C-reactive protein
19.07.2019

Protein dystrophy of the kidneys. Violation of mineral metabolism. Depending on the prevalence of the process

Fatty degenerations are associated with excessive accumulation of lipids (neutral fats, triglycerides, phospholipids, cholesterol) in the cytoplasm of parenchymal cells, or with their appearance in those cells where they are not normally found, or with the appearance of lipids of an abnormal composition in the cytoplasm of cells. A person's need for fat is 80-100 g per day.

The main functions of lipids in the body:

  • structural - lipids form the basis of cell membranes;
  • regulating;
  • providing energy, since lipids are one of the main sources of energy.

Depending on clinical manifestations highlight:

  • lipidoses;
  • obesity;
  • exhaustion.

The most common causes of acquired lipidosis are hypoxia and various intoxications. Therefore, fatty degenerations are a component of diseases accompanied by oxygen starvation. - coronary heart disease, hypertension, heart defects, chronic lung diseases (bronchiectasis, tuberculosis, emphysema). leading to the development of pulmonary heart failure. In addition, fatty degeneration is caused by various infections and intoxications, which are accompanied by both hypoxia and blockade of enzymes that catalyze lipid metabolism in cells by toxins. Lipidoses can sometimes be associated with a lack of vitamins and certain amino acids.

In pathology, fatty degenerations of the myocardium, liver and kidneys are of greatest importance.

Fatty degeneration of the myocardium develops by decomposition of fat-protein complexes of membranes of intracellular structures, as well as as a result of infiltration of cardiomyocytes with lipids. Regardless of the mechanism of dystrophy, small inclusions of fat first appear in myocardial cells (pulverized obesity), then they merge into droplets (small-droplet obesity), which gradually fill the entire sarcoplasm and can lead to cell death (Fig. 3).

for a sharp decrease in heart function and the development of heart failure.

Fatty liver, or fatty hepatosis

Rice. 4. Fatty degeneration of the myocardium (“tiger heart”). Yellow-white stripes are visible under the endocardium, corresponding to areas of lipid incorporation in cardiomyocytes.

At the same time, with many intoxications and infections, a mechanism of decomposition of the membranes of intracellular structures with the disintegration of their fat-protein complexes is possible. Finally, fatty hepatosis develops as a result of the transformation of proteins and carbohydrates into lipids, which is observed, for example, with chronic alcohol intoxication. In any case, in the cytoplasm of hepatocytes, mainly in the periphery of the hepatic lobules, dust-like obesity first develops, which transforms into small-droplet, and then into large-droplet obesity. In this case, the nucleus and intracellular structures are pushed to the periphery of the cells, which often die. In these cases, the fatty inclusions of dead hepatocytes merge, forming fatty cysts. Macroscopic changes in the liver depend on the severity of dystrophy. In severe cases, for example with alcoholism, the liver is enlarged in size, flabby, and on a section it is ocher in color - “goose liver”. With less pronounced fatty degeneration, the liver is also enlarged in size and has a yellowish-gray color when cut. With fatty hepatosis, liver function is preserved for a long time, but as the underlying disease and fatty degeneration progresses, it decreases, sometimes quite significantly.

Fatty kidney degeneration develops by infiltration of the tubular epithelium during hyperlipidemia, observed, in particular, with nephrotic syndrome. In this situation, lipids end up in primary urine ( hyperlipiduria) and are intensively reabsorbed by tubular epithelial cells, but in such large quantities that these cells are not able to metabolize the lipids that have entered them - small-droplet obesity of the tubular epithelium develops. Usually it is combined with their hyaline-droplet dystrophy. In this case, the kidneys are little changed in appearance, but in severe cases of the main pathological process, they acquire a grayish-yellow color, and when cut, their pyramids can take on a yellow color.

The outcome of parenchymal fatty degeneration depends on the degree of its severity - dust-like and small-droplet obesity is reversible when the cause that caused it is eliminated, large-droplet obesity can result in cell death.

