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ETHIOLOGY AND PATHOGENESIS.

Nephrolithiasis is a disease of the whole organism that characterizes the polyetiology and great complexity of the biochemical processes that determine its pathogenesis. Kidney stones are made up of substances found in the urine.

For stone formation, the following conditions are needed:

1) a specific reaction of urine;

2) supersaturated urine with salts that precipitate or are retained with difficulty in a soluble state;

3) the urine contains a known amount of colloids or organized protein substances (decayed epithelial cells, bacteria, fibrin, etc.), onto which salts subsequently settle and then turn into calculi.

Since there is no single reason for the formation of stones and the etiology has not yet been elucidated in many ways, it is more correct to speak not about the causes of stone formation, but about the factors contributing to this process.

The process of stone formation in the kidney can be partially considered as a result of insufficient formation of protective colloids by the renal elements. Discolloiduria is the most likely cause of urinary stone formation. An important factor in the occurrence of discolloiduria is a change in the function of the kidney, due to a violation of the regulation of blood circulation in it and impaired lymphatic outflow. In case of imbalance between colloids and crystalloids of urine, salts begin to precipitate and crystallize out. The colloids present in urine prevent crystalloids from falling out even from a supersaturated solution.

Thus, for stone formation, it is important not only to saturate the urine with crystalloids, but also to decrease the protective colloids in it.

Primary stone is often the result of a localized pathological process in the renal papilla. For the occurrence of a stone, a preliminary violation in the papilla of blood circulation, the appearance of lymphostasis, damage to the urothelium of the papilla is necessary. In the lumen of the collective canal of the renal papilla, lime salts are deposited near its apex, forming a matrix (core or "micelle") of the stone. The material for the formation of the nucleus can be fibrin, a blood clot, an amorphous precipitate, cell detritus, a foreign body. Stone growth occurs by depositing alternating concentric layers of mucopolysaccharides and crystalloids on it.

In many cases of nephrolithiasis, there is a close association between urinary infection and the occurrence of kidney stone. It is known, for example, that with pyelonephritis the occurrence of stone formation is a frequent occurrence (in 30% of patients with chronic pyelonephritis). Infection can cause necrotic changes in the tubule of the kidney in order to initiate the formation of a colloidal crystalline nucleus, followed by the development of a stone around it. Kidney infection contributes to the rapid growth of the stone, and the virulence of the infection is directly proportional to both the rate of stone growth and the frequency of nephrolithiasis recurrence.

In the genesis of nephrolithiasis, a violation of endocrine correlation is important. So, stone formation in the kidneys is known for diseases of the parathyroid and thyroid glands, etc.

Often there is stone formation in the kidneys with damage to the spinal cord as a result of dysregulation of the urinary organs.

An nutritional factor in the development of nephrolithiasis plays a significant role. Any uniform diet can be an incentive to the development of urolithiasis. Stones, consisting of uric acid and its salts (urates), are formed most often in individuals who eat mainly foods rich in purine bases (meat) and extractive substances, which decompose to form uric acid.

Stones, consisting of calcium salts of phosphoric acid (phosphates), are found mainly in people whose diet is dominated by dairy and vegetable products rich in calcium, especially milk. The influence of vitamin deficiencies (for example, the role of A-hypovitaminosis) is not excluded, however, this factor can only contribute to the formation of certain types of renal calculi. Of great importance in relapses of nephrolithiasis are liver function disorders. The formation of cystine stones or urates should be attributed to such violations. The basis of urolithiasis is the interaction of the genotype and the external environment, therefore, the role of hereditary factors in the genesis of the disease is noted by many authors.

Fermentopathy (tubulopathy) is a violation of metabolic processes in the body or renal tubule function as a result of insufficiency or absence of any enzyme. Genetically determined tubulopathies are called congenital metabolic errors. The most common tubulopathies that contribute to stone formation are oxaluria, uraturia, cystiuria, aminoaciduria, galactosemia, fructosemia. It should be noted that oxaluria, uraturia, cystiuria, generalized aminoaciduria, a change in carbohydrate metabolism, can be not only congenital, but also acquired. They occur after kidney and liver diseases (pyelonephritis, glomerulonephritis, cholecystitis, hepatitis, etc.) due to a violation of their function. In these cases, a combination of congenital and acquired tubulopathy may occur. So, for example, pyelonephritis, developed as a result of congenital oxaluria, can lead to acquired uraturia. As a result, stones of unequal composition are formed in the same kidney at different periods or in different kidneys of the same patient.

Thus, malnutrition, climatic conditions, metabolic and chemical disorders of urine, neurodystrophic, hormonal and bacterial-toxic effects on renal tissue, hemodynamic and urodynamic disturbances, etc. are pathogenetic in relation to urolithiasis. However, none of these factors taken separately is dominant and cannot lead to nephrolithiasis.
Obviously necessary;. joint participation in this complex process of many reasons.

