Terminal stage chronic renal failure is a stage of development of chronic renal failure, in which the disease enters the final stage and threatens human life and health.

If you do not urgently begin medical procedures or do not perform surgery on the patient, then no doctor will be able to say exactly how long he will live.

General information about chronic renal failure

Chronic renal failure is not a disease, but a condition that develops against the background of a long and uncompensated course of another, serious disease.

We can talk about both kidney diseases and other diseases that occur with damage to large vessels ().

The pathological process introduces changes into the functioning of the body; against the background of these changes, changes in the functioning of organs gradually (not abruptly, as in the acute stage of chronic renal failure) develop.

The performance of the kidneys decreases, their filtration function is impaired.

The peculiarity of chronic renal failure is that it can occur over a long period of time without pronounced symptoms.

Only with a long and uncompensated course of chronic renal failure is it dangerous for human life and health. But if you start treating pathological processes in a timely manner, you can get rid of chronic renal failure (partially or completely).

Kidney failure has several stages of development:

• compensated;
• intermittent;
• terminal.

The terminal stage, in turn, is divided into several additional stages of the flow.

Terminal stage

It all starts with a disruption of the filtration process, the outflow of urine gradually decreases, against the background of which the patient develops specific symptoms.

The human body is gradually “poisoned” by decay products; the kidneys cannot remove them in full. After a certain period of time it decreases significantly.

Liquid rich in toxins and harmful substances accumulates in the body, it enters other vital organs (lungs, heart, brain), causing irreversible changes in the body.

Carrying out medical procedures, as well as, only to a small extent compensate for the patient’s condition; only the situation can be completely corrected.

But it is carried out if the terminal stage is in the initial stages of development; in the final stages, when organs are damaged, transplantation is pointless.

Monitoring glomerular filtration will help determine that chronic renal failure has entered the terminal stage. If the indicator remains within 14-10 ml/min, then it is said that chronic renal failure has entered the terminal stage.

At this stage (while diuresis is maintained), the patient can still be helped. But further development of chronic renal failure is fraught with irreversible changes leading to death.

Causes of occurrence

There are several causes of end-stage chronic renal failure. All of them are chronic diseases that occur without appropriate drug correction.

Most often, the condition develops against the background of a long course of the following diseases:

• hypertension (with development);
• diabetes;
• autoimmune diseases of various kinds (vasculitis, systemic lupus erythematosus);
• some heart diseases (with the development of uncompensated heart failure).

Pathologies leading to the development of cardiopulmonary or renal failure can lead to the development of chronic renal failure in the terminal stage.

Endocrine diseases of various types can cause chronic renal failure, as well as some kidney diseases with a long course, heart disease and, in rare cases, gastrointestinal tract diseases.

Autoimmune diseases, provided that they occur with damage to the antibodies of the kidney tissue (directly the glomeruli), thereby reducing the filtration functions of the organs.

Stages of development

Nominally, the condition is divided into 4 main stages of the course (according to the severity of symptoms):

1. At the initial stage of development, a decrease is observed. In this case, diuresis is present, the excretory function has minor disturbances, and a person produces more than 1 liter of urine per day.
2. II and at this stage the amount of outgoing urine decreases (up to 500 ml), poisoning with decay products is observed, and the first changes in the functioning of the lungs and heart occur. But these changes are reversible.
3. II b – the severity of symptoms increases, characteristic signs of heart failure with damage to the lungs and liver appear. Liquid is excreted poorly and gradually occurs (complete absence of urination).
4. III – the final stage of the terminal stage. The patient develops characteristic signs of severe (with high intoxication). A decompensated degree of heart failure occurs. A person in this state is doomed, even carrying out the necessary medical procedures or connecting to dialysis will not be able to improve his condition. The procedures will only help save life.

Manifestation of the clinical picture

There are several characteristic signs, not all of them occur specifically during the terminal stage and are often superimposed on the symptoms of the underlying disease that led to the development of chronic renal failure.

Main features:

• significant reduction in the volume of urine output;
• disturbances in the functioning of vital organs;
• a significant increase in blood pressure levels;
• nausea, vomiting, general weakness;
• change in complexion, swelling;
• characteristic pain in the lumbar region.

The first thing you should pay attention to is a decrease in the volume of urine output. Fluid in the required volume is not removed from the body. Later, other signs that are more noticeable to others appear.

The person refuses to eat and suffers from prolonged diarrhea or vomiting. He is unable to take food, against the background of which severe exhaustion gradually develops.

Even if weight loss is not noticeable due to severe swelling, then when fluid gets into the lungs, swelling occurs and a painful, severe cough begins with or without sputum discharge.

Then the complexion changes, it becomes yellow, the person’s lips turn blue, and he falls into a semi-conscious state. This indicates the presence of encephalopathy (brain damage by decay products).

In this case, it is difficult to help the patient; he must be immediately hospitalized, since treatment of chronic renal failure is carried out only in a hospital setting.

Course of the disease

At the initial stage, only a decrease in the amount of urine excreted (diuresis) is observed. Pain in the lumbar region and swelling may be bothersome. There are no other pathological signs, since the glomerular filtration rate is reduced, but the kidneys are still functioning.

At stage 2, other signs of chronic renal failure appear, nausea occurs, and urine is excreted in the amount of 500 ml.

At stage 3, the fluid does not leave, diuresis stops. The kidneys completely fail, and acute renal failure develops.

Methods of therapy

Treatment of end-stage chronic renal failure comes down to dialysis using various methods and transplantation. Drug therapy is carried out, but its effectiveness is extremely low.

Conservative methods

The use of various drugs that improve kidney function accelerates the filtration capacity of organs.

But the use of medications cannot fully compensate for the patient’s condition. For this reason, dialysis is so important.

Most often, detoxification solutions are prescribed, which help remove toxins and harmful substances from the body.

Carrying out dialysis

It is carried out in 2 ways in order to save the patient’s life and avoid the development of severe complications.

Perinatal dialysis is carried out through the abdominal wall, with the introduction of a catheter and solutions to cleanse the body of harmful waste products. The solution is administered through a catheter, after some time it is withdrawn, along with it all toxic substances are removed from the body.

Hardware dialysis is a more complex but effective procedure performed in a hospital setting. Hardware dialysis lasts 5–6 hours, and allows you to do without medication for a long period of time. The procedure is carried out 2-3 times a month.

Organ transplantation

The operation is permissible only if chronic renal failure is at stage 1 or 2 of development. The procedure requires the presence of an organ (close relatives can act as such: brother, sister, parents, etc.).

If none of the relatives can act as a donor, then the patient is placed on the waiting list.

A donor organ can be obtained from a recently deceased person. But the waiting list for a transplant is very long and you will have to wait for more than one year for a kidney.

After surgery, additional therapy is carried out, it is aimed at reducing the risk of rejection.

Possible complications

A complication of chronic renal failure in the terminal stage can be considered the occurrence of:

• pathological changes in internal organs;
• development of encephalopathy;
• pulmonary and cerebral edema;
• development of severe heart failure.

The occurrence of complications directly indicates that pathological changes have occurred in a person’s body, which cannot be corrected with the help of medications.

Prognosis and life expectancy

It is difficult to predict exactly how long a person who has been diagnosed with this will live. According to some doctors, the average life expectancy depends on how quickly the patient received help and whether pathological changes in the body were diagnosed.

If we take the average, if medical procedures are carried out in a timely manner, it ranges from 10 to 15 years.

If the patient was admitted to a medical institution when pathological changes occurred in his body, and the terminal stage entered the final stage of development, then the prognosis is unfavorable.

Even with the necessary manipulations, it is possible to save a person’s life, but only for a while. Such a patient will no longer be able to fully recover and return to life.

Preventive measures

As part of preventive procedures, it is recommended to treat diseases of the endocrine system and cardiovascular system. Compensate for existing renal failure with medications and dialysis.

When treating kidney diseases: pyelonephritis, glomerular nephritis, pay attention to the effectiveness of therapy.

The terminal stage of chronic renal failure is the final stage of the development of the disease, at this stage it is important to provide timely assistance to the patient, and not to bring the condition to a pathologically dangerous level. If complications cannot be avoided, the likelihood of death is extremely high.