CONGENITAL PARENCYMATOUS LIPIDOSES

Congenital parenchymal lipidoses are hereditary enzymopathies, inherited in an autosomal recessive manner, and are characterized by the accumulation of lipids in cells that damage cell structures and are often accompanied by the death of the cells themselves. The most common lipid thesaurismoses are:

  • Gaucher disease caused by the absence of the enzyme beta-glucocerebrosidase. As a result, glucocerebrosides accumulate in the liver, spleen, bone marrow, brain, endocrine glands and lymph nodes, which leads to the death of cells in these organs and to progressive dementia, increased weight of the liver, spleen and wasting (cachexia).
  • Niemann-Pick disease develops in the absence of the enzyme sphingomyelinase, which breaks down sphingomyelin, which is part of many tissues, but especially nervous tissue. In sick children, it accumulates in the cells of most organs and at the same time there is an increase in the mass of the liver and spleen (hepato- and splenomegaly), a lag in mental development, neurological symptoms, hypotension, and exhaustion appear. Children die at the age of 2-3 years.

CARBOHYDRATE DYSTROPHIES

Carbohydrate dystrophies are associated with the accumulation of protein-polysaccharide complexes (glycogen, glycoproteins) in cells, or with the formation of these substances in those cells where they are not normally present, or with a change in their chemical composition.

Carbohydrates are an essential and most significant component of food. A person consumes 400-600 g of various carbohydrates per day. They are a necessary element of metabolism, an important component of the structure of cells and intercellular substances, and one of the main sources of energy to ensure the vital functions of the body.

ACQUIRED CARBOHYDRATE DYSTROPHIES

Hypoglycemia- conditions characterized by a decrease in blood glucose below 65 mg%, or 3.58 mmol/l. Normally, fasting blood glucose levels range from 65-110 mg%, or 3.58-6.05 mmol/l.

Causes of hypoglucemia are liver diseases - chronic hepatitis, cirrhosis of the liver, fatty degeneration, as well as prolonged fasting.

Disease results:

  • impaired transport of glucose from the blood to hepatocytes, a decrease in the level of formation of glycogenesis in them and, in connection with this, the absence of stored glycogen;
  • inhibition of the process of glycogen formation and glucose transport from hepatocytes to the blood.

Consequences of hypoglycemia

  • Hypoglycemic syndrome is a persistent decrease in blood glucose levels below normal (up to 60-50 mg%, or 3.3-2.5 mmol/l), leading to disruption of the body’s vital functions.
  • Hypoglycemic coma is a condition characterized by:
    • - a drop in blood glucose concentration below 40-30 mg%, or 2.0-1.5 mmol/l);
    • - loss of consciousness;
    • - life-threatening disorders of body functions.

Hyperglycemia- conditions characterized by an increase

Causes of hyperglycemia:

  • pathology of the endocrine system, accompanied by an excess of hormones that stimulate the flow of carbohydrates into the blood (glucagon, glucocorticoids, catecholamines, thyroid hormones, growth hormone) or a lack of insulin or a decrease in its effectiveness;
  • neuro- and psychogenic disorders, for example reactive psychoses, stress reactions and similar conditions, characterized by activation of the endocrine system;
  • overeating, especially long-term excessive consumption of confectionery products;
  • liver diseases in which hepatocytes lose the ability to transform glucose into glycogen.

Consequences

  • Hyperglycemic syndrome - a condition accompanied by a significant increase in blood glucose levels above normal (up to 190-210 mg%, 10.5-11.5 mmol/l or more), leading to disorders of the body’s vital functions.
  • Hyperglycemic coma , characterized by loss of consciousness, decreased or loss of reflexes, respiratory and circulatory disorders, often ending in the death of the patient.

Most often, hyperglycemia is observed in diabetes mellitus, which develops as a result of absolute or relative insulin deficiency (see Chapter 19).

HEREDITARY CARBOHYDRATE DYSTROPHY (GLYCOGENOSIS)

Glycogenoses- a typical form of pathology of carbohydrate metabolism of hereditary origin, characterized by the accumulation of glycogen in cells, which causes disruption of the body’s vital functions.

main reason- inherited or congenital anomaly of genes encoding the synthesis of enzymes for the breakdown (less often - formation) of glycogen. Inherited in an autosomal recessive manner. There are more than 10 types of glycogenosis. Among them, Gierke's disease is the most common. Pompe, fetal cystic fibrosis, as well as Forbes-Cori, Andersen, McArdle diseases.

Gierke's disease occurs in the absence of the enzyme glucose-6-phosphatase, which leads to the accumulation of glycogen in the cells of the liver and kidneys, but to the absence of carbohydrates in the blood. This is accompanied by secondary pituitary obesity. Most children die from acidotic coma.

