Nephrosclerosis: features of the clinical picture and therapy. Nephrosclerosis of the kidney (“wrinkled kidney”): causes, symptoms, signs, diagnosis and treatment I have right-sided nephrosclerosis, the left kidney is normal

Renal nephrosclerosis is a chronic disease that gradually causes the death of functional kidney cells (nephrons), resulting in the formation of connective tissue in their place, which is unable to perform the functions of the organ.

Classification of kidney nephrosclerosis

Nephrosclerosis as a wrinkled kidney, depending on the cause of the development of the pathology and the type of symptoms that appear, is divided into the following types:

• Primary nephrosclerosis - this form of the disease appears due to dysfunction of certain body systems.

• Secondary nephrosclerosis is a pathology of this type that develops as a result of the influence of unfavorable circumstances on the body.

• Hypertensive nephrosclerosis - in this case, the disease occurs due to hypertension and impaired blood flow through a narrowed artery. It is also called arteriolosclerotic nephrosclerosis. This type, in turn, is divided into two types - benign (slow development, when it is possible to stop the further development of the disease), which in most cases does not show characteristic symptoms, and malignant (loss of kidney cells occurs much faster).
• Atherosclerotic nephrosclerosis - the main feature of this type of disease is its unilateral spread (affects only one organ).

• Diabetic nephrosclerosis - with this form of pathology, both kidneys are damaged, which occurs in several stages. The first stage is characterized by the absence of symptoms. In the second stage, a slight increase in blood pressure is observed. A distinctive feature of the third stage is the appearance of severe swelling. At the fourth stage, renal failure begins to progress, which can appear a long time after.

Causes and symptoms of kidney nephrosclerosis

The following factors are most likely to cause this disease:

• age after 40 years;
• alcohol abuse;
• smoking;
• bearing a child;
• poor nutrition;
• hereditary predisposition to diseases of this type.

The causes of nephrosclerosis can be completely different. Primary factors in the occurrence of pathology:

• insufficient blood supply to organ systems;
• hypertension;
• the presence of blood clots that interfere with normal blood circulation, which is why organ infarction is possible;
• atherosclerosis - the arterial lumen begins to narrow as a result of the formation of fats on the walls of the arteries and their deposition;
• elderly age;
• impaired elasticity of the renal vessels.

Secondary causes of nephrosclerosis include:

• diabetes;
• hormonal imbalance during pregnancy (in this case, protein is removed from the body through urine, as a result of which nephrons die);
• glomerulonephritis in chronic form;
• pyelonephritis (inflammation due to pathogenic microorganisms entering the kidneys);
• the presence of stones in the kidneys;
• mechanical pressure of the ureter of various etiologies;
• tuberculosis;
• lupus erythematosus (with this disease the body fights its own cells);
• amyloid protein entering the kidneys;
• mechanical injury to the kidneys;
• consequences of surgery;
• use of radiation therapy.

The main danger of the disease is that at the beginning of its development there are practically no symptoms. Pathology is most often detected by chance - during general blood and urine tests. If the disease does not receive the necessary attention, it will cause complications over time, including end-stage renal failure.

At this stage of the disease, the symptoms are usually pronounced, but it is no longer possible to completely get rid of the pathology and bring the body’s condition back to normal.

With the development of nephrosclerosis, symptoms may be as follows:

• pronounced swelling on the face and legs;
• pain and discomfort in the lower back;
• hypertension;
• frequent attacks of headache, periodically intensifying;

• change in urine appearance (presence of sediment or blood impurities, dark color);
• false urge to urinate, especially at night;
• a small amount of urine excreted during the day (less than 0.5 l);
• constant thirst;
• aversion to meat food;
• increased body fatigue;
• lack of desire to eat;

• shortness of breath, tachycardia (even in the absence of physical activity);
• skin itching;
• sudden weight loss.

If one or more symptoms are detected, you must immediately consult a doctor and undergo a nephrological examination.

Diagnosis of kidney nephrosclerosis

If nephrosclerosis is suspected, an anamnesis is first collected and the patient is examined. After studying the symptoms of the disease, the patient’s abdomen is usually palpated. The combination of these methods makes it possible to establish a preliminary diagnosis and determine further research methods.

Laboratory diagnostic methods include:

• blood test for biochemistry (with nephrosclerosis, there is an increase in the level of urea, creatine, a decreased amount of protein, in subsequent phases of the disease the content of substances such as sodium, magnesium, potassium, phosphorus increases);
• blood test (decrease in hemoglobin level and platelet count);
• urine examination (increased protein level, decreased urine concentration, pronounced indicators of red blood cells and cylinders, which are absent in the normal state).

To establish a diagnosis, it is necessary to carry out a number of instrumental research methods, for example:

• ultrasound examination (in this case, the size of the organ is much smaller compared to normal, the cortical substance atrophies);
• renal angiography (localization of narrowed and deformed small vessels is revealed, thinning of the cortex occurs, the edges of the kidneys are slightly blurred);
• X-ray of the kidneys with a contrast agent (iodine preparations are injected, making it clear that the kidneys and their cortex are much smaller than normal);
• Dopplerography (slowing of blood flow in the renal vessels and nephrons is observed);
• scintigraphy (uneven isotope distribution);
• radionuclide renography;
• biopsy and histology of the biopsy sample (using a macroscopic specimen).

Treatment of the disease

In the case of a benign nature of the disease, treatment involves the use of diuretic drugs, as well as those that lower blood pressure. A long-term diet is mandatory, during which it is necessary to consume low-protein foods and low salt content. It is recommended to increase the amount of grains, fresh vegetables and fruits in the diet, and drink at least 2 liters of water per day.

The patient must undergo regular examinations to obtain information about the condition of the organ and its functioning.

During the period of therapy, it is necessary to treat chronic constipation, since the accumulation of toxins negatively affects the condition of the kidneys.

In order to improve renal blood circulation, regular exercise is recommended. Frequent walks in the fresh air and swimming will help improve a person's condition. In some cases, the doctor may advise the patient to visit the bathhouse and sauna, as this increases sweating and removes harmful substances from the body.

If the pathology is malignant, treatment must be carried out in a hospital setting. In this case, some caution must be taken when taking medications so as not to worsen the patient's condition. Sometimes surgery may be required to remove blockages in blood vessels or remove the atrophied part of the kidney. Most often, after such an operation, the patient undergoes hemodialysis or a kidney transplant.

With this type of nephrosclerosis, the prognosis is rarely favorable, since it is almost impossible to normalize the body’s condition.

Treatment can be carried out at home at the initial stage of the disease. If complications develop and there is a sharp deterioration in health, urgent medical attention is required.

• physiological and glucose solution (used to remove harmful substances from the body);
• polyionic solutions (used to regulate the acid-base balance);
• glandular preparations, erythropoietins;
• blood transfusion of some components (with the development of anemia);
• medicines to lower blood pressure;
• anticoagulants (used at the initial stage of the disease);

• diuretics (if there are symptoms of fluid retention in the body);
• potassium and calcium preparations;
• sorbents (used to reduce the amount of toxins in the intestines);
• multivitamin complexes;
• hepatoprotectors (drugs that protect the liver);
• choleretic agents (usually of plant origin).

