Pathological anatomy of chronic pyelonephritis under a microscope. Thyroid kidney. General mechanisms of the occurrence and development of kidney pathology

Morphological changes in chronic pyelonephritis vary depending on the duration of the process, the severity and activity of inflammation and the degree of sclerosis.

Chronic pyelonephritis is characterized by the development of the pathological process from the pelvis and medullary substance towards the cortex. This can be observed equally often with both urogenic and hematogenous or lymphogenous routes of infection into the kidney. The section reveals mostly roughly wrinkled tuberous buds of significantly reduced size. At the same time, an uneven decrease in the size and weight of the two kidneys, rough scars on their surface, reminiscent of infarctions, make it possible to differentiate this type of secondary wrinkled kidneys from those primarily wrinkled with arteriolosclerosis and secondary wrinkled with glomerulonephritis (see Fig. 1).

However, gross wrinkling and tuberosity are not always detected, and in some cases the nature of the process can only be determined histologically.

Histological studies primarily reveal pathological inflammatory infiltration of interstitial tissue, mainly in the intertubular region. For the most part, the inflammatory exudate of interstitial tissue is polymorphic in nature and consists of lymphocytes and plasma cells, histiocytes, and sometimes eosinophils. When the process worsens, neutrophils predominate. With less activity, plasma cells and lymphocytes often dominate. In the most advanced stages of pyelonephritic shriveled kidney, interstitial fibrosis is predominant, and lymphocytes and plasma cells are less common.

Chronic pyelonephritis is also characterized by the presence of colloidal casts filling dilated convoluted tubules and loops of Henle with flattened epithelium. Along with the expansion of the tubules and their filling with colloidal cylinders, tubular atrophy is observed. Colloidal casts in dilated tubules with atrophied epithelium can be predominantly or exclusively found in macroscopically visible scar areas, which indicates the uneven nature of kidney damage in chronic pyelonephritis. It is important to note that colloidal casts in dilated tubules are specific to chronic pyelonephritis and, as a rule, are not observed in nephrosclerosis of other origins (see Fig. 2).

The presence of pericapsular fibrosis is also characteristic, which is caused by periglomerular infiltration observed in the acute stage of pyelonephritis. Periglomerular fibrosis in chronic pyelonephritis, unlike glomerulonephritis, always has an extracapsular nature.

There are also signs of inflammation of the pelvis, which are manifested by an increased amount of connective tissue, as well as infiltration by plasma cells and lymphocytes (see Fig. 3).

In some cases, the pelvis and papillae may become necrotic. An increased amount of connective tissue in the renal capsule and its infiltration are also found.

Vascular changes in chronic pyelonephritis can be expressed in the form of productive endarteritis, hyperplastic arteriolosclerosis, hyalinosis and necrotic arteriolitis, as well as glomerulitis. These vascular changes are not specific to pyelonephritis, as they can also be observed in other vascular diseases of the kidneys. However, with pyelonephritis (in cases without hypertension), pronounced vascular changes are found mainly in scar areas. With unilateral pyelonephritis, accompanied by hypertension, vascular changes are more pronounced on the affected side.

Hyperplastic arteriolosclerosis may be observed in pyelonephritis before the development of hypertension and that vascular changes in the form of hyperplastic arteriolitis and hyalinosis may be primary to hypertension. Significant vascular changes in the kidney affected by the pyelonephritic process can be observed in the absence of hypertension. In the presence of hypertension in cases of unilateral pyelonephritis, the changes are more pronounced on the diseased side.