Pompe disease is associated with the absence of acid alpha-1,4-glucosidase in lysosomes, which leads to the accumulation of glycogen in the heart, striated and smooth muscles, including intercostal, diaphragmatic, tongue, esophagus, stomach, etc. Children die at an early age from heart or respiratory failure.

For the rest, cystic fibrosis is a disease associated with genotypic fermentopathy. leading to disruption of the exchange of mucoids that are part of the secretion of many glands. As a result, the secretion of the glands becomes viscous and thick, is difficult to remove, which leads to stretching of the glands, turning them into cysts, especially in the pancreas, mucous membranes of the gastrointestinal tract and respiratory tract, salivary, sweat, lacrimal glands, etc. In this case atelectasis often develops in the lungs with the development of pneumonia and bronchiectasis. Death most often occurs from pulmonary heart failure.

Dystrophies.

Dystrophy is a pathological process that occurs due to metabolic disorders, which occurs with damage to cellular structures, and as a result, normally undetectable substances appear in cells and tissues.Classification of dystrophies:

by scale of the process: local (local) and general

by reason, by the moment the reason appears: acquired and congenital. Congenital dystrophies are always genetically determined diseases, hereditary disorders of protein, or carbohydrate, or fat metabolism. Here there is a genetic deficiency of one or another enzyme that takes part in the metabolism of proteins, fats or carbohydrates. This leads to the accumulation of incompletely broken down products of carbohydrate, protein, and fat metabolism in the tissues. It occurs in a wide variety of tissues, but the tissue of the central nervous system is always affected. Such diseases are called storage diseases. Sick children die during the first year of life. The greater the enzyme deficiency, the faster the disease develops and the earlier death occurs.

By type of metabolic disorder: protein, carbohydrate, fat, mineral, water, etc. dystrophy

according to the point of application, according to the localization of the process, cellular (parenchymal) and non-cellular (mesenchymal) dystrophies, which are found in connective tissue, are distinguished; mixed (found in both parenchyma and connective tissue).

Pathogenesis. Pathogenetic mechanisms 4:

Transformation is the ability of some substances to transform into others that are quite similar in structure and composition. For example, carbohydrates have a similar ability when they transform into fats.

Infiltration is the ability of tissues or cells to be filled with an excess amount of a substance. Infiltration can be of 2 types: Infiltration of the 1st type is characterized by the fact that the cell, being in a state of normal functioning, receives an excess amount of one or another substance. There comes a limit at which it is unable to process and assimilate this excess. With type 2 infiltration, the cell is in a state of reduced vital activity, and therefore cannot cope even with the normal amount of substance entering it.

Decomposition. During decomposition, intracellular and interstitial structures (protein-lipid complexes that make up the membranes of organelles) decompose. In the membrane, proteins and lipids are bound and therefore not visible. When they break down, they appear in cells and become visible under a microscope.

Perverted synthesis. With perverted synthesis, cells form abnormal foreign substances that are not normally inherent in the body. For example, with amyloid dystrophy, cells synthesize an abnormal protein from which amyloid is then built. In patients with chronic alcoholism, liver cells (hepatocytes) begin to synthesize foreign proteins, from which the so-called alcoholic hyaline is then formed.

Each type of dystrophy has its own tissue dysfunction. With dystrophy, the function suffers in two ways: a quantitative and qualitative dysfunction, that is, the function decreases, and qualitatively, a distortion of the function is observed, that is, it has features that are unusual for a normal cell. An example of such a perverted function is the appearance of protein in the urine during kidney disease, when degenerative changes in the kidney occur; silt changes in liver tests in case of liver diseases, in case of heart pathology - changes in heart tones.

Protein parenchymal dystrophy: These are dystrophies in which protein metabolism suffers. The process develops inside the cell. Protein parenchymal dystrophies include: granular, hyaline-droplet, hydropic dystrophy.