Preventive actions

There are no special preventative methods for the disease. The main methods of preventing its occurrence and further development are maintaining proper nutrition, avoiding excessive mental and physical stress, regular rest, and constant monitoring of blood pressure levels.

It is worth remembering that the sooner you start treating this disease, the greater the chances of getting rid of the pathology and restoring the normal state of the body.

No kidney disease goes away without a trace; any pathological process in the kidney leads to damage and death of its structural and functional units - nephrons. The loss of single nephrons does not affect the function of the organ in any way. With the massive death of renal structures, they are replaced by connective tissue, and the function of the kidney is lost.

The process of replacing functioning nephrons with connective tissue is nephrosclerosis. This is not an independent disease, but a possible outcome of any pathological processes in the kidney. The outcome of nephrosclerosis is complete loss of function, reduction in size and ultimately shrinkage of the kidney. Sometimes doctors even replace the term “nephrosclerosis” with the concept of “wrinkled kidney”; in essence, they are the same thing.

Causes of nephrosclerosis

There are two forms of this pathology: primary and secondary wrinkled kidney.

• Primary nephrosclerosis is caused by vascular damage and impaired blood supply to the renal tissue as a result of renal vessels and renal infarctions, and impaired venous outflow. The structure of the kidneys undergoes sclerotic changes with age; by the age of 70, the number of active renal structural units in the kidneys decreases by 30-40%.
• The secondary form of the disease occurs as a result of damage to the kidney parenchyma during long-term autoimmune processes, kidney tuberculosis; severe nephropathy in pregnant women and organ trauma can lead to nephrosclerosis.

In recent decades, the main causes of this pathology are considered to be hypertension and diabetes mellitus, although literally 20 years ago glomerulonephritis was in the lead.

Main symptoms of nephrosclerosis

The disease can last for decades, with the deterioration of kidney function occurring gradually, and the symptoms initially do not bother patients much. A doctor is often consulted when edema appears, urination problems and signs of arterial hypertension appear. With such symptoms, changes in the kidneys are often irreversible, and the function of the organ is already significantly reduced.

Urinary dysfunction

This symptom includes polyuria (excessive urination - 2 liters per day or more) and nocturia (increased number and volume of urination at night).

In severe forms of nephrosclerosis, polyuria is replaced when the amount of urine, on the contrary, sharply decreases. Anuria (complete absence of urine may indicate end-stage renal failure).

Also, an admixture of blood appears in the urine, and it turns the color of meat slop - this symptom is called gross hematuria.

Arterial hypertension

When the blood supply to the kidneys is disrupted, a protective mechanism is activated aimed at increasing the pressure in the renal vessels, as a result of which substances are released into the blood that increase the pressure throughout the bloodstream. With nephrosclerosis, arterial hypertension reaches very high values, hypertensive crises are possible with an increase in systolic pressure to 250-300 mm Hg. Art., and it is very difficult to reduce the pressure.

Edema

Fluid retention in the body leads to the appearance. They first appear on the face in the morning and go away after a while. Then they gradually go down, the fingers on the hands swell (patients note that they cannot take off the rings in the morning) and shins (can’t put on shoes, can’t fasten boots). As the disease progresses, swelling spreads throughout the body, and anasarca occurs - generalized swelling of subcutaneous fat, soft tissues, and in the worst case, internal organs.

(cardiac asthma) occurs as a result of overload of the heart due to the increased amount of fluid in the body. As a result, blood stagnation occurs in the pulmonary capillaries. The patient experiences shortness of breath, cough, and during an attack there is sweating, cyanosis (blue discoloration of the skin), increased heart rate and respiratory rate. Cardiac asthma is a serious complication that can be fatal if left untreated.

Stages of nephrosclerosis

There are 2 periods in the development of this pathology:

1. In the first phase, there are no manifestations of nephrosclerosis, however, the patient has and may progress one or more diseases leading to the replacement of normal renal parenchyma with connective tissue. During this period, changes characteristic of kidney damage already appear in urine and blood tests.
2. Symptoms characteristic of nephrosclerosis, and, accordingly, renal failure, appear in the second stage of the process, when changes in the structure of the kidneys can be detected using ultrasound and other instrumental research methods.

Also, depending on the course of the pathological process, malignant and benign forms of nephrosclerosis are distinguished.

Fortunately, in the vast majority of patients, the second form of the disease occurs, in which the process progresses slowly; with successful treatment of the underlying disease, the progression of nephrosclerosis can be slowed down.

In a malignant course, nephrosclerosis progresses quickly and in a few years can lead to a complete loss of kidney function, severe and doom the patient to lifelong renal failure. Such an unfavorable outcome can be observed with malignant arterial hypertension and eclampsia in pregnant women.

Diagnosis of nephrosclerosis

Since the symptoms of a shriveled kidney appear in the later stages, it is very important to identify this pathology with the help of an examination as early as possible, since the effectiveness of treatment in this case will be much higher. Taking the patient's medical history plays an important role.

• General urine analysis. Any examination of the kidneys, of course, begins with a urine test; with initial nephrosclerosis, the following abnormalities can be detected: a decrease in the relative density of urine, the appearance of protein, single red blood cells and casts.
• Blood tests. In a clinical blood test, a decrease in the level of hemoglobin and platelets is possible. In biochemical – a decrease in the amount of total protein, an increase in the level of urea, creatinine, uric acid and sodium. An increase in glucose and cholesterol levels should alert you.

Such changes in urine and blood tests are very nonspecific and can be observed not only in kidney diseases. However, the combination of such deviations in the results of laboratory tests, in the presence of a history of factors that can lead to kidney damage, forces the doctor to think about further diagnosis.

For examination, many instrumental methods are used, such as ultrasound (x-ray of the kidneys with a contrast agent), angiography, radioisotope studies, etc. All of them reveal a decrease in the size of the kidney, the presence of calcium deposits, impaired blood flow in the renal vessels and other changes indicating proliferation connective tissue. A biopsy can give an accurate answer about the condition of the renal parenchyma.

Treatment of nephrosclerosis

There is no specific therapy aimed at treating nephrosclerosis. It is necessary to treat the disease, which has led to kidney damage and death of nephrons, followed by their replacement with connective tissue. That is why not only a nephrologist, but also a specialized specialist treats patients with nephrosclerosis.

In addition to therapy aimed at treating the underlying disease, patients must follow a diet. It is recommended to limit the amount of protein and table salt; the diet should contain enough vitamins and mineral salts. In the absence of arterial hypertension and edema, fluid and protein restriction is not required.

In end-stage renal failure, when both kidneys have lost their functions, patients are advised to undergo hemodialysis. The only way out in this situation is kidney transplantation; in recent years, this operation has been successfully carried out in Russia, and for citizens of our country it is free.

Nephrosclerosis- chronic kidney disease, in which functional kidney cells (nephrons) gradually die, and connective tissue grows in their place (not responsible for the functioning of the organ).

As a result, the kidneys become denser, wrinkle, decrease in size and cease to perform their functions - chronic renal failure develops (the international name is chronic kidney disease).