All diseases, depending on what is primarily affected - glomeruli or tubules, diseases are divided into: 1. Glomerulopathies a) glomerulonephritis b) idiopathic nephrotic syndrome (lipoid nephrosis) c) renal amyloidosis d) diabetic glomerulosclerosis e) Hepatic glomerulosclerosis
2. Tubulopathies a) acute (Acute renal failure - acute renal failure) b) chronic (myeloma kidney, gouty kidney)
GLOMERULONEPHRITIS – non-purulent inflammation of the glomeruli of the kidney. Classification of glomerulonephritis. According to etiology, they are: a) infectious-allergic b) of unknown nature. According to topography: a) extracapillary b) intracapillary. According to the nature of inflammation - a) serous b) fibrinous d) hemorrhagic e) mixed
According to the course: a) acute, b) subacute, c) chronic, d) terminal.
Chronic is divided into a) membranous b) mesangial c) fibroplastic
V.V. Serov identified 5 main forms of glomerulonephritis based on clinical and anatomical features: a) post-streptococcal, b) extracapillary proliferative c) membranous d) mesangial e) fibroplastic
The disease manifests itself with renal and extrarenal symptoms:
Renal symptoms include a) oliguria d) proteinuria e) hematuria e) cylindruria. Extrarenal symptoms include: 1) arterial hypertension 2) left ventricular hypertrophy, 3) dysproteinemia, 4) edema 5) hyperazotemia and uremia
In acute glomerulonephritis, the kidneys are slightly enlarged; based on their macroscopic appearance they are called variegated kidneys; the disease lasts for 10-12 months; the changes that occur are often reversible and patients recover. Less commonly, acute renal failure (ARF) occurs. In the glomeruli, changes occur in Stage 3: a) exudative, b) exudative-proliferative, c) proliferative. With necrosis of capillary loops, necrotizing glomerulonephritis occurs.
Chronic glomerulonephritis is divided into a) membranous b) mesangial c) fibroplastic. It leads to sclerotic changes, the kidneys decrease in size, their surface is fine-grained, the tissue is dense (secondary wrinkled kidney) - this ends in uremia (CRF).
AMYLOIDOSIS often occurs against the background of chronic infections, rheumatoid arthritis, and purulent diseases. Amyloidosis occurs in 4 stages a) latent - the kidney does not change externally b) proteinuric - the kidney is enlarged, dense, the cortex is wide pale, the medulla is full-blooded, called the “big sebaceous kidney” c) nephrotic - amyloid is deposited and in medulla, the kidney is called “large white” d) azotemic - the kidneys decrease in size, are dense, large-lumpy, called “amyloid-wrinkled kidneys” and patients often die from chronic renal failure
TUBULOPATHY. The leading one is acute tubulopathy or acute renal failure (ARF). The cause of the pathology is a) intoxication b) infection. The kidneys are enlarged in size, the boundary between the layers is clear, the cortex is pale, the medulla is full-blooded, there is edema in the stroma, dystrophy in the epithelium (hyaline droplet, vacuolar, fatty) patients can survive only with the use of hemodialysis. Macroscopically, such a kidney is called “sublimate” or “sulfanilamide” because occurs when poisoned by these substances. The morphological substrate of acute renal failure includes a) necrosis of the convoluted tubule epithelium, b) impaired blood and lymph circulation in the kidneys,
The disease occurs in 3 stages: a) initial (shock), b) oligo-anuric, c) restoration of diuresis. If the patient survives, the kidney structure is completely restored.
PYELONEPHRITIS is a purulent disease of the pelvis, calyces and stroma of the kidneys. More often caused by Escherichia coli, the infection penetrates the kidney in different ways: a) hematogenous (descending) b) urogenic (ascending) c) lymphogenic. Promote the development of inflammation: a) disruption of urine outflow b) urinary stasis. Pyelonephritis can be acute or chronic. Acute illness often ends in recovery. Chronic pyelonephritis ends with a pyelonephrotic wrinkled kidney. Microscopically, the kidney resembles thyroid tissue and is therefore called the “thyroid kidney.”
Complications of pyelonephritis include: a) carbuncle - accumulation of pus b) pyonephrosis - when the carbuncle communicates with the pelvis c) perinephritis - inflammation of the kidney capsule d) paranephritis - inflammation of the perirenal tissue e) papillonecrosis - necrosis of the papillae of the pyramids
URINOLOGICAL DISEASE - causes 1. General (metabolic disorders) 2. Local (inflammation and urinary stasis). As a rule, it is combined with pyelonephritis, so the complications are the same, but when the ureter is blocked, hydronephrosis is possible.
POLYCYSTIC KIDNEY is a congenital pathology when the kidneys sharply increase in size, consist of a large number of cysts, patients die from chronic renal failure.
NEPHROSCLEROSIS - kidney sclerosis is a morphological substrate of chronic renal failure (CRF). It is divided into a) primary wrinkled kidney, when the vessels are primarily affected (atherosclerosis, hypertension, less commonly periarteritis nodosa, etc.) and b) secondary wrinkled kidney, when the stroma or glomeruli are primarily affected (glomerulonephritis, pyelonephritis, amyloidosis, tuberculosis, kidney stone disease, etc.) The appearance of these kidneys is different. They are reduced in size, dense, wrinkled, but the surface in some cases is fine-grained (hypertension, glomerulonephritis) in other cases coarsely lumpy (atherosclerosis, pyelonephritis). With nephrosclerosis, blood pressure increases, causing left ventricular hypertrophy.
UREMIA is a chronic renal failure that occurs in most kidney diseases. The kidneys cannot excrete nitrogenous wastes (urea, creatinine), they accumulate in the blood and are then released through all organs of excretion - the gastrointestinal tract, skin, serous membranes, respiratory organs, and fibrinous or fibrinous-hemorrhagic inflammation occurs there (gastritis, enteritis, bronchitis, pneumonia, pleurisy, pericarditis, powdery skin, etc.)
KIDNEY TUMORS. Organ-specific cancers include a) hypernephroid cancer and b) nephroblastoma. Organ-nonspecific cancers arise from the pelvis. Histological forms of pelvic cancer include: a) transitional cell b) glandular (against the background of metaplasia) c) squamous cell, the most common of them is transitional cell

According to statistics, about 3% of the population suffers from kidney disease, leading to organ dysfunction due to problems with urine flow. Among the strong half of humanity, there is an increase in the number of patients by 10–12% annually. Signs of renal failure in men appear as a result of impaired metabolism and become the basis of anamnesis for diagnosis.

• Characteristic differences in the development of PN in men
• Kidney failure concept
• Acute renal failure
• Causes
• Symptoms
• Stages
• Initial
• Oligoanuric
• Diuretic
• Recovery
• Diagnostics of acute renal failure
• Treatment of acute renal failure
• ARF prognosis
• Chronic renal failure
• Symptoms of chronic renal failure
• Stages
• Hidden (latent)
• Compensatory stage
• Terminal stage
• Diagnostics
• Treatment of chronic renal failure
• Nutrition for renal failure syndrome
• Prevention
• Forecast

Characteristic differences in the development of PN in men

In case of renal failure, symptoms in men depend on the degree of damage and are often complicated by the presence of prostate cancer, drinking alcohol, drugs, and smoking.

The clinical picture includes:

• change in the volume of fluid released;
• swelling of the tissues of the face and legs;
• problems with mobility of the lower extremities;
• digestive disorders;
• hypertension.

In this case, abundant or weak urine outflow is observed spasmodically. In addition, a man is constantly susceptible to acute respiratory infections due to poor immunity.

Kidney failure concept

The term means partial or complete dysfunction of paired organs - loss of the ability to secrete, filter and drain urine. The acid-base balance is disrupted and osmotic homeostasis develops.

Important! If the disease is not diagnosed in a timely manner and treatment is not started, renal syndrome progresses, gradually causing cell necrosis.