Granular dystrophy. Histological examination reveals protein grains in the cells and cytoplasm. Granular dystrophy affects parenchymal organs such as the kidneys, liver and heart. This dystrophy is called cloudy or dull swelling. This is due to macroscopic features. The organs with this dystrophy are slightly swollen, and the cut surface is dull and cloudy, as if “scalded by boiling water.” Granular dystrophy is caused by a number of reasons that can be divided into 2 groups: infections and intoxications.In the kidneys with granular dystrophy, there is an increase in size, it is flabby, there may be a positive Schorr test (when the poles of the kidney are brought together, the kidney tissue tears). On section, the tissue is dull, the boundaries of the cortex and medulla are blurred or completely indistinguishable. With this type of dystrophy, the epithelium of the convoluted tubules of the kidney suffers. If normal kidney tubules have smooth lumens, then with granular dystrophy the apical section of the cytoplasm is destroyed and the lumen takes on a stellate shape. The cytoplasm of the epithelium of the renal tubules contains numerous grains (pink). Renal granular dystrophy has 2 outcomes: favorable: if the cause is removed, the tubular epithelium will return to normal; unfavorable, if the pathological factor continues to act, the process becomes irreversible, dystrophy turns into necrosis (often observed in case of poisoning with kidney poisons).Liver with granular dystrophy it is also slightly enlarged. When cut, the fabric becomes dull, the color of clay. Histological signs of granular liver dystrophy: protein grains may or may not be present. It is necessary to focus on the fact that the beam structure is preserved or destroyed. With this dystrophy, proteins break up into separate groups or separately lying hepatocytes, which is called discomplexation of the hepatic beams.Heart externally it is also slightly enlarged, the myocardium is flabby, and when cut it looks like boiled meat. Macroscopic characteristics: no protein grains. The histological criteria for this dystrophy are focal oxy- and basophilia. Myocardial fibers perceive hematoxylin and eosin differently. Some areas stain intensely lilac with hematoxylin, while others stain intensely with eosin blue.Hyaline-drip dystrophy found in the kidneys (the convoluted tubule epithelium suffers). Occurs in kidney diseases such as chronic glomerulonephritis, chronic pyelonephritis, and poisoning. Drops of a hyaline-like substance are found in the cytoplasm of the cells. This type of dystrophy is accompanied by severe impairment of renal filtration.

Hydropic dystrophy:

it can be observed in liver cells during viral hepatitis. Large light droplets appear in hepatocytes, often filling the cell.Fatty degeneration . There are 2 types of fats: mobile (labile) quantity, which varies throughout a person’s life, and which are represented by fat located in fat depots, and stable (immobile) fats, which are part of cellular structures and membranes. Fats perform a wide variety of functions - supporting, protective, etc. Fats are detected using special dyes:

Sudan III colors the fat orange-red.

Scarls in red

Sudan IV osmic acid colors fat black

Nile blue has metachromasia: it colors neutral fats red, and all other fats blue or light blue. Before dyeing, the material is processed in two ways: the first is alcohol wiring, the second is freezing. To identify fats, they use freezing tissue sections, since fats dissolve in alcohols.

Fat metabolism disorders are represented in humans by three pathologies:

Fatty degeneration itself (cellular, parenchymal)

General obesity or obesity

Obesity of the interstitial substance of the walls of blood vessels (aorta and its branches). This dystrophy underlies atherosclerosis.

Actually fatty degeneration.

The reasons can be divided into two main groups: infections intoxication.

Nowadays, the main type of chronic intoxication is alcohol intoxication. Drug intoxications and endocrine intoxications are common - for example, with diabetes mellitus. An example of an infection that causes fatty degeneration is diphtheria: diphtheria toxin can cause fatty degeneration of the myocardium. Fatty degeneration is localized in the same organs as protein degeneration - in the liver, kidneys and myocardium.

 With fatty degeneration, it increases in size, acquires density, and is dull and bright yellow when cut. The figurative name for this liver is “goose liver”.

Microscopic characteristics:

in the cytoplasm of hepatocytes, fat droplets of small, medium and large sizes can be seen. They can be located in the center of the lobule or occupy the entire hepatic lobule. There are several stages in the development of obesity:

simple obesity, when a drop occupies a hepatocyte, but if the influence of the pathological factor is stopped (the patient stops drinking alcohol), then after 2 weeks the liver returns to normal.

Necrosis: an infiltration of leukocytes appears around the focus of necrosis as a reaction to damage. The process at this stage is still reversible

fibrosis, that is, scarring. The process enters an irreversible cirrhotic stage.