Nephrosclerosis is not an independent disease. A large number of severe illnesses lead to its formation: diabetes mellitus, arterial hypertension and others.

Statistics

In Europe, according to statistics, chronic renal failure occurs in 600 cases per 1,000,000 inhabitants.

The number of patients with nephrosclerosis who are on hemodialysis (artificial kidney) with chronic renal failure ranges from 10 to 20%. Moreover, the mortality rate among patients with chronic renal failure reaches 22% per year.

Story

Then in 1914, Volgard and Fahr proved that arteriosclerotic changes (deposition of “harmful” fats) occur in the vessels of the kidneys, linking them with high blood pressure. They also identified nephrosclerosis as a separate disease, proposing to divide it into a simple and malignant form.

A doctor by training and a writer by vocation, Mikhail Bulgakov, passed away from nephrosclerosis. He authored famous works that have not lost their relevance even today: “The Master and Margarita”, “Notes of a Young Doctor” and others.

In a letter sent to his friend a few months before his death, Bulgakov wrote: “Dying is painful, boring and vulgar. As you know, there is one decent type of death - from a firearm, but, unfortunately, I don’t have that.”

Anatomy and function of the kidneys

The kidney contains renal tissue (parenchyma) and the pyelocaliceal system.

Kidney tissue consists of a cortex (contains nephrons, the smallest units of the kidney) and a medulla (contains urinary tubules). Urine is produced in the kidney tissue.

Pyelocalyceal system consists of calyces and pelvis, in which urine accumulates and is then excreted.

The outside of each kidney is covered with a capsule.

Nephron structure

The renal artery, having reached the renal tissue, decreases in diameter and branches, forming the afferent atreriole (a small-caliber artery).

Having entered the capsule, the afferent arteriole branches into the smallest vessels - a glomerulus is formed, which has about 50 loops. When leaving the nephron capsule, the vascular loops unite and form the efferent arteriole.

The walls of the glomerular vessels have a complex structure, due to which “windows” are formed.

Capsule structure

It consists of outer and inner leaves, and between them there is a cavity into which the liquid part of the blood from the glomerulus penetrates with the substances dissolved in it.

The urinary tubules of the nephron begin from the glomerular capsule, which flow into the collecting urinary tubules. Then they unite with each other and open into the renal cups of the pyelocaliceal system.

Mechanism of blood filtration and urine formation

Moreover, the “windows” allow both beneficial substances (for example, amino acids) and harmful substances (toxins, drugs) to pass through. However, with such filtration, blood elements (erythrocytes, leukocytes), blood proteins and large molecules are retained. This is how primary urine is formed (150-180 liters per day).

Next, primary urine enters the urinary tubules, in which beneficial substances (vitamins, fats, glucose) and water are reabsorbed, and harmful substances, on the contrary, accumulate. This is how primary urine turns into secondary urine (about 1.5-2.0 liters per day).

Then secondary urine enters the collecting ducts, then into the pyelocaliceal system of the kidney, then into the ureter and bladder. During the act of urination, secondary urine is removed from the body.

Kidney functions

• Removal from the body excess fluid, toxins, end products of metabolism of certain substances (urea, creatinine, bilirubin), allergens, medications and others.
• Hormone production:
  • Renin, which is involved in the regulation of vascular tone and blood pressure (the conversion of angiotensin I into angiotensin II), the content of sodium and potassium salts in the body, as well as the reabsorption of water in the urinary tubules,
  • Erythropoietin, which stimulates the formation of red blood cells (erythrocytes) in the bone marrow.
• Maintaining blood acidity(normal blood pH is from 7.37-7.44).
• Synthesis of a substance (urokinase), which regulates blood clotting.
• Converting vitamin D to its active form, improving the absorption of calcium and phosphorus in the small intestine.

Causes and classification of nephrosclerosis

Causes of primary nephrosclerosis (primary shriveled kidney)

A prolonged increase in blood pressure (BP) causes spasm and constriction of the blood vessels of the kidneys, they lose their elasticity, their pressure and resistance to blood flow increase.

Hypertensive nephrosclerosis occurs in two variants:

• Benign nephrosclerosis(arteriolosclerotic nephrosclerosis) - when connective tissue grows in the walls of the arteries of the kidneys, which leads to a decrease in their elasticity. The disease develops over 10 years or more. Often this form is combined with atherosclerosis (vascular disease).
• Malignant nephrosclerosis(arteriolonecrotic nephrosclerosis, Farah nephrosclerosis) develops over a short time (several years) with severe arterial hypertension (AH). In this disease, the arterioles and capillaries of the glomeruli die. Hemorrhages also occur in the wall of the urinary tubules, leading to atrophy of the cells of their inner layer (they decrease in size and lose viability).

There is a partial or complete blockage of the lumen of the renal artery by a detached blood clot (thrombosis) or embolus (for example, an accumulation of microbes in pyelonephritis). As a result, the lumen of the arteries narrows. Therefore, the flow of blood to the kidney or its individual zones decreases - heart attacks develop (areas of living tissue die).

In single and small heart attacks, the work of the kidney is compensated. Whereas with repeated and extensive infarctions, a larger number of nephrons die, leading to the development of nephrosclerosis.

Atherosclerosis

Fat-like substances - “harmful” fats (atherosclerotic plaques) - are deposited on the inner wall of the arteries throughout the body. Therefore, the lumen of the arteries narrows, and their walls thicken and become less elastic. As a result, the cells of organs and tissues are insufficiently supplied with blood, dying over time. The smaller the caliber of the arteries, the faster changes occur in them.

The most “favorite” areas of atherosclerotic plaques in the kidneys are the places where the renal artery enters the kidney, or where it divides into smaller branches.

Age-related changes

Starting from 40-50 years, the walls of the arteries thicken, and their lumens narrow. The reason is the deposition of calcium on the inner lining of the artery wall, the accumulation of smooth muscle fibers and connective tissue.

Age-related changes in the kidneys lead to thinning of the cortex and atrophy of the cells of the inner layer of the urinary tubules (lose function and viability).

By age 70, the number of nephrons in the kidneys decreases by about 40%.

Chronic venous congestion of the kidneys

It leads to disruption of the outflow of venous blood from the kidneys, creating conditions for excessive growth of collagen (the protein that is the basis of connective tissue) in the wall of the kidney vessels. Therefore, their elasticity decreases.

Changes develop over a long period of time (10 years or more) with nephroptosis (prolapse of the kidneys), narrowing of the renal vein and chronic venous thrombosis.

Causes of secondary nephrosclerosis (secondary wrinkled kidney)

Against the background of increased blood sugar levels, complex compounds are formed that are deposited on the inner wall of blood vessels (primarily small ones), damaging them. As a result, the vascular wall swells and thickens, and its permeability increases. Therefore, protein gets into the urine (diabetic nephropathy develops).

Also, when the cells of the inner wall of blood vessels are damaged, clotting factors are released into the blood. Therefore, the formation of blood clots in the lumen of the kidney vessels increases.

The changes lead to a slowdown in blood flow in capillaries (small vessels) and a decrease in the supply of oxygen to cells in almost all organs and tissues. That is, not only the kidneys are affected, but also other organs (eyes, heart).