Acute renal failure

ARF is characterized by partial or complete blockade of fluid outflow. As a result, nitrogen compounds accumulate, which provoke intoxication. A distinctive feature is the cyclical nature of symptoms, as well as a high probability of recovery with proper therapy.

Causes

Provocateurs of such pathology in men as acute renal failure are divided into 3 groups:

1. Problem of renal circulation, which often manifests itself in shock. The prerenal form develops.
2. Infections, poisoning, inflammatory processes leading to renal appearance.
3. Trauma, loss of a single organ, obstruction of the urinary tract - postrenal failure.

Symptoms

The clinical picture is characterized by 2 types of signs:

1. Specific symptoms appear - fluid secretion sharply decreases or urine output stops.
2. At the same time, nonspecific symptoms are observed: diarrhea, attacks of nausea, and vomiting. The liver enlarges, the patient’s arms and legs swell, and the nervous system becomes excitable or, conversely, inhibited.

Stages

As kidney failure develops, it goes through 4 main degrees.

Initial

Pathology manifests itself as a result of the presence of a primary disease. There is general malaise, pain in the abdominal area, intoxication, and pale skin.

Oligoanuric

A characteristic symptom is a sharp decrease in volume or complete blockage of urine output. As a rule, no more than 500 ml of liquid mixed with blood and an impressive sediment comes out per day. Over the course of several hours to 3 days, the man’s condition sharply worsens, swelling of the body and drowsiness appear. Diagnostics reveals hyperkalemia, acidosis, proteinuria, hyperphosphatemia, azotemia.

Important! Pulmonary edema is likely, leading to moist rales and shortness of breath. Complications from other organs are also possible - pancreatitis, uremic gastroenterocolitis, hepatitis.

Diuretic

From this moment, rehabilitation begins, which is differentiated into 2 distinct phases:

1. Early diuresis - the volume of discharge per day slowly increases, the ability of the kidneys to concentrate and filter urine is restored.
2. Polyuria - the amount of fluid leaking per day gradually comes to the standard and is approximately 2.5 liters. Other organs are also functioning normally. Duration 2.5–3 weeks.

Recovery

This stage often drags on for several months, since it requires a complete restoration of the functionality of all systems.

Diagnostics of acute renal failure

Acute renal failure clinical symptoms resemble urinary retention. In order for the examination to be carried out with maximum accuracy, it is important to describe the signs in detail and tell the doctor about the presence of pathologies that led to the problem. For example, the characteristics of pain in the lumbar region in a man will help determine the form in which PN develops.

1. Examine the condition of the bladder. If there is no fluid in the organ, this is a symptom that suggests acute renal failure. If urine is present, a sample is sent to the laboratory.
2. Blood is taken for biochemical analysis - the level of creatinine, urea, and electrolytes is determined.
3. However, the most informative method is considered to be an ultrasound of the kidneys to identify the structure of paired organs, size, and functionality.

Treatment of acute renal failure

Treatment is developed depending on the pathology provocateurs and stage.

1. The initial one requires eliminating the root cause. In case of shock, the patient's blood volume is replenished and blood pressure is normalized. If intoxication caused by poisons or drugs is suspected, the man's gastrointestinal tract is washed. To remove toxic substances, plasmaphoresis and hemosorption are used. They obstruct the urinary tract - excise tumor formations, crush stones blocking the passage, remove strictures.
2. At the stage of oliguria, the kidneys need to be treated comprehensively, restoring the outflow of fluid. Therefore, diuretics are included in the regimen, in particular Furosemide. For inflammation, antibiotics are prescribed. If complications in the patient's condition are likely, such as acidosis, uremia or overhydration, a course of hemodialysis is performed.
3. Depending on the cause, hormonal drugs, blood transfusions, and the introduction of solutions of calcium, potassium, and sodium salts may be used.

ARF prognosis

The outcome in case of timely access to medical help is favorable.

• 35–40% of patients completely get rid of the problem;
• partial recovery is observed in 10–15% of patients;
• 1–3% of men are forced to resort to hemodialysis for the rest of their lives.

Chronic renal failure

CRF, chronic renal failure, is characterized by the death of cellular structures. Kidney tissue is replaced by fibrous tissue, and organ volume decreases. This occurs as a result of dysfunction of the tubules and glomeruli, problems with blood supply, inflammatory processes, and tissue sclerosis. A persistent metabolic disorder develops.

Common causes of chronic renal failure in both men and women:

• systemic pathologies;
• diabetes;
• chronic pyelonephritis or glomerulonephritis;
• vascular diseases;
• abnormal kidney structure.

Symptoms of chronic renal failure

The clinical picture appears as the man’s condition worsens.

Important! At the first symptoms, it is necessary to undergo a thorough diagnosis, since the destruction of the cellular structures of organs is irreversible.

Stages

Kidney failure occurs in 4 stages.

Hidden (latent)

At this stage there are no obvious symptoms. However, a man feels increased fatigue even with little physical activity. If you undergo diagnostics at this time by submitting urine for biochemistry, a small amount of protein will be found in the sample. And this already allows one to suspect chronic renal failure.

Compensatory stage

The daily volume of fluid secreted increases. Urine and blood tests show changes in composition.

It is characterized by a sharp decrease in kidney performance, high levels of creatinine and urea in the blood. A man experiences the following symptoms:

• thirst and dry mouth;
• loss of appetite;
• nausea;
• gagging;
• weakness;
• decreased skin elasticity;
• muscle cramps;
• tremor of fingers;
• joint pain.

The clinical picture occurs periodically. In case of overwork, violation of the drinking regime and diet, infections, a rapid deterioration in the patient’s condition is observed.

