal stone patients with renal colic, should pay attention to and acute appendicitis for differentiation. Metastatic right lower abdominal pain is a characteristic of acute appendicitis. 70% to 80% of patients, at the beginning of the onset of epigastric pain, a few hours to a dozen hours after the transfer to the right lower abdomen. Epigastric pain is generally thought to be caused by visceral nerve reflexes, whereas right lower abdominal pain is caused by inflammatory stimulation of the right lower abdomen. The abdominal signs of acute appendicitis are limited, fixed and obvious pressure points in the right lower abdomen, and when the abdominal pain has not yet transferred to the right lower abdomen, the pressure pain has been fixed in the right lower abdomen, which is of great significance in the diagnosis. If the symptoms are atypical or the position of the appendix is abnormal, other symptoms and signs should be referred to for identification. If it is difficult to confirm the diagnosis, it should be closely observed and comprehensively analyzed to reduce misdiagnosis. 7, acute pancreatitis: abdominal pain is the main symptom of acute pancreatitis. Abdominal pain often begins in the upper abdomen, but can also be limited to the right upper abdomen or left upper abdomen, depending on the location of the lesion invasion. If the head of the pancreas and biliary tract disease, in addition to the right epigastric pain, can be radiated to the right shoulder or right waist; inflammation mainly invades the tail of the pancreas, epigastric pain can be radiated to the back of the left shoulder. The nature and intensity of the pain is mostly consistent with the extent of the lesion. Edematous pancreatitis is mostly persistent pain, may be accompanied by paroxysmal aggravation, mostly tolerable; hemorrhagic or necrotizing pancreatitis is mostly cut-like pain, not easy to be relieved by general analgesic drugs, and shock may occur in severe cases. According to the history, signs and blood, urine amylase measurement, most of the diagnosis of acute pancreatitis can be established. 8, ovarian cyst torsion: renal stone female patients with renal colic should pay attention to the ovarian cyst torsion to distinguish. Typical symptoms of ovarian cyst torsion are sudden onset of severe abdominal pain, even shock, nausea, vomiting. Gynecological examination reveals a mass with significant tenderness, high tension and limited muscle tension. If the torsion occurs slowly, the pain is mild, and sometimes the torsion can be reset by itself and the pain is relieved. Calcification of lymph nodes: If it is located in the kidney area, it can be misdiagnosed as kidney stone. Lymph node calcification is round granular dense shadow, internal uneven, and multiple, scattered, intravenous urography plus side view film can help to distinguish it from kidney stone. 10, other diseases: kidney stones should also be identified with other diseases that cause low back pain, abdominal pain, such as ruptured ectopic pregnancy, gastritis, gastric ulcer and other diseases. Complications] 1, urinary tract obstruction: renal calculi cause urinary tract lumen blockage can cause obstruction above the site of fluid accumulation. Stone obstruction is often incomplete obstruction, some stones have small grooves on the surface, the urine can pass along the small communication; sometimes the stone is larger, even cast stone, but the urine can still flow along the stone around, may also not cause fluid retention for a long period of time, the wall of the renal pelvis fibrotic tissue hyperplasia and thickening, then the expansion of the manifestation of the inconspicuous. The clinical manifestations of stone obstruction vary greatly depending on the urgency of its onset. Although all of them can eventually cause hydronephrosis, the clinical manifestation of hydronephrosis is not necessarily the main manifestation. Sometimes there are no clinical symptoms of hydronephrosis, and in some cases, hydronephrosis is not detected until the severity of hydronephrosis, abdominal swelling and renal insufficiency, or even anuria. 2, local damage: small and large activity of the stone, the damage to the local tissue is very light, large and fixed staghorn-shaped stone can make the renal calyx, renal pelvis epithelial cell detachment, ulcers, fibrous tissue hyperplasia, neutrophils and lymphocytes infiltration, resulting in fibrosis. After long-term stimulation of migrating epithelial cells by stones, squamous epithelial cell chemotaxis and even squamous epithelial cell carcinoma can occur, so urine exfoliative cytology should be done. Although an abnormal urine exfoliative cell does not necessarily lead to a definitive diagnosis, it may provide a hint of abnormal changes in the urinary tract epithelial cells. For the long-term existence of renal pelvis or bladder stones, the possibility of epithelial cell carcinoma should be thought of, and biopsies should be taken and sent for rapid frozen section examination at the time of surgery. Infection: the presence or absence of infection is of great significance to the treatment and prevention of kidney stones. The clinical manifestations of patients with urinary tract infection are fever, lumbago and pus cells in urine. When there are bacteria in urine culture, drug sensitivity test should be done at the same time. When stones are combined with infection, the growth of stones and damage to renal parenchyma can be accelerated. Before the stone is discharged or removed, this infection is difficult to cure, and pyelonephritis, renal pus, perinephritis, and even perinephric abscess can occur in severe cases; after adhering to the peritoneum, it can be penetrated into the intestinal tube. Microscopic renal interstitial inflammation, cellular infiltration and fibrosis, neutrophils and epithelial cells in the renal tubules, and renal tubular atrophy and glomerulosclerosis in the late stage. 4, renal insufficiency: renal stones in the combination of urinary tract obstruction, especially bilateral urinary tract obstruction or on the basis of the combination of serious infections, the patient may appear renal insufficiency. When the obstruction is lifted and/or the infection is effectively controlled, some patients. Renal function may improve or return to normal. In addition to the detection of serum urea nitrogen, creatinine and endogenous creatinine clearance, the method of determining renal function can also use intravenous pyelography and be judged according to the time and concentration of the contrast agent discharged.Although ultrasound can understand the dilatation of the urinary tract and the thickness of the renal parenchyma, it is more difficult to determine renal function. Static or dynamic nuclide scanning or videography can provide valuable clues. Because of the changes in obstruction and renal damage that occur with the site of stone mobilization and at different stages of treatment, patients with renal stones require follow-up monitoring, especially dynamic scans for renal parenchyma. When the stone is discharged, or after drainage, this examination can provide a basis for prognosis or further treatment. 5, renal calcium deposition: calcium deposits in the renal tissue, mostly occurring in patients with high blood calcium. Patients with primary hyperparathyroidism, renal tubular acidosis and chronic pyelonephritis may have renal calcium deposits. Calcium is mainly deposited in the medulla. In severe lesions, all of the renal parenchyma may have calcium deposits, leading to interstitial fibrosis, glomerulosclerosis and tubular atrophy.