Nephropathy of pregnancy (late toxicosis)

Against the background of hormonal changes in the body during pregnancy, the work of the brain changes, which sends “wrong commands” to all capillaries, leading to their spasm.

Therefore, resistance to blood flow in the vessels increases, and blood pressure rises. As a result, the blood supply to the kidneys deteriorates and nephrons die.

The permeability of the glomerular capillary wall also increases, so salts are retained in the body, and protein is lost in the urine. Such changes contribute to the formation of edema (the release of liquid into the surrounding tissues) and maintain blood pressure at high levels.

In response to an infection (sore throat, pharyngitis), the body produces antibodies (immune system proteins that fight “foreigners”), which, interacting with an antigen (bacterial protein or toxin), form circulating immune complexes (CICs) - the body’s protective reaction. Normally, CECs are destroyed by the liver and phagocytes (cells of the immune system). However, if there are disturbances in the functioning of the immune system, this does not happen.

With the blood flow, CECs enter the kidneys and damage the inner lining of the glomerular vessels. At the same time, substances are released into the blood that enhance the formation of blood clots in the lumen of the glomerular vessels, and hyaline (a protein substance of dense consistency) is deposited in their walls. As a result, the elasticity decreases and the permeability of the glomerular vessel wall increases, which leads to impaired blood flow.

Chronic pyelonephritis

Microbes with the blood flow or the reverse flow of urine from the bladder enter the renal glomeruli and the lumen of the urinary tubules, settling in them. White blood cells accumulate around bacterial clots. During recovery, scars form in their place; if recovery does not occur, ulcers form. When the disease lasts for a long time, the number of scars increases, leading to the death of a large number of nephrons.

Urolithiasis, narrowing or compression of the ureter

In the pyelocaliceal system and ureters, the outflow of urine is disrupted. Therefore, it stagnates, creating conditions for the proliferation of bacteria in it (normally urine is sterile, but during inflammatory processes it contains bacteria). Then the microbes enter the urinary tubules and glomerular vessels with the reverse reflux of urine, damaging their inner wall.

Kidney tuberculosis

With the flow of blood from the lesion (for example, easily), tuberculosis bacilli enter the kidneys, settling on the inner wall of the glomerular vessels. Leukocytes gather around the accumulation of bacteria, forming foci of inflammation. As a result, blood flow slows down and blood vessels narrow, disrupting the flow of blood to the glomeruli.

Systemic lupus erythematosus

With this disease, the immune system “does not recognize” its own tissues, mistaking them for “foreign” ones. Therefore, it tries to destroy normal cells of the body, damaging them. As a result, circulating immune complexes (CICs) are formed in the blood, which consist of an antibody (a protein of the immune system designed to fight “strangers”) and an antigen (particles from the surface of normal cells of the body).

CICs with the bloodstream reach the renal tissue and damage the inner wall of the glomerular vessels. Therefore, inflammation develops, which leads to the death of nephrons.

Kidney amyloidosis

There is a violation of protein metabolism: an abnormal protein is formed - amyloid, which becomes a “stranger” (antigen) for the body. Therefore, the immune system fights it by producing antibodies. The antibody and antigen, interacting, form CECs, which reach the kidneys through the bloodstream and damage the inner wall of the glomerular vessels. As a result, nephrons die. Simultaneously with kidney damage, the lungs, heart and other organs are involved in the process.

Kidney injury or surgery

Particles of kidney tissue can clog the lumen of the arteries and arterioles of the kidney. Therefore, the blood supply to a separate area of ​​the kidney is sharply disrupted, leading to the death of nephrons.

Ionizing radiation

Causes the development of disease years or months after exposure to the body. Moreover, changes occur in all vessels of organs and tissues. The degree of their severity depends on the dose and type of ionizing radiation.

What's happening? The walls of the kidney vessels gradually thicken, and their lumen narrows, therefore the blood flow in the nephrons decreases.

Symptoms

Signs of nephrosclerosis

Periods of nephrosclerosis

Second period characterized by the gradual death of nephrons and replacement of the renal parenchyma with connective tissue - chronic renal failure (CRF) develops. Depending on the volume of dead kidney tissue, CRF goes through several stages in its formation.

Stages of chronic renal failure

First stage

Patients get tired quickly during physical activity or in the evening. They have decreased ability to work, have slight dry mouth, thirst, polyuria, and nocturia. But in general the patients feel good. In a biochemical blood test, the content of sodium, phosphorus and calcium sometimes changes. Protein may be detected in the TAM, and the relative density of urine may decrease.

Second stage

Symptoms of azotemia appear: decreased appetite, lethargy, itching, nausea and vomiting. Vision is impaired, headaches occur, heart rate increases, and heart rhythm is disrupted. Blood pressure rises to high levels and is difficult to reduce. The volume of daily urine decreases. In a biochemical blood test, the level of urea and creatinine increases.

At this stage, as the course of the underlying disease improves, tests and the volume of daily urine are normalized, and the well-being of patients improves.

Third stage

Kidney function deteriorates sharply, the volume of daily urine decreases. Patients are weakened, get tired quickly, eat poorly, and are constantly thirsty. They are prone to frequent and severe bacterial or viral infections (ARVI, stomatitis, pustular infections on the skin). The skin is dry and acquires a yellowish tint - due to the accumulation of bile pigment derivatives in the body (normally excreted in the urine, turning it yellow). The level of creatinine and urea in the blood is increased.

Fourth stage

There is no urine, or its daily volume is sharply reduced, so symptoms of self-poisoning (uremia) increase. Sleep is disturbed, memory is reduced, pulmonary edema develops, there are blood clotting disorders, blood pressure remains high, and so on. There is a persistent increase in creatinine, uric acid and urea in the blood, and total protein is reduced.

All changes that occur at the fourth stage are irreversible.

Diagnosis of nephrosclerosis

Laboratory research

Blood chemistry

Indicators indicating renal dysfunction:

• Urea levels increase(2.5-8.3 mmol/l), creatinine(in women - 50-100 µmol/l, in men - 60-115 µmol/l) and uric acid(210 - 420 µmol/l).
• Total protein decreases(65-85 g/l).
• Potassium(3.5-5.5 mmol/l) in the initial stages remains normal or decreases, since it is excreted along with the fluid that the body loses in large volumes. At the final stage, the level of potassium increases, since it is not excreted in the urine, accumulating in the body.
• In the final stages, magnesium levels increase(0.8-1.2 mmol/l) and phosphorus(0.81-1.45 mmol/l). While the calcium content (2.15-2.65 mmol/l) decreases.
• Sodium rises(123-140 mmol/l). However, it may also decrease if the patient sharply limits the consumption of table salt.

General urine analysis

• Increased protein content(absent or present up to 0.033 g/l)
• Red blood cells appear(0-2-3 red blood cells in the field of view of the microscope) and cylinders (normally absent).
• Relative density of urine decreases (1.010 – 1.022 g/l)

General blood analysis

Hemoglobin levels decrease(in men - 130-160 g/l, in women -120-150 g/l), red blood cells (3.5 * 10 12

/l – 5.0*10 12 /l). While the level of leukocytes (4-9x10 9) due to self-poisoning, on the contrary, increases.