The heart is enlarged, the muscle is flabby, dull, and if you carefully examine the endocardium, under the endocardium of the papillary muscles you can notice transverse striations (this is the so-called “tiger heart”

Microscopic characteristics: fat is found in the cytoplasm of cardiomyocytes. The process is mosaic in nature: cardiomyocytes located along small veins are affected. Outcomes: a favorable outcome is a return to normal (if the cause is removed), and if the cause continues to operate, the cell dies and a scar forms in its place.

 In the kidneys, fat is found in the epithelium of the convoluted tubules. We encounter such dystrophy in chronic kidney diseases (nephritis, amyloidosis), or in cases of poisoning.

General obesity or obesity.

With obesity, the metabolism of neutral labile fats suffers, which appear in excess in fat depots; body weight increases due to the deposition of fats in the subcutaneous fatty tissue, in the omentum, mesentery, in the perinephric and retroperitoneal tissue, and finally, in the tissue covering the heart. With obesity, the heart appears to be clogged with a thick fatty mass, and then the fat begins to penetrate into the thickness of the myocardium, into the stroma, causing its fatty degeneration. Muscle fibers experience pressure from the obese stroma and atrophy from the pressure, which leads to the development of heart failure. Most often, the right ventricle is affected, which is why congestion occurs in the systemic circulation. In addition, obesity of the heart is fraught with myocardial rupture. In the literature, such a fatty heart is characterized as Pickwickian syndrome.In the liver, in obesity, fat can appear inside the cells. The liver takes on the appearance of a “goose liver”, just like in dystrophy. The origin of fat in liver cells can be differentiated by color staining: Nile blue stains neutral fat (in case of obesity) red, and in case of dystrophy the fat will be colored blue.

Obesity of the interstitial substance of the walls of blood vessels

. We are talking about cholesterol metabolism. By infiltration from the blood plasma, cholesterol enters the already prepared vascular wall and is deposited on the wall. Some of it is washed back, and some is eaten by macrophages. Macrophages loaded with fat are called xanthoma cells. Over the fat deposits, connective tissue grows, which protrudes into the lumen of the vessel, and an atherosclerotic plaque is formed.Causes of obesity:

genetically determined

endocrine (diabetes, Itsenko-Cushing's disease

physical inactivity

Fatty degeneration is a pathology that results from impaired tissue metabolism. The disease is characterized by lipid deposition mainly in organs such as the liver, kidneys, and myocardium.

In this disease, the liver enlarges and takes on a yellowish tint, becoming denser. Fatty droplets appear in the organ, which can occupy almost the entire liver lobule. The heart becomes large and loose, and you can see transverse stripes on it, reminiscent of a tiger coloring. Fat enters cardiomyocytes.

In the kidneys, it is found in the convoluted tubule epithelia.

Symptoms

With fatty degeneration in the liver, the symptoms are mild. Over time, pain may appear in the right hypochondrium. Vomiting and bowel dysfunction are possible. Very rarely the symptoms are severe. In such cases, bloating occurs and the patient loses a lot of weight. With any kind of physical activity, dizziness and fatigue appear. Lipodystrophy can develop into hepatitis or cirrhosis of the liver, so it is worth diagnosing immediately when the slightest symptoms appear.

With fatty degeneration of the myocardium, the patient at first has no reason to worry. His condition can be considered normal; only in case of heavy physical activity or during times of strong emotions can he feel a tingling sensation in his heart. Few people pay serious attention to this. But then it gets worse - shortness of breath and weakness appear. The feet and legs swell towards the end of the day. The pain in the heart intensifies and appears much more often, making itself felt. The patient's face may suddenly turn red, sweating may increase, and he/she often feels hot.

Causes of the disease

The reasons for the appearance of liver lipodystrophy are due to the fact that this organ cannot cope with the large amount of fats entering it and converts them into lipids. That is why the “residue” is deposited in the liver cells. It may also be a consequence of normal obesity.

The cause of this pathology in the myocardium can be various heart diseases. But another reason is extracardiac pathology, which has a negative effect on the muscles located in this area.

The disease appears in the kidneys due to impaired metabolism of a group of substances.

Treatment of the disease

Treatment of fatty degeneration begins mainly with eliminating the cause of the disease. For this, the patient is put on a certain diet prescribed by the doctor. If dystrophy appears against the background of some other disease, then the patient’s health is monitored by two doctors at once.