Terminal stage

Uremic intoxication develops with limited urine volume. The outflow of fluid may be completely blocked. Metabolic disorders lead to damage not only to the kidneys, but also to other organs. Often, a patient is diagnosed simultaneously with renal failure:

• pericarditis;
• encephalopathy;
• heart dystrophy;
• problems with the circulatory system;
• a sharp decrease in immunity.

Important! During this period, excretion occurs through the skin and this symptom can be identified by the characteristic smell of urine.

Diagnostics

1. A man suffering from a chronic form of the pathology gives a blood sample for biochemistry and urine for the presence of protein compounds.
2. A Rehberg-Toreev test is performed, which allows one to assess how far the renal failure has progressed and to calculate the rate at which filtration occurs.
3. To clarify the severity, an ultrasound of the kidneys is performed. For grades 1–2, additional radiography is recommended.
4. A biopsy is indicated if there is a suspicion of an oncological nature of the disease.
5. Symptoms such as anemia and increased bleeding are taken into account.

The degree of development of pathology can be determined by creatinine content:

• compensated – 0.2–0.45 mmol/liter;
• subcompensated – 0.46–0.9;
• decompensated – 0.91–1.33.

Treatment of chronic renal failure

Treatment tactics are entirely based on the stage at which the patient sought help.

1. During the initial course, signs of pathology are eliminated and the root cause is treated.
2. In the second stage, the progression of the process is noted, so drugs are prescribed that slow it down, as well as drugs that support the overall performance of the body.
3. In the third, in addition to the main treatment, medications are used to normalize the condition of other systems.
4. The fourth and fifth are indications for hemodialysis, as well as for peritoneal dialysis - self-purification of the blood using a catheter inserted into the abdominal cavity. Indicators are monitored monthly. The method is usually used when an organ transplant is needed, when a man is waiting for a transplant.

Pharmacological agents are used to eliminate symptoms and causes:

1. For hypertension, antihypertensive drugs are prescribed.
2. The presence of an autoimmune disease requires therapy with cytostatics and glucocorticoid hormones.
3. For severe edema, take diuretic medications.
4. When the pathology is a consequence of anemia, vitamins and iron compounds are recommended.
5. If renal failure is associated with anatomical features, an operation is performed to remove stones or widen the passage of the ureter.
6. At the last stage, the patient undergoes hemodialysis every 2 weeks or undergoes a kidney transplant.

Traditional methods also help relieve symptoms - treatment with decoctions of nettle, sage, and dandelion root. But before resorting to such therapy, it is necessary to discuss prescriptions with a urologist, and also take into account the likelihood of an allergic reaction.

Important! With the help of herbs, you can increase the flow of urine and improve its filtration. But the effect is short-lived, since herbal medicine does not eliminate the cause of disorders in the urinary system.

Nutrition for renal failure syndrome

When diagnosing renal failure, the doctor warns the patient about the need to follow a diet. A daily diet is developed with mandatory consideration of the severity of the pathology and the presence of complications. The amount of foods containing phosphorus, salt, and animal proteins is reduced. What should be the norms for carbohydrate and fat consumption are determined by a nutritionist.

1. It is advisable for patients to replace animal proteins with vegetable ones. If you use the former, limit their presence in the diet to 65 g throughout the day.
2. There should be more fruits and stewed or boiled vegetables on the table.
3. Control the water. The indicator is calculated using the formula - 800 ml + daily urine volume. Not only drinks are taken into account, but also soups.
4. If there is no severe swelling, up to 6 g of salt per day is allowed.
5. Reduce consumption of dairy products, bananas, apricots, and dried fruits due to their high potassium content.

Prevention

To prevent kidney failure from developing, a man should pay attention to provoking factors.

1. It is necessary to adhere to a proper diet, quit smoking and alcohol.
2. In the presence of inflammatory and infectious processes, promptly treat.
3. If a disease of paired organs is detected, adhere to the treatment regimen recommended by the urologist.
4. In case of deterioration of health and problems with urination, a man needs to undergo diagnostics as soon as possible. For preventive purposes, examination is recommended twice a year.

Forecast

1. Renal failure detected in the initial period responds well to therapy. At the same time, doctors completely restore the organ’s functionality.
2. With a prolonged course, the pathology becomes chronic, the treatment of which is much more difficult.
3. At a late stage, the structure of the kidney is destroyed, which leads to irreversible consequences. However, hemodialysis or transplantation helps prolong the patient's life. In the second case, the man will have to constantly take cytostatics to prevent rejection of foreign tissue.

If kidney failure is suspected in a man, there is no time to waste - it is necessary to diagnose the problem and begin treatment immediately. The sooner therapy is carried out, the better the prognosis and the greater the chances of complete healing.

What hormones do the adrenal glands produce and how do they affect the human body?

The adrenal glands are a component of the human endocrine system, that is, the organs responsible for the production of hormones. This is a paired gland, without which life is impossible. More than 40 hormones synthesized here regulate a huge number of important processes in the body. Adrenal hormones can be produced incorrectly, and then a person develops a number of serious diseases.

Adrenal glands and their structure

The adrenal glands are located in the retroperitoneum, located just above the kidneys. They are small in size (up to 5 cm in length, 1 cm in thickness), and weigh only 7-10 g. The shape of the glands is not the same - the left one is in the shape of a crescent, the right one resembles a pyramid. On top, the adrenal glands are surrounded by a fibrous capsule on which a fatty layer is located. The capsule of the glands is connected to the membrane of the kidneys.

The structure of the organs consists of an outer cortex (approximately 80% of the volume of the adrenal glands) and an inner medulla. The cortex is divided into 3 zones:

1. Glomerular, or thin superficial.
2. Beam, or intermediate layer.
3. Reticularis, or inner layer adjacent to the medulla.