Currently in foreign literature instead of the term chronic renal failure, considered outdated and characterizing only the fact of irreversible impairment of renal function, the term is used “chronic kidney disease” with mandatory indication of stage. It should be especially emphasized that establishing the presence and stage of CKD in no case replaces making the main diagnosis.

Clinical picture

The course of chronic renal failure varies, but more often it grows slowly and gradually, with periods of exacerbations and remissions. CRF increases sharply with exacerbation of the underlying pathological process in the kidneys(for example, glomerulonephritis or pyelonephritis), and when an infection occurs(acute respiratory infections, flu, sore throat, pneumonia, furunculosis, etc.). This is important because timely treatment can improve kidney function. A sign of exacerbation of chronic renal failure is a decrease in diuresis, a significant increase in urea and creatinine levels, a violation of the acid-base balance of the blood and an increase in anemia. In the most severe cases of malignant subacute glomerulonephritis, end-stage chronic renal failure can develop within 6-8 weeks from the onset of the disease.

In the initial (latent) stage, there are few clinical manifestations; the body more or less copes with maintaining a constant internal environment. But then deviations begin to increase. At this stage, symptoms are determined by the underlying disease, often general weakness, fatigue, decreased ability to work.

SKIN

In the initial stage of chronic renal failure, the skin is usually pale, which is associated with anemia, because produced in the kidneys erythropoietin- a hormone that stimulates the formation of red blood cells. Subsequently, the skin becomes yellowish-bronze tint, and the urine gradually becomes discolored, which resembles a picture of jaundice. However, this change in skin color is associated with retention of urinary urochromes in organism. In the terminal stage of chronic renal failure, patients suffer from itching, and the skin becomes covered with a peculiar white “ uremic frost"made of white urea crystals. Let me remind you that normally it is excreted in the urine 20-35 g of urea per day.

“Uraemic frost” from urea crystals on the skin of a black man.

Due to severe itching and decreased immunity, pustular infections.

Itchy skin with chronic renal failure.

BONE SYSTEM

Due to disturbances in phosphorus-calcium metabolism, a lot of parathyroid hormone, which “leaches” calcium from the bones. Arises osteomalacia- bones become less strong, they hurt, and they often have pathological fractures(bones break from small efforts, which does not happen normally). With chronic renal failure the content also increases uric acid in the blood (hyperuricemia), which leads to the deposition of urates in tissues and periodic attacks of inflammation in the joints - gout.

NERVOUS SYSTEM

Initially, patients realize that they have severe kidney disease; arises reaction to illness, which goes through a number of stages, starting with denial. Patients are depressed, their mood often changes, and thoughts of suicide are possible. This reaction to the disease more often occurs in cancer patients, but for additional information I will give these stages here:

1. Negation or shock (“this can’t be happening”).
2. Anger and aggression(“why me”, “why me”).
3. « Bargain"(search for treatment methods, drugs).
4. Depression and alienation (“I don’t want anything,” “I don’t need anything,” “everything is indifferent”).
5. Acceptance of your illness and building a new life (rethinking your life).

Subsequently, as nitrogenous metabolic products accumulate in the blood, muscle twitching, sometimes painful cramps in the calf muscles. In the terminal stage of chronic renal failure, severe nerve damage is characteristic ( polyneuropathy) with pain and atrophy (decrease in volume) of muscles.

Polyneuropathy in chronic renal failure causes pain and muscle atrophy.

Since chronic renal failure usually occurs malignant arterial hypertension(increased and very stable blood pressure), then strokes often occur.

THE CARDIOVASCULAR SYSTEM

The kidneys regulate blood pressure levels. In case of chronic renal failure due to renal blood flow disorders And activation of the renin-angiotensinogen-aldosterone system The blood pressure level steadily rises to high numbers and at the same time is extremely difficult to drop. This can be regarded as a kind of diagnostic sign: if a non-renal patient's blood pressure has become much more difficult to lower than before, he needs to have his kidneys checked(at a minimum - take a urine test according to Nechiporenko).

There may be headache, dizziness, discomfort and pain in the heart, arrhythmias, shortness of breath up to pulmonary edema due to overload of the left ventricle. In the future, they have an adverse effect anemia and acidosis. May develop uremic myocarditis and pericarditis.

RESPIRATORY SYSTEM

As mentioned just above, “ nephrogenic pulmonary edema“due to the accumulation of fluid in the body and weak heart function. Due to the penetration of urea, it happens irritation of mucous membranes, which leads to laryngitis, tracheitis, bronchitis and pneumonia due to reduced immunity.

DIGESTIVE SYSTEM

Mucous membranes of the stomach and small intestine highly permeable to urea, which can hydrolyze to ammonia irritating and damaging them. There may be perversion of taste, nausea, vomiting, ammonia odor in the mouth, increased salivation, ulceration of the oral mucosa, and gastrointestinal bleeding. The most common infectious complications are stomatitis and mumps.

Laboratory indicators

BLOOD with uremia (end-stage chronic renal failure): increasing anemia(hemoglobin drops to 40-50 g/l and below), toxic leukocytosis up to 80-100? 10 9 /l with the formula shifted to the left. The platelet count is reduced ( thrombocytopenia), which is one of the causes of bleeding in uremia and further reduces hemoglobin levels.

URINE: in the initial period, changes are determined by the underlying disease. As chronic renal failure increases, these changes smooth out, and it becomes difficult to determine the primary disease by urine analysis. Found in urine protein, leukocytes, erythrocytes, cylinders.

In the initial stages of chronic renal failure Blood potassium levels are usually low due to polyuria (“forced diuresis”). Sodium levels are also reduced due to restriction of its consumption with food and especially in case of damage to the tubules (for example, with pyelonephritis). Definitely developing acidosis(acidification of the internal environment) due to a violation of the secretion of acids by the kidneys, the formation of ammonia in the tubular cells and increased secretion of bicarbonates. Acidosis manifests itself drowsiness, itchy skin and low body temperature.

Because the the active form of vitamin D is produced in the kidneys, chronic renal failure leads to severe calcium malabsorption in the intestines and to a decrease in calcium levels in the blood (hypocalcemia). Hypocalcemia may occur paresthesias(tingling sensation and goosebumps on the skin), muscle twitching and cramps. By a feedback mechanism, more parathyroid hormone enters the blood, which “washes” calcium from the bones. In the terminal stage of chronic renal failure, the level of magnesium in the blood increases (drowsiness, weakness) and phosphorus (due to the “dissolution” of bones by parathyroid hormone).

About treatment

First of all, it is necessary to treat the underlying disease that caused chronic renal failure. Without this, the rest of the treatment will be ineffective. Important avoid nephrotoxic drugs(for example, aminoglycoside antibiotics).

In diet limit the amount of protein up to 50-40 g (up to 25-18 g) of protein per day, which reduces the formation of nitrogenous metabolic products. The high calorie content of food (1800-3000 kcal/day) is provided by carbohydrates and fats. The consumption of meat and fish is completely prohibited; eggs, butter and vegetable oil, honey, vegetables and fruits are allowed. Such a diet with a complete set of essential amino acids allows reuse urea nitrogen for protein synthesis. In a hospital setting, patients with chronic renal failure are prescribed a diet 7a(according to Pevzner), in the terminal stage on hemodialysis - diet 7g.

In the initial stages of chronic renal failure they use anticoagulants(heparin) and antiplatelet agents(chimes, trental), which improve blood circulation in the kidneys. In the terminal stage, these drugs are contraindicated, because increase bleeding.

Necessarily reduce high blood pressure, although this is difficult to do - you have to prescribe antihypertensive drugs from different groups. Furosemide (Lasix) is used in high doses, and thiazide diuretics (hydrochlorothiazide) are ineffective for chronic renal failure.

Imbalance of potassium and sodium eliminated by diet, administration of panangin, glucose with insulin and potassium, as well as the intake of table salt. To combat anemia, the use of erythropoietin preparations is most effective.