Platelet levels decrease(180 - 320 *10 9 /l). At the same time, the blood clotting time increases (the beginning of coagulation is from 30 seconds to 2 minutes, the end of coagulation is from 3 to 5 minutes) and the duration of bleeding (2-3 minutes).

Instrumental research methods

Ultrasound examination (ultrasound)

For nephrosclerosis there is atrophy (reduction in size and cessation of function) of the renal cortex in relation to the medulla. There is sometimes no separation (differentiation) between the two layers. Deposits of calcium salts in the kidney parenchyma (nephrocalcinosis) are also visible, which indicate the death of kidney tissue.

Excretory urography of the kidneys

The method is based on the fact that the kidneys are capable of secreting some radiopaque iodine-containing substances introduced into the body intravenously. As a result, X-rays taken at regular intervals provide images of the kidneys and urinary tract.

For nephrosclerosis the volume of the kidney and the size of the cortex are reduced. Deposits of calcium salts (nephrocalcinosis) are often detected.

Angiography of renal vessels

A contrast agent is given intravenously. Then a series of pictures are taken, in which the doctor then assesses the degree of narrowing of the kidney vessels, the presence of an obstruction to blood flow, and so on.

For nephrosclerosis there is deformation and narrowing of small arterial vessels, there is an uneven outer contour of the kidneys and thinning of the cortex. In addition, the symptom of “burnt wood” is visible - when the branches of the renal artery are narrowed and broken, and there is no fine pattern of the arteries.

Renal scintigraphy

A special radioisotope substance is injected intravenously, which is excreted by the kidneys, emitting radiation. This radiation is captured by special equipment and then transmits the image to a computer.

For nephrosclerosis The radioisotope substance is distributed unevenly. Sometimes only isolated areas of kidney tissue are preserved, and sometimes the kidney is not visible at all.

Doppler of renal vessels

Special equipment emits and directs ultrasonic waves, which, upon reaching the organ, are reflected and captured by special equipment. The information is then transferred to a computer where the data is processed.

For nephrosclerosis the method reveals a slowdown in blood flow in the renal vessels and nephrons.

Radionuclide renography

It is considered the most sensitive method in the early stages of kidney disease. Since it allows you to evaluate the function of each kidney, the state of blood flow in the glomeruli, as well as the excretion of urine by the tubules.

A radiopharmaceutical is injected intravenously, which is filtered by the glomeruli and excreted from the body. The drug emits radiation, which is detected by special equipment.

For nephrosclerosis the special drug accumulates and is excreted more slowly by the kidneys.

CT scan

To diagnose nephrosclerosis, CT and angiography are combined (administration of a contrast agent intravenously before examination). This allows you to evaluate the structure, structure and position of the kidney, as well as the condition and function of the kidney vessels.

For nephrosclerosis small arterial vessels are narrowed and deformed, the cortex is thinned, and the kidney itself may be reduced in size. There are changes in the vessels: narrowed and broken.

Kidney biopsy

Using a special needle inserted through the skin into the kidney, the doctor obtains a small area of ​​kidney tissue. Then he sends it for research.

Treatment of nephrosclerosis

Regarding the treatment of nephrosclerosis, drugs are prescribed comprehensively and for a long time (for years and months), courses of treatment are often repeated, but with short breaks between them.

Treatment of nephrosclerosis: hemodialysis and kidney transplantation

During hemodialysis The patient's blood is passed through a special membrane in an artificial kidney machine. Due to this, the body is cleansed of toxins and end products of metabolism, and the balance of water and salts is normalized.
The frequency of the procedure depends on the degree of renal dysfunction and the model of the device used.

A patient undergoing hemodialysis is prescribed medications to lower blood pressure, vitamins, potassium and other medications.

Kidney transplant - a radical method that allows patients to lead an active lifestyle. The donor organ is taken either from a corpse (subject to all conditions) or from a living donor (for example, a brother or sister - with their consent).

After a transplant, patients take special medications that suppress the activity of the immune system so that it does not reject the donor organ.

Is hospitalization necessary for nephrosclerosis?

However, if the condition worsens, there is a need treatment in a hospital setting:

• Increased loss of fluid (polyuria) and salts
• The acid-base balance in the body is disturbed (blood acidification) - when the pH is lower than 7.2
• Self-poisoning with metabolic products
• High urea and creatinine levels
• Increased bleeding
• Severe anemia (hemoglobin below 40-50 g/l)

Lost fluid is replenished with intravenous solutions solutions of glucose, isotonic sodium solution and others.

When salts are lost solutions for intravenous administration or oral preparations containing sodium and potassium are used.

To reduce creatinine and urea levels A glucose solution is administered as a drink or intravenously in combination with insulin.

Acid-base balance restored with sodium bicarbonate solution administered intravenously.

For the treatment of anemia red blood cells (the component of blood containing red blood cells - erythrocytes) are transfused.

In case of self-poisoning Solutions (glucose, rheopolyglucin and others) and hemodez are administered intravenously.

On a note

A patient undergoing hemodialysis must carry with him a card (memo) indicating the diagnosis and frequency of procedures, telephone numbers and address of the dialysis center. Because in emergency cases (poisoning, accident, loss of consciousness on the street), doctors must know which patient they are dealing with in order to create conditions for timely hemodialysis.

Nutrition for nephrosclerosis (diet)

Nephrosclerosis: diet and drinking regimen

Nutrition principles include creating conditions to reduce the load on the nephrons, but taking into account the stage of nephrosclerosis.

Protein restriction

Justified, since 100 grams of protein produces 30 grams of urea. Also, a protein-restricted diet encourages the body to reuse urea for protein synthesis.

In the absence of renal protein deficiency is practically unlimited.

However if chronic renal failure has developed, it should be limited. In the early stages of the disease, protein is limited to 50-60 grams per day, in the later stages - to 30-40. Moreover, 2/3 of the protein should be high-value: poultry, lean beef, egg whites, fish, dairy products. Whereas only 1/3 of the protein should come from potatoes, bread, cereals and other products containing protein. However, you should not overuse dairy products and fish, as they contain phosphorus.

Limiting salt intake

Justified, since sodium attracts water, increasing swelling. However Depending on the stage of chronic renal failure and symptoms, the approach is different:

• In the absence of edema and normal blood pressure numbers salt is not limited.
• In the initial stages of chronic renal failure salt is limited to 10-15 grams per day , in later- up to 3-7.

Maintaining potassium, calcium and phosphorus levels close to normal

Traditionally, lactic acid products are rich in calcium. However, in case of nephrosclerosis, they should be limited because they contain phosphorus. Whereas its level in the body is already increased in nephrosclerosis. Therefore, it is necessary to consume more other foods in which contains calcium: legumes (peas, beans), green vegetables, whole grain flour.

Products containing potassium are consumed if there is not enough potassium in the body (in the initial stages). Whereas if potassium is in excess (late stages), foods containing it are limited. Lots of potassium in raisins, dried apricots, bananas, chocolate, baked potatoes.