Both cortical and brain tissue are responsible for the production of different hormones. Each adrenal gland has a deep groove (gate), through which blood and lymphatic vessels pass and spread to all layers of the glands.

Cortical hormones

Adrenal hormones are a huge group of special substances that are produced by the outer layer of these glands. All of them are called corticosteroids, but different zones of the cortex produce hormones that have different functions and effects on the body. To produce corticosteroids, a fatty substance is needed - cholesterol, which a person gets from food.

Hormonal substances of the zona glomerulosa

Mineralocorticosteroids are created here. They are responsible for the following functions in the body:

• regulation of water-salt metabolism;
• increased smooth muscle tone;
• control of potassium, sodium and osmotic pressure metabolism;
• regulation of the amount of blood in the body;
• ensuring myocardial function;
• increasing muscle endurance.

The main hormones of this group are corticosterone, aldosterone, and deoxycorticosterone. Since they are responsible for the condition of blood vessels and the normalization of blood pressure, when the level of hormones increases, hypertension occurs, and when the level decreases, hypotension occurs. The most active is aldosterone, the rest are considered minor.

Zona fasciculata of the adrenal glands

This layer of glands produces glucocorticosteroids, the most important of which are cortisol and cortisone. Their functions are very diverse. One of the main functions is glucose control. After the release of hormones into the blood, the volume of glycogen in the liver increases, and this increases the amount of glucose. It is processed by insulin secreted by the pancreas. If the amount of glucocorticosteroids increases, this leads to hyperglycemia; when it decreases, insulin hypersensitivity appears.

Other important functions of this group of substances:

• increased muscle tone;
• maintaining brain function in terms of the ability to sense tastes, aromas, and the ability to comprehend information;
• controlling the functioning of the immune system, lymphatic system, thymus gland;
• participation in the breakdown of fats.

If a person has an excess of glucocorticosteroids in the body, this leads to a deterioration in the body’s defenses, accumulation of fats under the skin, on internal organs, and even increased inflammation. Because of them, for example, in diabetic patients, the skin regenerates poorly. But with a lack of hormones, the consequences are also unpleasant. Water accumulates in the body, many types of metabolism are disrupted.

Reticulate layer substances

Sex hormones, or androgens, are produced here. They are very important for humans, and they have a particularly great influence on the female body. In women, androgens are converted into testosterone, which the female body also needs, albeit in small quantities. In men, their growth, on the contrary, contributes to their conversion into estrogens, which causes the appearance of female-type obesity.

During menopause, when ovarian function slows down significantly, the work of the reticular layer of the adrenal glands allows you to receive the bulk of sex hormones. Androgens also help muscle tissue grow and become stronger. They help maintain libido, activate hair growth in certain areas of the body, and participate in the formation of secondary sexual characteristics. The highest concentration of androgens is observed in humans aged 9-15 years.

Adrenal medulla

Hormones of the adrenal medulla are catecholamines. Since this layer of glands is literally penetrated by small blood vessels, when hormones are released into the blood, they quickly spread throughout the body. Here are the main types of substances produced here:

1. Adrenaline is responsible for the activity of the heart and the body’s adaptation to critical situations. With a prolonged increase in the substance, growth of the myocardium is observed, and the muscles, on the contrary, atrophy. Lack of adrenaline leads to a drop in glucose, memory and attention problems, hypotension, and fatigue.
2. Norepinephrine - constricts blood vessels, regulates blood pressure. Excess leads to anxiety, sleep disturbances, panic, deficiency leads to depression.

Symptoms of hormonal imbalance

When the production of hormonal substances by the adrenal glands is disrupted, various disorders develop in the body. A person's blood pressure may rise, obesity may occur, the skin will become thinner, and the muscles will become weak. Osteoporosis is very typical for this condition - increased bone fragility, because excess corticosteroids wash away calcium from bone tissue.

Other possible signs of hormonal imbalances:

• menstrual irregularities;
• severe PMS in women;
• inability to conceive;
• stomach diseases - gastritis, ulcers;
• nervousness, irritability;
• insomnia;
• erectile dysfunction in men;
• baldness;
• swelling;
• weight fluctuations;
• skin inflammation, acne.

Diagnosis of hormonal balance in the body

A blood test from a vein to study hormonal levels is recommended if the above symptoms are present. Most often, an analysis is performed to study sex hormones for indications such as delayed sexual development, infertility, and recurrent miscarriage. The main hormone is dehydroepiandrosterone (the norm in women is 810-8991 nmol/l, in men - 3591-11907 nmol/l). Such a wide range in numbers is due to different concentrations of the hormone depending on age.

An analysis of the concentration of glucocorticosteroids is prescribed for menstruation disorders, osteoporosis, muscle atrophy, skin hyperpigmentation, and obesity. Be sure to stop taking all medications before donating blood, otherwise the test may give an incorrect result. Studies of the level of aldosterone and other mineralocorticosteroids are indicated for abnormalities in blood pressure, hyperplasia of the adrenal cortex, and tumors of these glands.

How to influence hormone levels?

It has been established that hunger, stress and overeating lead to disruption of the adrenal glands. Since corticosteroids are produced at a specific rhythm, you need to eat according to that rhythm. In the morning you need to eat heavily, because this helps to enhance the production of substances. In the evening, meals should be light - this will reduce the production of hormonal substances that are not required in large quantities at night.

Physical activity also helps normalize corticosteroid levels. It is useful to exercise before 15:00 in the afternoon, and in the evening only light exercise can be used. To keep your adrenal glands healthy, you need to eat more berries, vegetables, fruits, take vitamins and supplements of magnesium, calcium, zinc, and iodine.