Herbal preparations are used to reduce azotemia Lespenefril and Chophytol, which increase renal blood flow. May be assigned anabolic steroid, which enhance protein synthesis and reduce urea formation. Exists method of removing nitrogen metabolism products through the intestines with controlled diarrhea. For these purposes, a choice of magnesium sulfate, sorbitol (xylitol) or a special solution (NaCl, KCl, CaCl 2, Na 2 CO 3, mannitol) is used. However, there is a danger here dehydration and electrolyte (ion) imbalance, therefore it is safer to use hemodialysis. In the absence of arterial hypertension and heart failure, prescribe sauna with dry hot air, after which the general condition of many patients improves significantly.

For end-stage chronic renal failure, the so-called renal replacement therapy(PTA), which includes program hemodialysis, continuous peritoneal dialysis and kidney transplantation. The methods are complex and cannot be described here in a nutshell. The mortality rate among patients with end-stage chronic renal failure is 22% per year.

The conservative stage of chronic renal failure requires transfer of patients to disability group II, terminal - to group I.

References:

1. « A practical guide to nephrology» ed. A. S. Chizha, 2001.
2. « Problems of diagnosis and conservative therapy of chronic renal failure", magazine "Medical Council", No. 11-12 for 2010. http://medi.ru/doc/a240513.htm

Read also:

19 comments to the note “Chronic renal failure (CRF)”

Diabetes mellitus is not the main cause of chronic renal failure.

On the mentioned page medi.ru/doc/a240513.htm it is stated that " Diabetes mellitus is currently the leading cause of development terminal chronic renal failure in both developed and developing countries - it is a major disease in 20-40% patients starting renal replacement therapy for the first time".

They also write on the fence.
The main cause is essential and symptomatic arterial hypertension. And then diabetes.

The main cause is essential and symptomatic arterial hypertension. And then diabetes.

Is this very important? Therapy-resistant hypertension, as a rule, (except for tumors of the endocrine system, central nervous system damage, vascular stenosis) is a consequence of kidney damage.

It is important because both symptomatic and essential are treated effectively. And the presence of a large number of chronic renal failure patients in the country is a sign of its rapid marginalization and degradation.

This is no longer a question for medicine... but for the “country”

Important because both symptomatic and essential can be treated effectively

POORLY responsive to therapy, especially in patients with ESRF. I speak responsibly, because... I have something to do with this.

My mother has end-stage chronic renal failure, but she is not given group 1. Which law or other document states that the first group is included in the terminal stage? I can’t find a specific document on the Internet where this is clearly stated.

The first disability group is reserved for those patients who cannot care for themselves. If a patient with end-stage chronic renal failure regularly undergoes hemodialysis, then his condition is satisfactory and he is able to care for himself.

If a patient with terminal chronic renal failure for some reason lives without renal replacement therapy, then his condition worsens significantly, and he may well be classified as 1st group of disability.

If you do not agree with the decision of the medical and social examination bureau, you can appeal it:
invalid.ru/expert.htm#appeal

Group 1 is given to people who have irreversible changes in the body - terminal chronic renal failure - is such! And dialysis patients are potential for disability group 1 - definitely! It’s just that in this state “socially oriented policy” is aimed at eliminating the sick and old...

The 1st group of disability is given if the patient cannot care for himself and needs outside help. For regular dialysis, group 2 should be given.

It is precisely these doctors that my last words of comment relate to.

After all, it is those who sit on the commission who determine how you, the patient, live and how self-care is available to you! They don’t see when a patient from dialysis is dragged home and also to dialysis! And yet, dialysis is not available in all places - people go God knows where in this condition!

I wonder if they themselves have not tried to be in this shoes and “enjoy” their disability and just live on that handout that they called a pension from the state? Thank God, I came across a DOCTOR, a MAN! Former military doctor! — He knew for sure that he was in group 1 for life on dialysis!

And you, dear Emergency Doctor, don’t get sick! And remember that NO ONE is immune from such a disaster! Be merciful to the sick, and not to the state - all the same - they will steal!

I am not a member of the commission and I will not be able to get on it even if I wanted to, since they hire narrow specialists in certain specialties. I'm just trying to convey to patients how they will be viewed and what they can expect.

Disability is benefits, pension supplements (yes, small, but there are a lot of disabled people) and one of the indicators of health care performance, so the commission is forced to conduct strict screening.

I simply have no words for your comment, dear emergency doctor...

You try to explain to patients who are in difficult life situations about benefits, about the large number of disabled people, and so on... yes, your competence includes “taking care” of our budget... Continue, just leave this profession, please, don’t treat the sick thinking about money, and not about the end result of your profession...

Dear my “fellow soldiers” - patients of the hemodialysis department and after transplantation! Living in our country and still finding yourself in a situation of illness, all of you are potentially heroes! Please do not give up, fight for yourself, strive for adequate dialysis and obtain all necessary medications - the Constitution, Laws and the Convention on the Rights of Persons with Disabilities have not yet been repealed! Write to all authorities, to patient nephrology organizations - adequate therapy is the key to the safety of your body!

Those who are on dialysis - this is 1 g. disability! Know this! After transplantation, if you came to her with a group that is not lifelong, they give you both groups 2 and 3, so your doctors should write as clearly as possible in the extracts for the commission all life-threatening disorders of your health - in detail and truthfully with a recommendation about a high degree of the group! severe diseases of internal organs, with a progressive course, severe joint deformities, etc. etc.

Know that the country has had a budget surplus for a long time, the regional tax authorities are collecting huge amounts of money - and there will never be any for the population alone! And if you don’t declare yourself. contact the prosecutor's office, the press, etc. - they will simply “forget” about you, and this can only benefit our system - do not let yourself be destroyed!

Remember that you have loved ones who care about you!

I live in Belarus, money is tight here. We exist largely thanks to the help of Russia.

In the Russian Federation, the budget surplus is primarily due to high prices for exported oil. If it falls, as has happened before, the budget will immediately burst at the seams. And what should you do when you have to sharply cut social spending, as recently in Greece? Psychologically, it is much easier not to receive something at all than to receive it and then return it.

Whatever the reason for the surplus, sick people should not worry about this at all - they are citizens of the state! And if there are worthless managers in this state, they need to be changed, the sooner the better.

In Russia there is an immensely huge bureaucracy, corruption and fabulous salaries and benefits for officials! And what’s happening at the medical market is actually Yaroslavna’s crying! Even drugs under DLO are actually purchased above the commercial retail price, and are written off at an even higher price! And you think that patients should take something else into account... Hmm... yeah, no, it’s easier to put everything in its place at the place of residence and defend yourself once, the next time the officials will not want to mess with you. But this is my opinion and my experience - for example, my conscience will not allow me to “rob” my family, forcing me to spend additional money on what can be shaken out of this empty state.

Just because there is some money somewhere does not mean that it is in medicine. About 20 cents are allocated for food per patient per day, the same amount for medicines, and the doctor receives about 15 cents per day for one patient.

According to the clinical course, acute and chronic renal failure are distinguished.

Acute renal failure

Acute renal failure develops suddenly, as a consequence of acute (but most often reversible) damage to the kidney tissue, and is characterized by a sharp drop in the amount of urine excreted (oliguria) to its complete absence (anuria).

Causes of acute renal failure

Symptoms of acute renal failure

• small amounts of urine (oliguria);
• complete absence (anuria).

The patient's condition worsens, this is accompanied by nausea, vomiting, diarrhea, lack of appetite, swelling of the extremities occurs, and the liver increases in volume. The patient may be inhibited or, on the contrary, agitation may occur.

In the clinical course of acute renal failure, several stages are distinguished:

Stage I- initial (symptoms caused by the direct impact of the cause that caused acute renal failure), lasting from the moment of exposure to the main cause until the first symptoms of the kidneys have a different duration (from several hours to several days). Intoxication may appear (pallor, nausea,);

Stage II- oligoanuric (the main symptom is oliguria or complete anuria, also characterized by a severe general condition of the patient, the occurrence and rapid accumulation of urea and other end products of protein metabolism in the blood, causing self-poisoning of the body, manifested by lethargy, adynamia, drowsiness, diarrhea, arterial hypertension, tachycardia , body edema, anemia, and one of the characteristic signs is progressively increasing azotemia - an increased content of nitrogenous (protein) metabolic products in the blood and severe intoxication of the body);

Stage III- restorative:

• early diuresis phase - the clinic is the same as in stage II;
• the phase of polyuria (increased urine production) and restoration of the concentrating ability of the kidneys - renal functions are normalized, the functions of the respiratory and cardiovascular systems, the digestive canal, the support and movement apparatus, and the central nervous system are restored; the stage lasts about two weeks;

IV stage- recovery - anatomical and functional restoration of renal activity to initial parameters. It can take many months, sometimes it takes up to one year.