Ensuring you get enough calories and vitamins

Because if there are not enough calories, the body uses its own resources to work - its own proteins. Whereas, by breaking down, proteins increase the level of urea.

Therefore, the patient should receive food rich in carbohydrates, fats and vitamins: rice, potatoes, sweets, fresh vegetables and fruits, butter and vegetable oil, honey.

However, the patient should plan his diet taking into account the underlying disease. For example, if you have diabetes, you should limit your carbohydrate intake.

Drinking regime

In the initial stages When there is no edema and blood pressure does not rise to high levels, water restriction is not required. Moreover, with sufficient water intake (2-2.5 liters per day), blood passes through the kidneys faster, creating conditions for better removal of toxins from the body.

In later stages(in the presence of edema and high blood pressure), the patient is recommended to take 500 ml of fluid more than he excreted in the previous day.

Consequences of nephrosclerosis

However, with an unfavorable course of the underlying disease, kidney function deteriorates, so a large number of nephrons die. As a result, chronic renal failure develops over time, and after several years the patient often needs hemodialysis or a kidney transplant.

Kidney nephrosclerosis is a pathological condition of the organ in which the standard type of tissue is completely replaced by connective tissue. The functional component of the new type does not allow the organ to perform its functions, since it is not intended for this. The morphology of renal tissue in this pathology changes diametrically. The circulatory system also suffers, which leads to shrinkage of the kidney and complete loss of its functions.

The prognosis for this disease is ambiguous, as it depends on the stage at which the pathology was diagnosed. Late detection and lack of proper therapy leads to the death of the patient. To understand what nephrosclerosis is, you need to look at the etiology of the disease.

Renal sclerosis is a pathology that does not occur as an independent disease, but is an associated pathology. Among the reasons that provoke the development of the disease are:

• Hypertension.
• Atherosclerotic lesions of blood vessels of the urinary system.
• Other pathological disorders of the blood supply to the kidneys.

Depending on the factors that led to the occurrence of pathology, several types of nephrosclerosis are distinguished.

The cause of nephrosclerosis is a violation of the blood supply to the kidneys, which leads to their dysfunction

Classification

Atherosclerotic vascular lesions and the presence of blood clots are the main causes of the formation of the first stage of the pathology: primary nephrosclerosis.

Primary nephrosclerosis

With this type of renal sclerosis, the trophic capabilities of the organ tissues are severely impaired. This causes ischemic conditions. And in the absence of proper medical care, they provoke a kidney infarction. The potential risk of this pathology is that if the blood supply is completely inhibited, the excretory system stops functioning. This entails a condition. Such complications are life-threatening for the patient.

The main consequence of primary nephrosclerosis is primary kidney shrinkage. This is typical for acute hypertension.

In turn, nephroangiosclerosis is divided into several types:

Atherosclerotic nephrosclerosis

A pathological condition that develops as a consequence of atherosclerotic disease affecting the arterial vessels and arterioles of the kidney. As a result, the lumen of the vessels is greatly narrowed or completely blocked. Degenerative conditions of the organ arise as a result of decreased permeability due to thickening of the arterial walls.

The early stage is asymptomatic, while a characteristic complication of renal sclerosis is ischemia, as a result of which changes occur on the surface of the organ and scars form. The prognosis for this type is positive, because not all kidney tissue is affected by destruction, continuing to perform its functions normally.

Shriveled kidney

Hypertensive nephrosclerosis

This type of pathology owes its name to the etiological factor that caused spastic conditions of the blood vessels. As with the previous form, pathogenesis includes ischemic damage to the organ, as well as the replacement of normal tissues with connective tissue.

In turn, the hypertensive type of pathology is divided into:

1. Arteriolosclerotic nephrosclerosis. This is a malignant disease.
2. Arteronecrotic nephrosclerosis. Benign course.

Involutive form

This form of renal sclerosis occurs in older patients. This is mainly due to calcium deposits on the walls of blood vessels. When the lumen narrows, the pathological condition develops according to the standard pattern.

Secondary nephrosclerosis

The development of this form of the disease is due not only to atherosclerosis, but is also a consequence of other pathologies. Various infectious and inflammatory processes in the kidney system lead to this disease.

Main reasons:

• in a chronic course.
• in a chronic course.
• Severe forms.
• Tuberculosis.
• Amyloidosis.
• Nephropathy in pregnant women.
• Consequences of injuries and surgical interventions.

Symptoms

In the first stages, the symptoms of renal sclerosis are practically absent. Diagnosis of pathology occurs after preventive testing or during the diagnosis of another disease. In the absence of measures taken, the pathology develops and with each subsequent stage of development the severity of symptoms increases.

With nephrosclerosis, the main clinical picture relates to functional disorders of the organ, which provides symptoms:

• Swelling of the face and lower extremities.
• Lumbalgia.
• Hypertension associated with headaches. The pain syndrome is practically not overcome by painkillers.
• Changes in the physical properties of urine, as well as the presence of various inclusions in it - flaky sediment, changes in color to reddish, turbidity.
• Nocturnal enuresis.
• A sharp decrease in diuresis.
• Dry mouth and thirst.
• Apathy, weakness, lack of appetite. Also, patients with nephrosclerosis experience an aversion to meat foods.
• Dermatological disorders.
• Losing weight.
• Tachycardia, shortness of breath.

Symptoms and manifestations of nephrosclerosis

Such symptoms in adults and children require immediate diagnosis.

Diagnostic procedures

If the first symptoms of pathology appear, then biochemical studies of blood, urine, and instrumental studies of the organs of the urinary system are carried out.

Since the risk of developing the disease increases in the presence of chronic pathologies, patients suffering from diabetes mellitus, hypertension, atherosclerosis, and pathological weight gain are recommended to undergo tests once a year and undergo a full functional diagnosis.

This includes:

• Blood analysis. General and biochemical. Particular attention is paid to creatinine clearance.
• Analysis of urine. The density of urine is important.
• Ultrasonography.
• X-ray procedures, including contrast ones.

Therapy

Treatment of nephrosclerosis is based on two principles. The first is drug therapy, the second is surgical intervention.

If high blood pressure is diagnosed, drugs are selected that reduce blood pressure at a general level. The approach to the selection of funds is individual. Therapy is prescribed only by the attending physician. The choice of medications is based on the characteristics of the patient’s body and the possibility of using combinations of drugs.

There are several main groups of drugs:

• ACE inhibitors.
• Angiotensin receptor blockers.

A fundamentally important point is the correct diet. Salt is completely excluded. In some cases, carbohydrates are contraindicated.

Timely diagnosed first stage of the disease implies a classical approach to treatment:

• Hormonal therapy. Prednisolone, methylprednisolone. Dosages are determined by the doctor based on the functionality of the kidney.
• Cytostatic agents.
• Drugs that improve the functional abilities of the urinary system.

If the main cause is atherosclerosis, then medications from the statin group are prescribed. This allows you to reduce cholesterol levels in the blood, which has a beneficial effect on the functioning of the cardiovascular system. It also helps stop nephrosclerosis.