The main exogenous and endogenous factors involved in the genesis of nephrolithiasis include the following.

1. Changes in the kidneys and urinary tract:

1) congenital anomalies creating urinary stasis;

2) processes leading to obstruction of the urinary tract;

3) neurogenic diseases (dyskinesias) of the urinary tract;

4) inflammatory and parasitic diseases of the urinary organs (pyelonephritis, cystitis, urethritis, etc.);

5) trauma to the urinary organs;

6) a foreign body in the urinary tract.

2. Functional disorders of the liver and gastrointestinal

tract:

1) latent hepatopathies;

2) hepatogenic gastritis;

3) colitis, etc.

3. Diseases of the endocrine glands:

1) hyperparathyroidism (adenoma, hyperplasia);

2) hyperthyroidism;

3) hyperpituitary diseases.

4. The presence of infectious foci outside the genitourinary system.

5. Metabolic disorders:

1) idiopathic hypercalciuria;

2) violations of membrane permeability in relation to colloids;

3) renal rickets, etc.

6. Diseases requiring prolonged rest of the body:

1) fractures of the spine and limbs;

2) osteomyelitis;

3) diseases of the osteoarticular system;

4) chronic visceral diseases, diseases of the nervous system.

7. Clinical and geographical factors:

1) a dry, hot climate with a large evaporation of moisture;

2) limitation of water consumption, etc .;

3) iodine deficiency in the external environment.

8. Eating disorders, vitamin balance:

1) lack of vitamins A and C in food;

2) excess vitamin D.

9. Vicious antiphysiological swaddling of children in some countries of the East (swaddling in cradles “beshik”, “gavora”, fettering movements and disrupting normal urination). According to the chemical composition of stones, oxalates, phosphates, urates, carbonates are distinguished. Less common are cystine, xanthine, protein, cholesterol stones. The stones are usually layered, the number of stone-forming minerals is not more than three, the remaining minerals can be found in the form of an impurity. Stone is a mixture of minerals and organic matter.

Oxalate

oxalic acid calcium salts

dense black-gray with a prickly surface stains urine in dark brown or black

Phosphate

calcium salts of phosphoric acid

the surface is smooth, slightly rough, the shape is diverse, the consistency is soft, white or light gray in color formed in an alkaline environment quickly grow easily crushed

Urate

uric acid and its salts

yellow-brown color with a smooth surface, solid consistency

Carbonate

calcium salts of carbonic acid

have white color, smooth surface, soft, various in shape

Cystine

from a sulfur compound of the amino acid cystine

yellowish white, roundish, soft texture, with a smooth surface

Protein

from fibrin mixed with salts and bacteria

small, flat, soft, white

Cholesterol

from cholesterol

black color, easy to crumble



Kidney stones can be single or multiple. Their size is the most diverse - from 0.1 to 10-15 cm or more, weight from fractions of a gram to 2.5 kg or more. Often, the stone performs the cup-pelvis system as an impression with thickenings at the ends of the processes located in the cups. Such stones are called coral-shaped.

Ureter stones are almost always displaced kidney stones by their origin. They are diverse in shape and size. Single stones are more common, but there may be two, three stones or more in one ureter. The stone most often lingers in places of physiological narrowing of the ureter: at the exit from the pelvis, at the intersection with the iliac vessels, in the periblastic (juxtavesical) and intramural sections.

PATHOLOGICAL ANATOMY. Morphological changes in nephrolithiasis are extremely diverse and depend on the anatomical features of the kidney, the location of the stone, its size and shape, the degree of activity of pyelonephritis. The absence of bacteria in the urine during its study does not mean the absence of inflammatory changes in the kidney, which in these cases are interstitial nephritis.

As a result of impaired urine outflow with “aseptic” nephrolithiasis caused by stone, sclerosis and tissue atrophy begin in the pelvis, and then pass to the interstitial tissue of the kidney. The canals expand, the elements of the renal parenchyma change and lose their function, some of them die. Interstitial tissue gradually turns into scar-connective tissue, at the same time it is replaced.

With calculous pyelonephritis, i.e. “Infected ™” stones, the inflammatory process spreads from the brain to the cortical layer. Inflammatory infiltrates and suppuration lead to a sharp change in the cells of the tubules and glomeruli. Calculous pyelonephritis, especially with coral nephrolithiasis, can be the cause of purulent fusion of renal tissue, i.e. pyonephrosis. The inflammatory process spreads to the papillae, causing necrotic pallitis, and then affects the deeper sections of the renal pyramids. Gradually, the surrounding fiber is gradually involved in the process, in connection with which peripyelitis, periurethritis, pedunculitis develop. Ureter stones can cause stricture, pressure sores and rarely perforation of its wall.
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