The diet is aimed not only at eliminating excess fat intake, but also at reducing the patient’s weight, which is monitored by a specialist. Significant weight loss is unacceptable, as this is an extra burden on the body. It is necessary that these changes occur gradually. Under the supervision of doctors, the patient can lose 11-20 kilograms in weight per year.

This result is achieved not only through diet, but also through physical exercise, which should help improve the condition of the body, train it, and force it to fight lipodystrophy.

If this does not help improve the functioning of any organ, the doctor may prescribe the use of medications.

Do not forget that the prescription of any drugs should be made only by a specialist in this field, observing all the individual characteristics of the patient’s body.

Preventive measures

Prevention for this disease includes proper nutrition and exercise. At the same time, do not forget that the load should be regular, but not too heavy.

You should not self-medicate, as this will only worsen the patient’s condition. It is better to get examined and start treatment with a doctor. Of course, it is advisable not to get sick at all, so do not forget about prevention and maintaining a healthy lifestyle.

This word is translated from Greek as “eating disorder.” This term refers to a complex of quantitative and qualitative changes in tissues and organs, which leads to disruption of their functions - a decrease or distortion of cell metabolism. There are general and local dystrophy.

Depending on the metabolism of which substances is disturbed (it can be fats, carbohydrates or proteins, as well as water or mineral micro- and macroelements), dystrophies are classified.

According to the degree of involvement of the body, there are local and generalized or general dystrophies, from the point of view of the cause of the disease - congenital and acquired, and according to the place of occurrence - parenchymal (arising inside cells), mesenchymal (appearing in the intercellular space, connective tissue) and mixed.

Kidney dystrophy - what is happening?

Kidney dystrophy is a local phenomenon, since it affects only one organ, although as a result not only the urinary system, but the entire body suffers. Another name for this disease is nephrosis.

As you know, the main function of the kidneys is to remove metabolic end products from the body. The exchange itself occurs in the renal glomeruli, where blood and an aqueous solution come into contact, into which substances unnecessary in the body are removed. These, by the way, also include toxins, so the kidneys always suffer during various intoxications, along with the main center for counteracting toxins - the liver.

Diagnosing dystrophies is not an easy task for a specialist.

Kidney dystrophy can be asymptomatic for a long time, and appear only when they can no longer cope with their functions. Then substances appear in the body that are not products of normal metabolism. It is their search that is the task of biochemical research of blood and urine.

Most of the abnormal metabolites clearly indicate a specific dystrophy, and, therefore, are its unique markers. For example, the appearance of free renal epithelial cells in the urine is a sign of the development of febrile nephrosis, and a sign of amyloid nephrosis is the appearance of amyloid protein in the urine, which gave the name to this pathology. To make a diagnosis, an ultrasound examination is performed - the affected kidneys increase in size, become loose and flabby.

What does dystrophy do to normal kidney function?

There are various mechanisms for the occurrence of nephrosis.

  • Infiltration. This is the process of accumulation of an excess amount of any substance in an organ or tissue. It has two forms of manifestation - either the level of this substance in the body is too high, and the cell cannot process it normally, or the reduced vital indicators of the cell do not allow it to metabolize the normal level of this substance.
  • Transformation. The process of transforming substances that are similar in structure or origin into each other. A typical example is fats and carbohydrates.
  • Decomposition. As a result of this process, the cell organelles disintegrate into their constituent substances and these bricks begin to accumulate in the cell, their aggregates forming typical inclusions in the cell.
  • Perverted synthesis. Some kidney dysfunctions cause kidney tissue to produce substances that are not normal metabolic products. For example, amyloid protein or alcoholic hyaline. It is these products that are specific markers for making the correct diagnosis and prescribing treatment.

You need to understand that all four mechanisms give the overall picture of the disease. Moreover, they can be involved at different stages of disease development, have different degrees of severity, and provide different diagnostic opportunities. It is the combination of mechanisms that is the reason that in renal dystrophy both qualitative and quantitative impairment of renal function occurs.

Protein metabolic dystrophies are a serious danger to your kidneys.

Since the kidneys take the most active part in protein metabolism, protein dystrophies are most common. They usually affect the cells of the kidney tissue (parenchyma), which is why they are called “parenchymatous”. They can be caused by connective tissue diseases, suppuration, the appearance of tumors, and chronic inflammation.