Chronic renal failure

Chronic renal failure is a gradual decline in kidney function until it disappears completely, caused by the gradual death of kidney tissue as a result of chronic kidney disease, the gradual replacement of kidney tissue with connective tissue and shrinkage of the kidney.

Chronic renal failure occurs in 200-500 out of every million people. Currently, the number of patients with chronic renal failure is increasing annually by 10-12%.

Causes of chronic renal failure

The causes of chronic renal failure can be various diseases that lead to damage to the renal glomeruli. This:

• kidney diseases: chronic glomerulonephritis, chronic pyelonephritis;
• metabolic diseases diabetes mellitus, gout, amyloidosis;
• congenital kidney diseases, polycystic disease, underdevelopment of the kidneys, congenital narrowing of the renal arteries;
• rheumatic diseases, scleroderma, hemorrhagic vasculitis;
• vascular diseases arterial hypertension, diseases leading to impaired renal blood flow;
• diseases leading to disruption of the outflow of urine from the kidneys: urolithiasis, hydronephrosis, tumors leading to gradual compression of the urinary tract.

The most common causes of chronic renal failure are chronic glomerulonephritis, chronic pyelonephritis, diabetes mellitus and congenital anomalies of kidney development.

Symptoms of chronic renal failure

There are four stages of chronic renal failure.

1. Latent stage. At this stage, the patient may not have any complaints, or fatigue during physical activity, weakness that appears in the evening, and dry mouth may occur. A biochemical blood test reveals slight disturbances in the electrolyte composition of the blood, sometimes protein in the urine.
2. Compensated stage. At this stage, the patients’ complaints are the same, but they occur more often. This is accompanied by an increase in urine output to 2.5 liters per day. Changes are detected in the biochemical parameters of blood and in.
3. Intermittent stage. Kidney function is further reduced. There is a persistent increase in the blood products of nitrogen metabolism (protein metabolism), an increase in the level of urea and creatinine. The patient experiences general weakness, fatigue, thirst, dry mouth, appetite decreases sharply, an unpleasant taste in the mouth is noted, nausea and vomiting appear. The skin acquires a yellowish tint, becomes dry and flabby. Muscles lose tone, small muscle twitching, tremors of fingers and hands are observed. Sometimes there is pain in the bones and joints. The patient may have a much more severe course of common respiratory diseases, sore throats, and pharyngitis.

   During this stage, periods of improvement and deterioration in the patient's condition may be expressed. Conservative (without surgical intervention) therapy makes it possible to regulate homeostasis, and the general condition of the patient often allows him to still work, but increased physical activity, mental stress, errors in diet, restriction of drinking, infection, surgery can lead to deterioration of kidney function and aggravation of symptoms.

4. Terminal (final) stage. This stage is characterized by emotional lability (apathy is replaced by excitement), disturbance of night sleep, daytime drowsiness, lethargy and inappropriate behavior. The face is puffy, gray-yellow in color, the skin is itchy, there are scratches on the skin, the hair is dull and brittle. Dystrophy increases, and hypothermia (low body temperature) is characteristic. No appetite. The voice is hoarse. There is an ammonia smell from the mouth. Aphthous stomatitis occurs. The tongue is coated, the abdomen is swollen, vomiting and regurgitation are often repeated. Often - diarrhea, foul-smelling, dark-colored stools. The filtration capacity of the kidneys drops to a minimum.

   The patient may feel satisfactory for several years, but at this stage the amount of urea, creatinine, and uric acid in the blood is constantly increased, and the electrolyte composition of the blood is disturbed. All this causes uremic intoxication or uremia (uremia urine in the blood). The amount of urine excreted per day decreases until it is completely absent. Other organs are affected. Cardiac muscle dystrophy, pericarditis, circulatory failure, and pulmonary edema occur. Disorders of the nervous system are manifested by symptoms of encephalopathy (sleep disturbances, memory, mood, and the occurrence of depressive states). The production of hormones is disrupted, changes occur in the blood coagulation system, and immunity is impaired. All these changes are irreversible. Nitrogenous waste products are excreted in sweat, and the patient constantly smells of urine.

Prevention of kidney failure

Prevention of acute renal failure comes down to preventing the causes that cause it.

Prevention of chronic renal failure comes down to the treatment of such chronic diseases as: pyelonephritis, glomerulonephritis, urolithiasis disease.

Forecast

With timely and correct application of adequate treatment methods, most patients with acute renal failure recover and return to normal life.

Acute renal failure is reversible: the kidneys, unlike most organs, are able to restore completely lost function. However, acute renal failure is an extremely serious complication of many diseases, often foreshadowing death.

However, in some patients, the decrease in glomerular filtration and the concentrating ability of the kidneys remains, and in some, renal failure takes a chronic course, with associated pyelonephritis playing an important role.

In advanced cases, death in acute renal failure most often occurs from uremic coma, hemodynamic disorders and sepsis.

Chronic kidney failure must be monitored and treated early in the disease, otherwise it can lead to complete loss of kidney function and require a kidney transplant.

What can you do?

The main task of the patient is to notice in time the changes that occur to him both in terms of his general well-being and in the amount of urine, and consult a doctor for help. Patients who have a confirmed diagnosis of pyelonephritis, glomerulonephritis, congenital kidney anomalies, or systemic disease should be regularly monitored by a nephrologist.

And, of course, you must strictly follow the doctor’s instructions.

What can a doctor do?

The doctor will first determine the cause of kidney failure and the stage of the disease. After which all necessary measures will be taken to treat and care for the patient.

Treatment of acute renal failure is aimed primarily at eliminating the cause that causes this condition. Measures are applicable to combat shock, dehydration, hemolysis, intoxication, etc. Patients with acute renal failure are transferred to the intensive care unit, where they receive the necessary assistance.

Treatment of chronic renal failure is inseparable from treatment of the kidney disease that led to kidney failure.

Modern methods of treating chronic renal failure
Modern methods of treating chronic renal failure

CHRONIC RENAL FAILURE

Until recently, chronic renal failure (CRF) was defined as a clinical and biochemical syndrome that occurs with kidney damage of any etiology, caused by a gradually progressive loss of excretory and endocrine functions of the organ due to the irreversible loss of functioning nephrons.
In this case, unlike acute renal failure, the pathophysiological processes are irreversible, which lead to these disorders. Their development only partially depends on the etiology of the underlying renal disease, since the leading pathogenetic mechanisms of damage to functioning nephrons in this situation are intraglomerular hypertension, hyperfiltration in the glomerulus and the nephrotoxic effect of proteinuria (more precisely, disorders of renal protein transport).
The discovery of the unity of the mechanisms of pathogenesis of kidney tissue damage in chronic diseases of this organ was one of the important factors that led to the creation of a fundamentally new concept - chronic kidney disease (CKD).
Reasons for the emergence of the concept of CKD.
Currently, there is a dramatic increase in the number of patients with chronic renal pathology.
This is primarily determined by the increase in the incidence of diabetes mellitus, the aging of the population and, accordingly, the increase in the number of patients with kidney damage of a vascular nature.

The progressive increase in the number of such patients is regarded as a pandemic. The above factors have led to a catastrophic increase in the number of people who require renal replacement therapy (RRT) - various types of dialysis or kidney transplantation.
The long-standing approach to secondary prevention of end-stage renal disease (ESRD) has also contributed to the increase in the number of patients on RRT.

When a certain degree of decline in renal function was achieved, it was not considered necessary to resort to any special methods to slow the progression of the pathological process in the renal tissue.
In addition, over the past decades, the quality of RRT technologies has continuously improved, which has caused a sharp increase in life expectancy for patients receiving such treatments.

All this has led to an increased need for dialysis beds, organ transplants and rising costs.
Already in the sixties of the last century, it became clear that many mechanisms of progression of chronic kidney diseases are quite universal and largely operate regardless of etiology. Equally important was the identification of risk factors for the development and progression of a chronic pathological process in renal tissue.
Like the mechanisms of progression, they turned out to be basically the same in various chronic kidney diseases and quite similar to cardiovascular risk factors.