If the disease is diagnosed at one of the last stages, when the patient is experiencing serious problems, then the following methods are indicated:

• Blood dialysis. An effective procedure that cleanses the blood of toxins that are not filtered by the kidneys due to illness. Usually up to five procedures are performed. Already by the third procedure the patient feels much better.
• Peritoneal dialysis. It is also an effective method that can be carried out even at home.
• Nephrectomy or transplantation. It includes a whole range of procedures for adaptation of a new organ in the patient’s body. Consequences of surgery include the possibility of rejection by the patient's immune system.

Knowing the dangers of nephrosclerosis, the patient must strictly follow the doctors’ instructions.

Treatment with folk remedies

Treatment of kidney nephrosclerosis with folk remedies includes a set of measures aimed at reducing cholesterol levels in the blood and improving the functional abilities of the kidneys. And also, additional to the main anti-inflammatory and antiseptic therapy of renal diseases with herbal medicines.

Ayurveda is an Indian herbal medicine that is very popular. The main drug that is often used by patients and prescribed by doctors is Cyston. Treatment with this remedy is long-term and ensures normalization of renal pressure, alleviation of inflammatory processes and increased diuresis.

• Birch buds.
• Lingonberry extracts.
• Mixtures of flax seeds, strawberry leaves, birch buds, nettle leaves, knotweed, horsetail.
• Licorice root infusion.

Pediatric pathology

A child cannot develop kidney nephrosclerosis without the presence of congenital diseases of the organ. This is due to the fact that pathology appears as a result of a large number of damaging factors, the accumulation of negative effects of which occurs over years. In a child's body this is impossible.

Preventive measures

Among the preventive measures are:

• Dietary recommendations. Doctors do not advise neglecting fruits and vegetables. It is also not recommended to abuse meat.
• Body weight control.
• Maintaining proper water regime.
• Playing sports and giving up bad habits.
• Exclusion of self-medication.
• Periodic diagnostic procedures.
• No poisoning or intoxication by chemicals.

Conclusion

What is renal nephrosclerosis? This is the outcome of diseases that can be successfully treated in the early stages, thereby excluding the development of such a life-threatening pathology. Most patients, unfortunately, do not pay attention to the first symptoms, allowing the disease to develop slowly. Only timely access to a doctor and correct diagnosis gives a person a chance to live a full life.

This is a pathological condition caused by the death of nephrons, their replacement by connective tissue with an increase in renal failure. It manifests itself as polyuria, nocturia, hypertension, swelling, discomfort in the lower back, and in the later stages - oliguria, hematuria, intoxication. Diagnosed using laboratory tests, ultrasound, CT, MSCT of the kidneys, nephroscintigraphy, angiography of the renal vessels, urography, biopsy. For treatment, etiopathogenetic therapy of the underlying disease, anticoagulants, antiplatelet agents, antianemic, detoxification, vitamin and mineral agents, replacement therapy, and kidney allotransplantation are used.

General information

Nephrosclerosis is a secondary clinical and anatomical condition, manifested by compaction, wrinkling of the kidneys and a decrease in their functional capacity due to the replacement of parenchyma with fibers and interstitial substance of connective tissue. The shriveled kidney was first described in 1914 by the German clinician F. Volhard and pathologist K.T. Farom.

Typically, nephrosclerosis complicates the course of urological and other somatic pathologies. In the twentieth century, its leading cause was considered to be glomerulonephritis, currently - arterial hypertension and diabetes mellitus (more than 60% of all diagnosed cases). The prevalence of nephrosclerosis in European countries is 0.06%. At the same time, 10-20% of patients require regular hemodialysis, and mortality from chronic renal failure reaches 22%.

Causes of nephrosclerosis

Kidney shrinkage is a polyetiological process that complicates various vascular disorders and urological diseases. Depending on the type of nephrosclerosis, experts in the field of urology and nephrology identify two groups of causes that cause primary or secondary replacement of the renal parenchyma with fibrous structural elements of connective tissue. A primarily wrinkled kidney is formed against the background of damage to the renal vessels caused by diseases such as:

• Arterial hypertension. In patients with essential hypertension and symptomatic hypertensive conditions, the renal vessels persistently spasm and narrow, and the nutrition of the parenchyma is disrupted. Connective tissue compaction of the vascular wall or death of arterioles and glomerular capillaries ends, respectively, with the formation of slowly progressive arteriosclerotic nephrosclerosis or malignant arteriolenecrotic glomerulosclerosis of Farah.
• Atherosclerosis of the renal arteries. The deposition of atherosclerotic plaques on the inner lining makes the vascular wall less elastic and narrows the lumen of the vessels feeding the renal parenchyma. A decrease in tissue perfusion provokes the destruction of nephrons and tissue hypoxia, which promotes excessive formation of connective tissue. As a result, as a result of atherosclerosis, the cortical substance becomes thinner, the cells of the urinary tubules atrophy, which reduces the functional capacity of the kidney.
• Chronic venous congestion. Against the background of stagnation caused by nephroptosis, narrowing or chronic thrombosis of the renal veins, parenchymal vessels dilate paretically, the flow of oxygenated arterial blood decreases, and ischemia increases in the tissues. The situation is aggravated by compaction of the vascular walls, which further disrupts tissue metabolism. Under hypoxic conditions, partial cell death occurs, and nephrosclerosis occurs within 10-15 years.

In some patients, angiogenic renal destruction occurs acutely with partial or complete thromboembolism of the renal artery. A sharp disruption of blood circulation causes a kidney infarction - massive death of nephrons as a result of acute ischemia. Subsequently, the necrotic area is gradually replaced by connective tissue, and nephrosclerosis develops.

A secondarily wrinkled kidney is spoken of in cases where the patient initially suffers from a urological disease, in which the renal parenchyma is destroyed under the influence of infectious agents, autoimmune complexes, mechanical factors (stretching, trauma by stones), etc. The main causes of secondary (nephrogenic) nephrosclerosis are:

• Kidney diseases. Hardening of the parenchyma can result in pyelonephritis, kidney tuberculosis, glomerulonephritis, urolithiasis, and polycystic disease. A separate group of causes of nephrosclerosis consists of secondary nephropathies, which complicate the course of other pathological processes - diabetes mellitus, systemic lupus erythematosus, malignant neoplasia, preeclampsia.
• Diseases of the lower urinary tract. Nephrosclerosis can develop against the background of hydronephrosis, caused by obstructive stagnation of urine during sclerosis of the bladder neck, the formation of uretero-vaginal fistulas, and compression by pelvic tumors. Atrophic processes are observed in 30-60% of patients suffering from vesicoureteral reflux.

Pathogenesis

Despite the variety of causes that cause nephrosclerosis, the mechanism of development of the disease as a whole is common. Initially, under the influence of various damaging factors (hypoxia, inflammatory and dystrophic processes caused by pathogenic factors of microorganisms, autoimmune complexes, direct traumatic effects, etc.), destruction of the glomerular and tubular epithelium occurs with the exclusion of some nephrons from the general blood supply.