In case of disturbances in the level of these substances, treatment with drugs is prescribed, including insulin, vitamin D and calcium, adrenal replacement hormones and their antagonists, vitamins C, group B, diuretics, and antihypertensive drugs. Lifelong therapy with hormonal drugs is often required, without which severe disorders develop.

The infection, having penetrated the kidney or pelvis by hematogenous or urinogenic routes, invades the interstitial tissue of the kidney and the tissue of the renal sinus.

Hematogenous pyelonephritis

In hematogenous pyelonephritis, inflammatory foci are located mainly in the cortex, around intralobular vessels. The inflammatory process, involving interstitial tissue, damages mainly the tubular system. With urinogenic, ascending pyelonephritis, the infection affects the kidney in separate foci, fan-shaped, in the form of wedges, extending from the pelvis to the surface of the kidney. Between these foci of inflammation and subsequent fibrosis are areas of normal renal tissue. With bilateral pyelonephritis, the pathological process in the kidneys spreads unevenly, asymmetrically, in contrast to glomerulonephritis and nephrosclerosis.

Acute pyelonephritis

Pyelonephritis, being at first a focal process, becomes diffuse in nature with each new attack. Interstitial tissue plays a very important physiological role in intercellular metabolism. After the disappearance of inflammatory infiltrates, there is no true restoration of the interstitial tissue; In place of the dead elements of the renal parenchyma, scar tissue develops. Primary and secondary acute pyelonephritis can occur first in the form of serous, then purulent interstitial inflammation. Taking this into account, it is customary to use the terms “acute serous pyelonephritis” and “acute purulent pyelonephritis”. While acute serous pyelonephritis is observed in 64%, acute purulent - only in 36% of patients with acute pyelonephritis. In the stage of acute serous inflammation, the kidney is enlarged and tense.

The perinephric tissue is significantly swollen. Microscopically, numerous perivascular infiltrates are detected in the interstitial tissue.

Under the influence of appropriate treatment, this stage undergoes reverse development, but serous acute pyelonephritis can also progress to the stage of purulent inflammation.

Acute purulent pyelonephritis occurs in the form of apostematous nephritis, abscess and carbuncle of the kidney.

Apostematous nephritis is a metastatic suppurative process, one of the subsequent stages of acute pyelonephritis.

In this case, the cortical substance of the kidney, both on the surface and on the section, is dotted with small ulcers that look like beads.

Apostematous nephritis

With apostematous nephritis, the kidney is enlarged and gray-cherry in color. The perinephric tissue is sharply swollen. After removing the fibrous capsule, multiple small (from a pinhead to a pea in size) abscesses, located singly or in groups, are visible. On a section of the kidney, small abscesses are often found in the medulla. Microscopically, multiple foci of purulent inflammation are detected in the interstitial tissue. In the circumference of the Malpighian glomeruli, clusters of small cell infiltrates with foci of necrosis are visible. The urinary tubules are compressed by infiltrates, which are located both in the interstitial tissue and in the perivascular spaces.

Apostematous nephritis is combined with renal carbuncle in 24% of cases. These two types of purulent kidney damage represent a single pathological process, manifesting itself only in different sequences and intensity of its development. If apostematous nephritis is characterized by multiple small abscesses, then a renal carbuncle is a localized suppurative focus, characterized by a tumor-like progressive growth of inflammatory infiltration without a tendency to large abscess formation. In appearance, this process in the kidney is very similar to a skin carbuncle. This circumstance gave rise to Israel in 1891 calling this disease a kidney carbuncle.

The size of the carbuncle ranges from 0.3 to 2 cm, rarely more. Carbuncle can be single or multiple, in 25% of cases it is combined with apostematoenous nephritis. Usually the purulent process affects one kidney, rarely both (5%). With a favorable course of acute purulent pyelonephritis, infiltrates are reabsorbed and connective tissue grows in their place. Replacement of purulent foci with connective tissue leads to the formation of scar retractions on the surface of the kidney, first dark red and then white-gray. On a section of the kidney, these scars have the shape of a wedge, reaching the pelvis.

And so, in acute pyelonephritis, the inflammatory process is first localized in the interstitial tissue, and then the tubules and, lastly, the glomeruli are involved in it. When the process enters the chronic stage, productive endarteritis, hyperplasia of the medial vascular lining, and arteriolar sclerosis occur. Arteriolar sclerosis is one of the causes of further kidney atrophy.

Pyelonephritis shrinkage of the kidney due to atrophy of its parenchyma can be so significant that the kidney has a mass of only 30-50 g. In children, especially young children, pyelonephritis is extremely active and is accompanied by the death of the kidney parenchyma in large areas.

pyelonephritis children kidney dispensary

Kidney diseases are many and varied. The modern classification of kidney diseases, based on the structural and functional principle, provides for the identification of 5 groups of diseases: glomerulopathies, tubulopathies, stromal diseases, neoplasms and congenital anomalies.

Glomerulopathies are based on primary and predominant damage to the glomeruli, leading to impaired filtration of urine. Examples of glomerulopathies are glomerulonephritis, diabetic and amyloid nephropathy, Alport syndrome, etc. Glomerulopathies are classified into congenital and acquired, inflammatory and non-inflammatory. The degree of damage to the glomeruli of the kidney can be different, and therefore they distinguish: a) focal (focal) damage - a small part of the glomeruli is affected, b) diffuse - at least 70% of the glomeruli are affected, c) total - one or another glomerulus is affected entirely, d ) segmental - only part of the glomerulus is affected. In this case, a combination of these terms can be used to designate a pathological process (for example, focal segmental sclerosis).

Non-inflammatory glomerulopathies include: a) minimal change glomerulopathy, b) focal segmental glomerular sclerosis, c) membranous nephropathy. An example of inflammatory glomerulopathy is glomerulonephritis.