Clarification of the pathogenetic mechanisms of progression of chronic kidney diseases, identification of risk factors for their occurrence and development has made it possible to develop well-founded treatment regimens that can actually delay the onset of RRT or reduce the number of lethal complications.
Approaches to renoprotection for different kidney diseases turned out to be basically identical (angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor antagonists, non-dihydropyridine calcium channel blockers, low-protein diet).
All of the above required rethinking, primarily to develop effective measures to further improve medical and social care for patients with chronic kidney disease.
One of the prerequisites for this should be unity or at least similarity of criteria for identifying, describing, assessing the severity and rate of progression of renal pathology.
However, there was no such unity among nephrologists. For example, in the English-language literature one could find about one and a half dozen terms used to designate conditions associated with the appearance of chronic renal dysfunction.

It should be noted that in domestic nephrology the terminological problem was less acute. The phrase “chronic renal failure” (CRF) or, in appropriate cases, “end-stage renal failure”, “end-stage chronic renal failure”, etc. was usually used.
However, there was no common understanding of the criteria for chronic renal failure and assessment of its severity.

Obviously, the adoption of the concept of CKD should sharply limit the use of the term “chronic renal failure”.

In the NKF classification, the phrase “renal failure” remains only as a synonym for stage V. CKD.
At the same time, in the English-language nephrological literature, the name “end-stage renal disease” has become widespread.
NKF thought it would be appropriate to retain the term because it is widely used in the United States and refers to patients who are treated with various dialysis modalities or transplantation, regardless of their level of kidney function.
Apparently, in domestic nephrological practice it is worth preserving the concept of “end-stage renal failure”. It is advisable to include patients, both already receiving RRT, and patients with stage V CKD, for whom replacement treatment has not yet been started or for whom it is not carried out due to organizational problems.
Definition and classification of CKD.
A number of issues briefly mentioned above have been addressed by the National Kidney Foundation (NKF). The Foundation created a group of experts who, as a result of analyzing many publications on diagnostics and treatment, assessing the significance of a number of indicators in determining the rate of progression of kidney diseases, terminological concepts and agreements with administration representatives, proposed the concept of chronic kidney disease (CKD). ).

When developing the concept of CKD, the experts of the NKF working group pursued several goals: Definition of the concept of CKD and its stages, regardless of the cause (etiology) of renal failure (disease).
Selection of laboratory parameters (research methods) that adequately characterize the course of CKD.
Determination (study) of the relationship between the degree of renal dysfunction and complications of CKD.
Stratification of risk factors for the progression of CKD and the occurrence of cardiovascular diseases.

NKF experts proposed a definition of CKD, which is based on a number of criteria:
Kidney damage lasting > 3 months, which manifests itself as structural or functional impairment of the organ with or without a decrease in GFR.
These damages are manifested either by pathomorphological changes in the renal tissue, or by changes in the composition of the blood or urine, as well as changes when using methods of visualization of the structure of the kidneys GFR< 60 мл/мин/1,73 м2 в течение трех и более месяцев, при наличии или отсутствии других признаков повреждения почек.
In other words, chronic kidney disease can be defined as “the presence of kidney damage or decreased levels of kidney function for three months or more, regardless of diagnosis.”

NKF experts have identified five stages of CKD depending on the severity of the decrease in GFR

Let us again draw attention to a very important point.
In the classification, risk factors for the development and progression of CKD are highlighted in a separate line.
One of the most important among them is systemic arterial hypertension or proteinuria.
It should be borne in mind that, according to the conclusion of NKF experts, the presence of risk factors alone does not provide grounds for making a diagnosis of CKD, but requires a certain set of preventive measures).

The concept of CKD, which is not directly related to a nosological diagnosis, does not negate the nosological approach to the diagnosis of a specific kidney disease.
However, it is not a purely mechanical combination of chronic kidney damage of various natures.
As noted earlier, the development of this concept is based on the unity of the leading pathogenetic mechanisms of progression of the pathological process in renal tissue, the commonality of many risk factors for the development and progression of kidney diseases and the resulting similarity in methods of therapy, primary and secondary prevention.

In this sense, CKD is close to the concept of coronary heart disease (CHD).
The term CKD, as soon as it appeared, won citizenship rights not only in the United States, but also in many other countries.
The VI Congress of the Scientific Society of Nephrologists of Russia, held on November 14-17, 2005 in Moscow, clearly supported the need for widespread introduction of the concept of CKD into the practice of domestic healthcare.

General clinical manifestations of late stages of CKD.
Signs associated with the development of renal dysfunction and little dependent on the underlying pathological process in the kidneys usually begin to appear at the third stage of CKD and reach maximum severity by the fifth. At first, moderate polyuria, nocturia, decreased appetite, and a tendency to anemia are usually recorded.

A drop in GFR below 30% of the normal level leads to the appearance of symptoms of uremic intoxication, an increase in hyporegenerative anemia (due to a decrease in erythropoietin production), disturbances in phosphorus-calcium metabolism and the formation of symptoms of secondary hyperparathyroidism (due to a decrease in the intrarenal synthesis of the active metabolite of vitamin D-1, 25(OH)2D3; synonyms: 1,25-dihydroxy-cholecalciferol, calcitriol, D-hormone, etc.), metabolic acidosis (due to a decrease in renal excretion of hydrogen ions and suppression of bicarbonate ion reabsorption).

Compensation for metabolic acidosis is carried out by the lungs by increasing alveolar ventilation, which leads to the appearance of deep, noisy breathing. Secondary hyperparathyroidism, along with acidosis, leads to the development of osteodystrophy, which can manifest itself as pathological fractures. In addition, disturbances in calcium-phosphorus homeostasis often cause the appearance of extraosseous calcifications, including vascular calcification. Secondary hyperparathyroidism, skeletal damage, and soft tissue calcification are most severe in patients receiving RRT and represent a very serious clinical problem in these patients.
As CKD progresses, patients develop hemocoagulation disorders, which is accompanied by the slight formation of subcutaneous hematomas and an increased risk of bleeding, including gastrointestinal bleeding.

The skin is dry ("brights don't sweat"), and many patients experience painful itching, leading to scratching.
The initially present polyuria can be replaced by oliguria, leading to overhydration and swelling of the internal organs, including edema of the lungs and brain.
In the later stages of CKD, uremic polyserositis can develop, in particular uremic pericarditis, which is a poor prognostic sign and requires immediate initiation of RRT.

Sometimes the so-called "terminal nephrotic syndrome".
General cerebral symptoms gradually increase: lethargy, drowsiness, apathy, and sometimes sleep rhythm disturbances.
Almost all patients are characterized by uremic dyslipoproteinemia, leading to acceleration of atherogenesis processes and increased cardiovascular risks.

Diagnostics. Provided early detection of the underlying renal pathological process (GN, secondary nephropathies, diabetic nephropathy, etc.) and follow-up of the patient, diagnosis usually does not cause difficulties. To monitor renal function in practical work, the level of plasma creatinine and GFR are monitored over time.
Some diagnostic difficulties may arise when managing patients in whom azotemia is detected for the first time. In these cases, the issue of distinguishing between acute and chronic renal failure may become relevant.

Now a little mathematics, which, unfortunately, cannot be done without in this section.
The problem of estimating glomerular filtration rate in practical medicine. Glomerular ultrafiltration is the initial and main mechanism of urine formation.
The way the kidneys perform all their diverse functions depends decisively on its condition.
It is not surprising that members of the NKF working group chose glomerular filtration rate (GFR) not only as the main criterion for distinguishing specific stages of CKD, but also as one of the most important basis for making a diagnosis of chronic kidney disease. The developers of the National Kidney Foundation have convincingly shown that the degree of decline in GFR is very closely associated with other clinical or metabolic changes that occur as chronic nephropathies progress.

It is clear that the introduction of the concept of CKD requires the availability of a reliable, simple and inexpensive method of measuring GFR in clinical practice.

To date, a very large number of methods and their modifications have been developed that make it possible to estimate GFR with varying degrees of accuracy. However, their use in widespread clinical practice is limited by complexity and high cost.
Therefore, they are usually used for specific research purposes.