With the development of this pathology, swelling develops, and in the urine, in addition to protein, blood cells (erythrocytes and leukocytes), as well as casts, which are conglomerates of epithelial cells of the renal tubules, appear. However, many nephrologists believe that urine analysis alone in the case of this disease is not sufficiently informative.

During the development of these conditions, proteins can either accumulate into aggregates - coagulate, or, on the contrary, liquefy with a decrease in the viscosity of the matrix - this process is called colliquation.

  • Granular dystrophy of the kidney. In addition to the kidneys, this type of dystrophic changes can occur in the liver and heart and is also called dull or cloudy swelling. The cause of this pathology may be intoxication or infection.

With the development of this disease, histological examination shows that protein grains are clearly visible in the cells, and the normal shape of the convoluted tubules of the kidney changes. If intoxication is removed in time, the kidney will return to its original state, but with prolonged exposure to poisons, irreversible necrosis of the kidney occurs.

Granular dystrophy of the kidneys most often affects the liver, which acquires a clayey tint and also becomes dull, however, grains in the liver cells may or may not appear, the liver beams become disorganized, its cells lose their connection and become isolated.

With this pathology, the heart also enlarges and becomes flabby. There are no grains in its tissues, however, foci of basophilic and oxyphilic cells appear - the myocardium begins to perceive dyes differently and areas of lilac and blue color appear on the preparations, which are absent normally.

  • Hyaline droplet renal dystrophy. The target of this lesion is the epithelium lining the convoluted tubules of the kidneys and is directly involved in the exchange of substances between the blood and the kidney matrix. The cause may be diseases such as chronic pyelonephritis, glomerulonephritis, as well as poisoning. This type of dystrophy received its name due to the presence in the cells of drops of a substance similar to hyaline, which serve as a diagnostic sign of this condition.
  • Hydropic dystrophy of the kidney. Its other name is vacuolar dystrophy, which is associated with the appearance in cells of atypical large vacuoles filled with a matrix - intracellular fluid. The main causes of this pathology are glomerulonephritis, amyloidosis, diabetes mellitus, as well as glycol poisoning or a sharp decrease in potassium levels in the body, which lead to an increase in the level of filtration, as well as disruption of the enzymes of kidney cells. The prognosis for this condition is unfavorable - most often necrosis of the affected cells occurs.

Fatty kidney degeneration - what to do?

Another name is lipoid kidney dystrophy. Normally, free lipids are always found in the kidneys in the area of ​​the collecting ducts and the narrow segment. However, in obesity, fat deposits also appear in the epithelium of the distal and proximal renal tubules. These can be various phospholipids, cholesterol and free lipids. The kidneys increase in size, and a typical yellowish fatty speck appears on them. The main reason for the development is tissue degeneration or oxygen starvation, which develops, for example, with heart failure, lung diseases, alcoholism, and anemia. Other reasons may be poisoning with arsenic, chloroform or phosphorus, infections (tuberculosis, diphtheria), unbalanced low-protein diet, vitamin deficiency.

Glycogenous kidney dystrophy - the presence of problems with carbohydrate metabolism.

It occurs in diabetes mellitus and is associated with the accumulation of glycogen in the kidney (this occurs in the distal section and loops of the nephron), which is a form of deposition (accumulation) of carbohydrates in the human body. Occurs in diabetes mellitus.

Two special types of dystrophies.

  • Necrotizing kidney dystrophy. Kidney necrosis often occurs during poisoning with so-called renal poisons. These are salts of heavy metals, organic acids, and kidney poisons. Another cause is extensive damage to the skin (burns), as well as infections.
  • Feverish nephrosis. This is a degenerative condition of the kidneys caused by the rapid development of an infectious disease. Its diagnosis is associated with the appearance of epithelial cells in the urine that are not united into cylinders. The condition goes away on its own as the infection is treated and does not require special treatment.

How to protect your kidneys from nephrosis?

Most infectious infections, intoxications, the presence of chronic inflammatory processes, tumors always have a negative effect on the kidneys. The vast majority of medications that have to be taken during treatment also affect their work. You should remember this and monitor the condition of the kidneys - after all, in the early stages, most dystrophies are reversible, and the lack of treatment can result in the inevitable death of the kidney.

Problems can be solved by regularly visiting resorts, choosing an appropriate diet, avoiding drugs that kill the kidneys, and alcohol. Take care of your health!
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