Tubulopathies are characterized by primary predominant damage to the tubules, leading to disruption of the concentration, reabsorption and secretory functions of the kidneys. Tubulopathies can be congenital and acquired, acute and chronic, obstructive and necrotizing. In particular, acquired necrotizing acute tubulopathies include necrotic nephrosis, which underlies acute renal failure, and acquired obstructive chronic tubulopathies include “myeloma kidney” and “gouty kidney”.

Stromal (interstitial) kidney diseases are characterized by predominant damage to the interstitial tissue with subsequent involvement of the entire nephron in the process. This group includes tubulointerstitial nephritis and pyelonephritis.

Congenital kidney anomalies usually occur in childhood. The most common diseases are polycystic disease, renal dysplasia and aplasia, horseshoe kidney, etc.

Kidney tumors are very diverse. The most common are epithelial organ-specific and organ-nonspecific neoplasms.

GLOMERULONEPHRITIS is a disease of infectious-allergic or unknown etiology, which is based on bilateral focal or diffuse non-purulent inflammation of predominantly the glomeruli with characteristic renal and extrarenal symptoms. Renal symptoms include oliguria, proteinuria, cylindruria, and hematuria; to extrarenal - hypo- and dysproteinemia, edema, symptomatic arterial hypertension, myocardial hypertrophy of the left ventricle of the heart, hyperazotemia and uremia.

According to the nosological affiliation, glomerulonephritis is primary and secondary, according to the course - acute, subacute and chronic, according to the topography of the inflammatory process in the glomeruli - intra- and extracapillary, according to the prevalence of the process in the kidney - focal and diffuse. With intracapillary glomerulitis, inflammation is localized in the capillary loops and mesangial space and usually goes through 3 successive stages: exudative, exudative-proliferative and proliferative, with extracapillary - in the cavity of the glomerular capsule, and can be exudative (serous, fibrinous, hemorrhagic) or proliferative (with the formation of cavity of the capsule "crescent").

ACUTE GLOMERULONEPHRITIS, being usually an immune complex disease, is associated with infectious agents, most often P-hemolytic streptococcus. Primary infection usually manifests itself in the form of sore throat and pharyngitis. The provoking factor in a sensitized organism is hypothermia. Microscopic examination of the kidneys reveals intracapillary glomerulitis. It is characterized by “hypercellularity” of the glomeruli due to infiltration of lymphocytes, monocytes, segmented leukocytes, as well as proliferation of mesangial cells and endothelium of the glomerular capillaries. Electron microscopy and immunofluorescence reveal deposits of immune complexes in the basement membrane and mesangium. When segmented leukocytes predominate in the infiltrate, we speak of the exudative phase of glomerulitis; when the proliferation of glomerular cells is combined with leukocyte infiltration, we speak of an exudative-proliferative phase; if the proliferation of endothelial and mesangial cells predominates, we speak of a proliferative phase. In addition to the glomeruli, an inflammatory infiltrate is also detected in the stroma of the kidney; dystrophy, necrobiosis and even necrosis occur in the tubular epithelium. Macroscopically, the kidneys in some cases appear enlarged in size with a wide flabby cortical layer and red speckles (“motley kidney”), and in some cases they appear practically unchanged.

Thanks to the use of anti-inflammatory and immunosuppressive therapy, in 95% of patients clinical recovery can occur within 6 weeks, but complete recovery occurs within a year. In some cases, acute glomerulonephritis can be more severe, with the development of fibrinoid necrosis of the glomerular capillaries and their thrombosis (necrotizing glomerulonephritis), which can cause acute renal failure and death.

SUBACUTE GLOMERULONEPHRITIS is characterized by the presence of “crescents” in most glomeruli, filling the capsule cavity. They consist of nephrothelium, podocytes, macrophages and fibrin. Subsequently, fibrosis of the crescents occurs. The latter compress the capillary loops, which leads to their thrombosis and necrosis. Mesangial cell proliferation also occurs in response to capillary damage. The pathological process progresses rapidly, nephrosclerosis develops, within several months - 1.5 years - chronic renal failure, symptomatic hypertension. In this regard, subacute glomerulonephritis is also called rapidly progressive or malignant. Macroscopically, the kidneys may be sharply enlarged, flabby, with a thickened, swollen pale cortex (“large white kidney”); the cortex can be yellow-gray with red speckles and clearly demarcated from the medulla (“large mottled bud”); in some cases, the cortical layer is red and merges with the full-blooded pyramids - (“big red kidney”).

CHRONIC GLOMERULONEPHRITIS is usually characterized by a long latent course. In 20% of patients, chronic renal failure is detected already at the first time they seek medical help. The cause of the development of chronic glomerulonephritis often remains unidentified; in some cases, there are indications in the anamnesis of previous renal diseases. Chronic glomerulonephritis can be diffuse mesangioproliferative and mesangiocapillary. The first form is characterized by proliferation of mesangial cells in response to the deposition of immune complexes. Mesangial cells increase matrix production, which subsequently leads to glomerular sclerosis. The lesion is usually diffuse in nature, but can also be focal segmental. The disease progresses rather slowly, the long-term prognosis is poor, since chronic renal failure, symptomatic hypertension and other complications gradually appear.