Throughout the world in practical medicine, the main estimates of GFR until recently remained the serum creatinine concentration (Cgr) or endogenous creatinine clearance (Ccreatinine clearance).
Both of these methods have a number of significant disadvantages. Serum creatinine concentration as an index of GFR.

Creatinine is a low molecular weight product of nitrogen metabolism.
It is mainly excreted by the kidneys by glomerular filtration, although some is secreted in the proximal tubules. In streets with unimpaired filtration capacity, the proportion of creatinine secreted by the tubules is small. However, the contribution of tubular secretion to the distortion of estimates of glomerular filtration rate may increase sharply with a decrease in renal function.

The process of creatinine formation in healthy people occurs at an almost constant rate.
This determines the relative stability of Cgr.
Despite the relative stability of creatinine production, there are a significant number of reasons, including those not directly related to the functional state of the kidneys, that can affect the level of Cgr. The main determinant of serum creatinine levels.
apparently, is the volume of muscle mass, since the production of this metabolite is proportional to this volume.
An important factor influencing serum creatinine levels is age.
GFR in adults declines progressively after age 40.
Decreased creatinine generation caused by age naturally increases GFR levels. Sgr in women is usually slightly lower than in men. The main significance in the appearance of these differences, apparently, is also associated with lower muscle mass in females.
Thus, clinical assessment of GFR based on serum creatinine levels cannot be carried out without taking into account the anthropometric, gender and age characteristics of the patient.

Under conditions of pathology, including kidney pathology, all factors that determine the level of serum creatinine can be modified to one degree or another.
The available information does not make it possible to come to a final conclusion about whether creatinine formation is increased, unchanged, or decreased in patients with chronic kidney disease.

However, when GFR decreases to 25-50 ml/min, patients usually spontaneously reduce protein intake (nausea, vomiting, anorexia).
Serum creatinine levels can be affected by various medications.
Some of them (amnoglycosides, cyclosporine A, platinum preparations, X-ray contrast agents, etc.) are nephrotoxic drugs, when prescribed, an increase in Cg reflects a real decrease in GFR.
Others are capable of undergoing the Jaffe reaction.
Finally, some drugs selectively block proximal tubular creatinine secretion without any significant effect on GFR.
Cimetidine, trimethoprim and, possibly, to some extent phenacetamide, salicylates and vitamin D3 derivatives have this property.

The determined value of creatinine concentration in blood serum depends quite significantly on the analytical methods used to measure this indicator. Until now, the level of creatinine in biological fluids is most often assessed using the Jaffe reaction.
The main disadvantage of this reaction is its low specificity.
This reaction can involve, for example, ketones and keto acids, ascorbic and uric acids, some proteins, bilirubin, etc. (“non-creatinine chromogens”). The same applies to some cephalosporins, diuretics, if they are prescribed in high doses, phenacetamide, acetohexamide and methyldopa (when administered parenterally). With normal serum creatinine values, the contribution of non-creatinine chromogens to its total concentration can range from 5 to 20%.

As kidney function declines, serum creatinine concentrations naturally rise.
But this increase is not accompanied by a proportional increase in the level of non-creatinine chromogens.
Therefore, their relative contribution to the concentration of total chromogen (creatinine) in the serum decreases and usually in this situation does not exceed 5%. In any case, it is clear that creatinine levels measured using the Jaffe reaction will underestimate the true GFR values.
Rapid changes in the latter parameter also lead to disruptions in the clarity of the inverse relationship between the concentration of serum creatinine and GFR.
In relation to them, the increase or decrease in Cgr may be delayed by several days.
Therefore, special care must be taken when using Cgr as a measure of renal function during the development and resolution of acute renal failure.
Use of creatinine clearance as a quantitative measure of GFR. The use of SSG compared to Sgr provides one significant advantage.
It allows you to obtain an estimate of the glomerular filtration rate, expressed as a numerical value with a dimension corresponding to the nature of the process (usually ml/min).

However, this method of assessing GFR does not resolve many issues.
Obviously, the accuracy of the measurement of CVg largely depends on the correctness of urine collection.
Unfortunately, in practice, the conditions for determining the volume of diuresis are often violated, which can lead to either an overestimation or an underestimation of Cg values.
There are also categories of patients in whom quantitative urine collection is almost impossible.
Finally, when assessing the value of GFR, the amount of tubular secretion of creatinine is of great importance.
As noted above, in healthy people the proportion of this compound secreted by the tubules is relatively small. However, under conditions of kidney pathology, the secretory activity of proximal tubular epithelial cells in relation to creatinine can increase sharply.

However, in a number of individuals, including those with a significant decrease in GFR, creatinine secretion may even have negative values. This suggests that they actually have tubular reabsorption of this metabolite.
Unfortunately, it is impossible to predict the contribution of tubular secretion/reabsorption of creatinine to the error in determining GFR based on CFR in a particular patient without measuring GFR using reference methods. “Calculation” methods for determining GFR.

The very fact of the presence of an inverse, although not direct, relationship between Cgr and GFR suggests the possibility of obtaining an estimate of the glomerular filtration rate in quantitative terms based only on the concentration of serum creatinine.

Many equations have been developed to predict GFR values ​​based on Cgr.
Nevertheless, in real practice of “adult” nephrology, the Cockcroft-Gault and MDRD formulas are most widely used.

Based on the results of the multicenter study MDRD (Modified of Diet in Renal Disease), a series of empirical formulas were developed that make it possible to predict GFR values ​​based on a number of simple indicators. The best agreement between the calculated GFR values ​​and the true values ​​of this parameter, measured by the clearance of 125I-iothalamate, was shown by the seventh version of the equations:

However, it should be borne in mind that there are situations where “calculated” methods for determining GFR are unacceptable.

In such cases, at least a standard creatinine clearance measurement should be used.
Situations in which it is necessary to use clearance methods for determining GFR: Very old age. Non-standard body sizes (patients with limb amputations). Severe emaciation and obesity. Diseases of skeletal muscles. Paraplegia and quadriplegia. Vegetarian diet. Rapid decline in kidney function.
Before prescribing nephrotoxic drugs.
When deciding whether to start renal replacement therapy.
It must also be remembered that the Cockcroft-Gault and MDRD formulas are not applicable in children.

Cases of acute deterioration of renal function in patients with pre-existing chronic kidney pathology, the so-called “acute on chronic renal failure”, or, in the terminology of foreign authors, “acute on chronic renal failure” deserve special attention.
From a practical point of view, it is important to emphasize that timely elimination or prevention of factors leading to acute impairment of kidney function in patients with CKD can slow the rate of progression of deterioration of organ function.

The causes of acute renal dysfunction in patients with CKD may be: dehydration (limited fluid intake, uncontrolled use of diuretics); CH; uncontrolled hypertension; the use of ACE inhibitors in patients with bilateral renal artery stenosis; obstruction and/or urinary tract infection; systemic infections (sepsis, bacterial endocarditis, etc.); nephrotoxic drugs: NSAIDs, antibiotics (aminoglycosides, rifampicin, etc.), thiazides, radiocontrast agents.
It should also be mentioned that patients with CKD are especially sensitive to any potentially nephrotoxic factors, and therefore the problems of iatrogenicity and self-medication (herbs, sauna, etc.) in these cases should be given special attention.

Another important indicator of the rate of progression of CKD is proteinuria.
In an outpatient setting, to assess it, it is recommended to calculate the protein/creatinine ratio in the morning urine, which is almost equivalent to measuring daily protein excretion.
An increase in daily proteinuria always means an acceleration in the rate of progression of CKD.