Since kidney cells are not capable of regeneration, after phagocytosis of destroyed cellular elements, nephrosclerosis begins - the damaged area is replaced by connective fibers, and the kidneys themselves become denser. In the remaining glomeruli, blood circulation and filtration increase, resulting in an increase in the volume of urine excreted and a decrease in its relative density. Against the background of blood flow disturbances, the synthesis of renin, which regulates glomerular filtration, increases, which contributes to the occurrence or worsening of arterial hypertension.

Due to the high compensatory capabilities of the renal tissue, clinical signs of renal failure appear only with severe nephrosclerosis with the loss of 70% of the nephrons of both kidneys or 85% of one. When 5% of cells or less are retained, functional failure of the organ occurs, requiring replacement therapy.

Symptoms of nephrosclerosis

The clinical picture of the disease at an early stage is characterized by an increase in the amount of daily urine (more than 2 liters), increased frequency of urination at night (more than 3 times per night), constant nagging pain in the lumbar region, and an increase in blood pressure. As nephrosclerosis progresses, swelling appears: first on the face, then it spreads evenly throughout the body. Swelling is most pronounced in the morning.

At a later stage, the symptoms worsen: the volume of daily urine decreases to 0.5–0.8 l, an admixture of blood may appear in the urine, the patient is bothered by dry mouth and constant thirst. General symptoms of intoxication arise and increase: headache, nausea and vomiting, weakness, muscle pain.

Complications

Serious disturbances in the processes of filtration and reabsorption, which occur with the destruction of more than 70-75% of the initial number of nephrons, lead to the formation of chronic renal failure. Because the shriveled kidney stops producing erythropoietin, which is necessary for the maturation of red blood cells in the bone marrow, iron deficiency anemia often develops. Patients with nephrosclerosis have an increased risk of nephrogenic arterial hypertension due to excess renin production. When vitamin D metabolism is disrupted, osteoporosis occurs with increased bone fragility and a tendency to form pathological fractures.

Diagnostics

Patients with suspected nephrosclerosis are prescribed a comprehensive examination to determine the features of the morphological structure of the kidneys, identify signs of parenchymal atrophy, and assess the functional viability of the organ. The most informative laboratory and instrumental methods for diagnosing a wrinkled kidney are:

• General urine analysis. For nephrosclerosis, a significant decrease in the relative density of urine (up to 1.005-1.015 g/l) is indicative. With increasing signs of chronic renal failure, erythrocyturia (up to 2-3 red blood cells in the field of view), cylindruria, proteinuria (up to 0.033 g/l) are possible.
• General blood analysis. In patients with a shriveled kidney, the content of hemoglobin and red blood cells decreases, moderate thrombocytopenia, and an increase in the duration of bleeding and blood clotting time are noted. Slight leukocytosis often occurs.
• Blood biochemistry. Assessment of functional capacity using biochemical parameters reveals renal failure. With nephrosclerosis, the content of uric acid, creatinine, urea, magnesium, phosphorus, and sodium may be increased. The level of protein and potassium decreases.
• Sonography. Characteristic echographic signs of nephrosclerosis are a decrease in the size of the affected organ, thinning of the parenchyma, atrophy of the cortex, and its unclear differentiation with the medulla. Often, kidney ultrasound reveals nephrocalcinosis.
• X-ray methods. With survey and excretory urography, the size of the kidneys and the cortical layer are reduced, and calcifications are detected in the parenchyma. Impaired filling of the pyelocaliceal system with a contrast agent may indicate the development of chronic renal failure.
• Angiography. On renal angiograms, the arteries are usually narrowed and deformed. In some patients, the fine arterial pattern may be absent (the “burnt wood” symptom). The cortex is thinned. Irregularity of the outer contour of the kidneys is typical.
• Dynamic nephroscintigraphy. When the kidney shrinks, it accumulates and excretes nephrotropic radionuclide more slowly. The study is complemented by static nephroscintigraphy, which reveals parenchymal defects by the uneven distribution of the radiopharmaceutical.
• Renal tomography. Three-dimensional models and layer-by-layer images obtained during CT and MSCT reveal thinning of the cortical layer and a decrease in the size of the organ. Signs of nephrosclerosis are narrowing and deformation of small arterial vessels.
• Needle biopsy of the kidneys. Histological analysis of a kidney biopsy reveals a significant decrease in the number of nephrons and a large number of connective tissue fibers. During the study, the condition of arterioles and capillaries is assessed.

Differential diagnosis of nephrosclerosis is carried out with diabetes mellitus and diabetes insipidus, acute renal failure, rapidly progressive glomerulonephritis, hepatorenal syndrome, hypochloremic azotemia. If necessary, the patient, in addition to a nephrologist and urologist, is consulted by a therapist, cardiologist, phthisiatrician, rheumatologist, endocrinologist, oncologist, and oncohematologist.

Treatment of nephrosclerosis

Conservative therapy for the initial stages of kidney shrinkage is aimed at correcting the underlying disease that provoked the sclerotic process and increasing renal failure. Taking into account the pathology that caused nephrosclerosis, the patient is prescribed antibiotics, antihypertensive drugs, statins, glucocorticosteroids, antiglycemic, diuretic, non-steroidal anti-inflammatory and other etiopathogenetic drugs. To relieve disorders caused by functional renal failure, the following can be used:

• Anticoagulants and antiplatelet agents. By influencing the rheological properties of blood, they improve blood flow in the renal arterioles and capillaries and, by restoring tissue perfusion, they slow down nephrosclerosis. Prescribed with caution when chronic renal failure increases.
• Vitamin and mineral complexes. To correct changes in the biochemical composition of the blood caused by impaired filtration, potassium, calcium, vitamin D, multivitamin formulations, and bisphosphonates are used. Taking them improves metabolism and prevents osteoporosis.
• Antianemic drugs. If anemia is detected, erythropoietin preparations are prescribed, which stimulate the formation of red blood cells, and iron, necessary for the synthesis of hemoglobin. Reducing hemic hypoxia makes it possible to slow down sclerotic processes in the kidney tissues.
• Detoxification therapy. To speed up the elimination of toxic metabolites that accumulate in the body during nephrosclerosis, enterosorbents are used, which bind metabolic products in the intestine. Herbal remedies based on artichoke can be prescribed to reduce urea levels.

If kidney shrinkage is combined with stage III-IV chronic renal failure, renal replacement therapy is indicated - peritoneal dialysis, hemodialysis, hemodiafiltration, hemofiltration. A radical treatment method recommended for nephrosclerosis with a decrease in the number of viable nephrons to 5% or less is kidney transplantation after abdominal or laparoscopic nephrectomy.

Prognosis and prevention

With timely detection of the disease, the prognosis is relatively favorable; the appointment of adequate therapy allows one to achieve a long-term state of compensation for nephrosclerosis. Over time, nephron function deteriorates and chronic renal failure develops: such patients require an organ transplant or regular hemodialysis.

To prevent nephrosclerosis, it is necessary to follow the recommendations of a specialist in the treatment of nephrological diseases (especially of an inflammatory nature), monitor the level of blood pressure, blood glucose, avoid hypothermia, and do not abuse salt and meat foods. An important role in preventing the development of a wrinkled kidney is played by regular visits to a family doctor for early detection and correction of somatic pathology.