Mesangiocapillary glomerulonephritis is characterized not only by the proliferation of mesangial cells, but also by thickening of the basement membranes of the glomerular capillaries, and therefore proceeds aggressively. There are 2 main types of mesangiocapillary glomerulonephritis (type 3 is currently described). In type 1, thickening of the basement membrane occurs due to the deposition of immune complexes; in type 2, electron-dense deposits are detected in the basement membranes of capillaries, but there are no immune complexes in them. In this regard, this type of glomerulonephritis is also called “dense deposit disease” or “dense deposit disease.” As chronic glomerulonephritis progresses, it loses the morphological features characteristic of one type or another. Gradually, diffuse sclerosis and hyalinosis of the glomeruli occurs, and the corresponding tubules atrophy and die. The remaining nephrons expand and fill with urine containing protein (“thyroidization” of the kidney). Connective tissue grows in the stroma of the kidney. Macroscopically, the kidneys become significantly reduced in size, the cortex is thinned with a fine-grained surface. In the section, the boundary of the layers is unclear, the vessels are well contoured due to the thickening of their walls. This collective type of kidney damage is called fibroplastic glomerulonephritis, and the wrinkled kidneys are called secondary wrinkled.

For chronic glomerulonephritis, in addition to progressive chronic renal failure, hypertrophy of the myocardium of the left ventricle of the heart, systemic changes in arteries (elastofibrosis, atherosclerosis), arterioles (plasma impregnation, sclerosis and hyalinosis), as well as organ changes due to vascular damage and symptomatic hypertension are very characteristic. The most common causes of death in the terminal stage of the disease are uremia, stroke, and cardiovascular failure.

PYELONEPHRITIS is an infectious disease in which the renal pelvis, calyces and kidney substance, mainly interstitial tissue, are involved in the pathological process. Pyelonephritis can be primary and secondary, unilateral and bilateral, focal or diffuse, acute or chronic.

The causative agents of pyelonephritis are many microorganisms, but most often - Escherichia coli, Enterobacter, Proteus. Infection of the kidney can occur by ascending (urogenic), descending (hematogenous) and lymphogenous routes. It is important to remember that infection entering the kidneys alone is not enough. The development of the disease is determined by the reactivity of the body and a number of local factors that cause disruption of the outflow of urine, urinary stasis and, as a consequence, reflux (vesicoureteral, pyelo-renal, pyelovenous). Ascending pyelonephritis usually complicates urolithiasis, tumors of the urinary tract, ureteral strictures, etc. The hematogenous route is characteristic of sepsis, the lymphogenous route is characteristic of inflammatory diseases of the genital organs and intestines.

ACUTE PYELONEPHRITIS can be serous, serous-purulent and purulent. The most typical is purulent inflammation, in which purulent exudate accumulates in the pelvis and calyces, their epithelium dies and desquamates. Purulent inflammation also appears in the stroma of the kidney, often in the form of multiple abscesses. As a result, dystrophy, necrobiosis and necrosis occur in the epithelium of the tubules, and cylinders appear in the lumen of the tubules. Complications of acute pyelonephritis include purulent peri- and paranephritis, pyonephrosis, papillonecrosis (necrosis of the pyramidal papillae), urosepsis, etc.

CHRONIC PYELONEPHRITIS is characterized by a recurrent course in the form of attacks of acute pyelonephritis and progressive proliferation of connective tissue in the kidney. Characteristically, there is unevenly expressed cicatricial wrinkling, the formation of adhesions between the kidney tissue and the capsule, and sclerosis of the renal pelvis. The surviving nephrons hypertrophy, the tubules appear dilated, with protein content (“thyroid kidney”). The asymmetry of the process in both kidneys is characteristic. As a result, pyelonephritic nephrosclerosis occurs. Characteristic complications of chronic pyelonephritis are chronic renal failure and nephrogenic symptomatic hypertension with its various manifestations.

RENAL FAILURE is a violation of the basic homeostatic functions of the kidneys with the development of azotemia, disturbances of acid-base balance and electrolyte-water balance. Kidney failure can be acute or chronic. Acute renal failure is understood as a sudden impairment of renal function - oliguria develops. The morphological substrate of acute renal failure is necrotic nephrosis. Etiopathogenetic factors of acute renal failure are usually classified into renal and prerenal. Prerenal factors include shock of any etiology, hemolysis, myolysis, severe hydrochloropenia, intoxication associated with peritonitis, pancreatitis, etc. Renal factors include exogenous nephrotoxins (mercury, lead, etc.), toxic-allergic kidney damage (“sulfanilamide kidney”) , acute kidney diseases (glomerulonephritis, pyelonephritis), blockage of the urinary tract (stones, tumor), etc.

The main link in the pathogenesis of acute renal failure is a violation of renal hemodynamics as a reflection of general hemodynamic disorders in the body. In the kidney, a spasm of the cortical vessels occurs and the bulk of the blood is discharged through the juxtamedullary nephrons. Such reduced blood circulation in the kidneys leads to progressive ischemia of the cortex, impaired renal lymphatic drainage with the development of interstitial edema. Cortical ischemia is accompanied by dystrophy, necrobiosis and necrosis of the epithelium of the kidney tubules. This action is also complemented by the direct effect of nephrotoxic poisons on the epithelium. There are 3 stages of acute renal failure: initial (shock), oligo-anuric and restoration of diuresis. With timely treatment with hemodialysis, recovery usually occurs; progressive acute renal failure leads to death.

CRF is a syndrome of gradually occurring renal dysfunction, the morphological substrate of which is nephrosclerosis, and the most striking clinical expression is uremia. Nephrosclerosis can be primary (atherosclerotic and arteriolosclerotic) and secondary, caused by glomerulonephritis, pyelonephritis, urolithiasis, renal amyloidosis, tuberculosis, etc.

The occurrence of uremia is associated with retention of nitrogenous waste in the body, acidosis, and electrolyte imbalance. This leads to autointoxication and profound disturbances in cellular metabolism. Excretory organs (skin, mucous and serous membranes, respiratory and digestive organs) are especially severely affected. They cause blood and lymph circulation disorders, alterative and inflammatory changes and, in particular, polyserositis, laryngo-tracheo-bronchitis, esophago-gastro-enterocolitis and many others. etc.).