Treatment. Dietary recommendations.
The basic principles of the diet for CKD come down to the following recommendations:
1. Moderate limitation of NaCl consumption depending on the level of blood pressure, diuresis and fluid retention in the body.
2. The maximum possible fluid intake depending on diuresis, under the control of body weight.
3. Limiting protein intake (low-protein diet).
4. Limit foods rich in phosphorus and/or potassium.
5. Maintaining the energy value of the diet at the level of 35 kcal/kg body weight/day.
Taking into account the fact that as tubulointerstitial sclerosis develops, the ability of the kidneys to reabsorb Na may decrease, in some cases the salt regime must be expanded to 8 or even 10 g of salt per day. This is especially true for patients with the so-called “salt-losing kidney.”
In any situation, it is necessary to take into account the concomitant use of diuretics and their dose.
In a number of patients taking loop diuretics in large doses (over 80-100 mg/day of furosemide), restrictions on the consumption of table salt with food are not required.
The most adequate method of monitoring NaCl intake is daily urinary Na excretion.
A healthy person excretes at least 600 milliosmoles (mosm) of osmotically active substances (OAS) per day.
Intact kidneys are capable of significantly concentrating urine, and the total concentration of OAS (osmolality) in urine can be more than four times higher than the osmolality of blood plasma (1200 or more and 285-295 mOsm/kg H2O, respectively).
The kidneys cannot eliminate OAS (mainly urea and salts) without excreting water.
Therefore, a healthy individual is theoretically capable of excreting 600 mol in 0.5 liters of urine.

With the progression of CKD, the concentrating ability of the kidneys steadily decreases, the osmolality of urine approaches the osmolality of blood plasma and amounts to 300-400 mOsm/kg H20 (isosthenuria).

Since in the advanced stages of CKD the total excretion of OAV does not change, it is easy to calculate that to excrete the same 600 my OAV, the volume of diuresis should be 1.5-2 l/day.
This makes it clear that polyuria and nocturia appear; ultimately, limiting fluid intake in such patients accelerates the progression of CKD.

However, it should also be taken into account that with CKD stages III-V. The ability to excrete osmotically free water is gradually impaired, especially if the patient takes diuretics.
Therefore, fluid overload is fraught with the development of symptomatic hyponatremia.

Guided by the above principles, it is permissible to allow patients a free water regime, taking into account self-monitoring of daily diuresis, adjusted for extrarenal fluid losses (300-500 ml/day). Regular monitoring of body weight, blood pressure, clinical signs of overhydration, determination of daily Na excretion in urine and periodic testing of Na levels in the blood (hyponatremia!) are also necessary.

For many decades, in practical nephrology there has been a recommendation to limit the intake of proteins with food, which is based on a number of theoretical premises.
However, only recently has it been proven that a low protein diet (LPD) reduces the rate of progression of CKD.

Adaptive mechanisms of MBD in patients with CKD include: improvement of intraglomerular hemodynamics; limiting hypertrophy of the kidneys and glomeruli; positive effect on dyslipoproteinemia, effect on renal metabolism, limitation of O2 consumption by renal tissue; reduction in oxidant production; effects on T cell function; suppression of AN and transforming growth factor b, limiting the development of acidosis.
MBD is usually prescribed to patients starting from stage III. CKD.
At II st. A diet with a protein content of 0.8 g/kg body weight/day is advisable.

The standard MBD involves limiting protein intake to 0.6 g/kg/day.
In order to enrich the diet with essential amino acids, a low-protein diet can be prescribed with supplements.
Low protein diet options:
- standard MBD - protein 0.6 g/kg/day (again, regular food);
- MBD, supplemented with a mixture of essential amino acids and their keto analogues (preparation “Ketosteril”, Fresenius Kabi, Germany); food protein 0.4 g/kg/day + 0.2 g/kg/day ketosteril;
- MBD supplemented with soy proteins, protein 0.4 g/kg/day + 0.2 g/kg/day soy isolate, for example “Supro-760” (USA).

As mentioned above, when using MBD it is very important to maintain the normal energy value of the diet due to carbohydrates and fats at the level of 35 kcal/kg/day, since otherwise the body’s own proteins will be used as energy material.
In practical work, the issue of monitoring patient compliance with the MBD is essential.

The amount of protein consumed per day can be determined based on the concentration of urea in the urine and knowing the amount of daily diuresis using the modified Maroni formula:
PB = 6.25 x EMM + (0.031 x BMI) + *SP x 1.25
where PB is protein consumption, g/day,
EMM - urea excretion in urine, g/day,
BMI - ideal body weight (height, cm - 100),
*SP - daily proteinuria, g/day (this term is entered into the equation if SP exceeds 5.0 g/day).
In this case, the daily excretion of urea can be calculated based on the volume of daily urine and the concentration of urea in the urine, which in the practice of Russian clinical laboratory diagnostics is usually determined in mmol/l:
EMM = Uur x D/2.14
where Uur is the concentration of urea in daily urine, mmol/l;
D - daily diuresis, l.

Renoprotection.
In modern nephrology, the principle of renoprotection has clearly been formed, which consists in carrying out a set of therapeutic measures in patients with kidney disease, aimed at slowing the rate of progression of CKD.

The complex of treatment measures is carried out in three stages, depending on the degree of renal dysfunction:
Stage I - nitrogen excretion function of the kidneys is preserved (CKD stages I-II), a decrease in functional reserve may be noted (no increase in GFR by 20-30% in response to a protein load).
Stage II - kidney function is moderately reduced (CKD stage III).
Stage III - kidney function is significantly reduced (CKD stage IV - beginning of stage V CKD).

Stage 1:
1. Adequate therapy for the underlying renal disease in accordance with the principles of evidence-based medicine (evaluation indicator - reduction of daily proteinuria below 2 g/day).
2. In diabetes, intensive control of glycemia and the level of glycosylated hemoglobin (evaluation indicator - control of microalbuminuria).
3. Adequate control of blood pressure and proteinuria using ACE inhibitors, ATj receptor antagonists to AII, or a combination thereof.
4. Timely and adequate treatment of complications: heart failure, infections, urinary tract obstruction.
5. Exclusion of iatrogenic causes: medications, Rg-contrast studies, nephrotoxins.
6. Normalization of body weight with a mass index >27 kg/m2.
Successful pathogenetic therapy of the underlying renal disease is of paramount importance in preventing the formation of glomerulo- and tubulointerstitial sclerosis, and, consequently, in slowing the rate of progression of CKD.
In this case, we are talking not only about the treatment of newly diagnosed pathology, but also about the elimination of exacerbations.
The activity of the main inflammatory process (or its relapses) involves the activation of humoral and tissue immune reactions, naturally leading to the development of sclerosis.
In other words, the more pronounced the activity of the inflammatory process and the more often its exacerbations are noted, the faster sclerosis forms.
This statement is in full agreement with the traditional logic of the clinician and has been repeatedly confirmed by clinical studies.
In glomerular diseases, hypertension is usually formed long before the decline in renal function and contributes to their progression.
In parenchymal diseases, the tone of preglomerular arterioles is reduced and the system of their autonomous autoregulation is disrupted.
As a result, systemic hypertension leads to an increase in intraglomerular pressure and contributes to damage to the capillary bed.

When choosing antihypertensive drugs, it is necessary to proceed from the main three pathogenetic mechanisms of parenchymal renal hypertension; Na retention in the body with a tendency to hypervolemia; increased RAS activity; increased activity of the sympathetic nervous system due to increased afferent impulses from the affected kidney.

For any renal pathology, including diabetic nephropathy, if the creatinine level is normal and the GFR is more than 90 ml/min, it is necessary to achieve a blood pressure level of 130/85 mm Hg. Art.
If daily proteinuria exceeds 1 g/day, it is recommended to maintain blood pressure at 125/75 mm Hg. Art.
Considering modern data that nocturnal hypertension is the most unfavorable from the point of view of kidney damage, it is advisable to prescribe antihypertensive drugs taking into account the data of 24-hour blood pressure monitoring and, if necessary, transfer their use to the evening hours.

The main groups of antihypertensive drugs used for nephrogenic hypertension:
1. Diuretics (for GFR< 70мл/мин - преимущественно петлевые диуретики). 2. Ингибиторы АПФ и антагонисты АТ1 рецепторов к АII.
3. Non-dihydropyridine calcium channel blockers (diltiazem, verapamil).
4. Dihydropyridine CCBs are exclusively long-acting.
5. b-blockers.
Medicines are listed in descending order of recommended frequency of use.
Any antihypertensive therapy for parenchymal renal disease should begin with the normalization of Na metabolism in the body.
In kidney diseases, there is a tendency to Na retention, which is higher, the higher the proteinuria.
At least in experimental studies, the direct damaging effect of sodium contained in the diet on the glomeruli, regardless of blood pressure levels, has been proven.
In addition, sodium ions increase the sensitivity of smooth muscles to the action of AII.

The average dietary salt intake for a healthy person is approximately 15 g/day, so the first recommendation for patients with kidney disease is to limit salt intake to 3-5 g/day (an exception may be tubulointerstitial kidney damage - see above).
In an outpatient setting, a measure to monitor patient compliance with prescribed recommendations is to monitor urinary sodium excretion per day.
In cases where there is hypervolemia or the patient is not able to follow a hyposodium diet, diuretics are the first-line drugs.
If renal function is preserved (GFR > 90 ml/min), thiazides can be used; if GFR decreases< 70мл/мин назначаются петлевые диуретики (допустима комбинация петлевых диуретиков с тиазидами).
Potassium-sparing diuretics are absolutely contraindicated.

During treatment with diuretics, careful dose monitoring is necessary to prevent the development of hypovolemia. Otherwise, kidney function may acutely deteriorate - “ACF on chronic renal failure.”

Drug renoprotection.
Currently, many prospective placebo-controlled studies have proven the renoprotective effect of ACE inhibitors and AT1 receptor antagonists, which is associated with both hemodynamic and non-hemodynamic mechanisms of action of AN.

Strategy for using ACE inhibitors and/or AT1 antagonists for the purpose of nephroprotection:
- ACE inhibitors should be prescribed to all patients in the early stages of the development of any nephropathies with SPB > 0.5-1 g/day, regardless of blood pressure levels.
ACE inhibitors have renoprotective properties even at low plasma renin levels;
- the clinical predictor of the effectiveness of the renoprotective effect of drugs is partial (SPB< 2,5 г/сут) или полная (СПБ < 0,5 г/сут) ремиссия протеинурии через несколько недель или месяцев после начала приема медикаментов.
When treating with ACE inhibitors, a dose-dependence phenomenon is observed: the higher the dose, the more pronounced the antiproteinuric effect;
- ACE inhibitors and AT1 receptor antagonists have a renoprotective effect regardless of the systemic hypotensive effect.
However, if the blood pressure level does not reach the optimal level during their use, it is necessary to add antihypertensive drugs of other pharmacological groups. If you are overweight (body mass index > 27 kg/m2), it is necessary to achieve weight loss, which enhances the antiproteinuric effect of the drugs;
- if the antiproteinuric effect of any drug from one of the groups (ACE inhibitors or AT1 antagonists) is insufficient, a combination of them can be used.

The third-line drugs are non-dihydropyridine CCBs (diltiazem, verapamil). Their antiproteinuric and renoprotective effects have been proven in diabetic and non-diabetic nephropathies.
However, they can only be considered as an addition to basic therapy with ACE inhibitors or AT1 antagonists.

Less effective, from the point of view of nephroprotection, is the use of dihydropyridine CCBs.
This is associated with the ability of these drugs to dilate the glomerular afferent arterioles.
Therefore, even with a satisfactory systemic hypotensive effect, conditions are created that promote intraglomerular hypertension and, consequently, the progression of CKD.
In addition, short-acting dihydropyridine CCBs activate the sympathetic nervous system, which in itself has a damaging effect on the kidney.
The negative effect of non-extended dosage forms of nifedipine on the course of diabetic nephropathy has been proven.
Therefore, the use of this drug in DN is contraindicated.
On the other hand, in recent years, data have emerged indicating the effectiveness of the renoprotective properties of a combination of ACE inhibitors and long-acting dihydropyridine CCBs.

Today, b-blockers occupy the last place as renoprotective drugs.
However, in connection with recent experimental studies that have proven the role of activation of the sympathetic nervous system in the progression of chronic nephropathy, the view on the validity of their use in nephrogenic hypertension should be reconsidered.

Stage II(patient with any renal pathology and GFR 59-25 ml/min).
The treatment plan at this stage includes:
1. Dietary measures.
2. Use of loop diuretics to control hypertension and hypervolemia.
3. Antihypertensive therapy, taking into account possible side effects of ACE inhibitors. If the blood plasma creatinine level is 0.45-0.5 mmol/l, do not use ACE inhibitors in high doses.
4. Correction of phosphorus-calcium metabolism disorders.
5. Early correction of anemia using erythropoietin.
6. Correction of dyslipoproteinemia.
7. Correction of metabolic acidosis. When GFR decreases below 60 ml/min (CKD stage III), all drug therapy is carried out against the background of a low-protein diet.
In order to avoid the occurrence of hypo- or hypervolemia, a more strict regimen regarding sodium and fluid intake is necessary.
Only loop diuretics are used as diuretics. Sometimes their combination with thiazides is acceptable, but the use of thiazide diuretics alone is not recommended.
It is necessary to take into account the possibility of side effects from the use of ACE inhibitors with a GFR of 59-30 ml/min, namely: deterioration of renal excretory function, which is explained by a decrease in intraglomerular pressure; hyperkalemia, anemia.
At a plasma creatinine level of 0.45-0.5 mmol/l, ACE inhibitors are not first-line drugs and are used with caution.
A combination of long-acting dihydropyridine CCBs and loop diuretics is more preferable.
When GFR is below 60 ml/min, treatment for disorders of phosphorus-calcium metabolism, anemia, dyslipoproteinemia, and acidosis begins. A low-protein diet with limited dairy products helps reduce the total amount of inorganic calcium entering the body. In addition, in CKD, the adaptive capabilities of the intestine to increase calcium absorption are impaired (due to 1,25(OH)2D3 deficiency).
All these factors predispose patients to the development of hypocalcemia.
If a patient with CKD has hypocalcemia with a normal level of total blood plasma protein, it is recommended to use 1 g of pure kalysh per day exclusively in the form of calcium carbonate to correct the blood calcium level.
This type of therapy requires monitoring calcium levels in the blood and urine. Hyperphosphatemia in patients with chronic renal failure contributes to the occurrence of calcifications of soft tissues, blood vessels (aorta, aortic valve) and internal organs. It is usually recorded when GFR decreases below 30 ml/min.

A low-protein diet usually involves restricting the intake of dairy products, and therefore the intake of inorganic phosphorus into the patient’s body is reduced.
However, it should be taken into account that prolonged and significant restriction of protein intake can lead to negative protein catabolism and exhaustion.
In these cases, it is recommended to add complete proteins to the diet with the simultaneous administration of drugs that interfere with the absorption of phosphates in the intestine.

The most well-known and widely used in practice at present are calcium carbonate and calcium acetate, which form insoluble phosphate salts in the intestine.
The advantage of these drugs is the additional enrichment of the body with calcium, which is especially important for concomitant hypocalcemia. Calcium acetate is distinguished by greater phosphate-binding capacity and less release of calcium ions.

Calcium preparations (acetate and carbonate) should be taken with food, doses are selected individually and on average range from 2 to 6 g/day.
Currently, aluminum hydroxides are not used as phosphate binders due to the potential toxicity of the latter in patients with CKD.

Several years ago, phosphate binding agents that did not contain aluminum or calcium ions appeared abroad - the drug Renagel (sevelamer hydrochloride 400-500 mg).
The drug has high phosphate-binding activity; no side effects are observed with its use, but it is not registered in the Russian Federation.

In patients with CKD due to impaired endocrine renal function, there is a deficiency of the active form of vitamin D.
The substrate for the active form of vitamin D3 is 25(OH)D3 - 25-hydroxycholecalciferol, which is formed in the liver.
Kidney disease itself usually does not affect 25(OH)D3 levels, but in cases of high proteinuria, cholecalciferol levels may be reduced due to loss from vitamin D-carrying proteins.
Reasons such as insufficient insolation and protein-energy deficiency should not be ignored.
If the level of 25(OH)D3 in the blood plasma of patients with chronic renal failure is below 50 nmol/l, then patients require cholecalciferol replacement therapy.
In cases where high concentrations of parathyroid hormone are observed (more than 200 pg/ml) with normal concentrations of cholecalciferol, the use of drugs 1,25(OH)2D3 (calcitriol) or 1a(OH)D3 (alpha-calicidiol) is necessary.
The last group of drugs is metabolized in the liver to 1.25(OH)203. Low doses are usually used - 0.125-0.25 mcg based on 1,25-dihydroxycholecalciferol. This treatment regimen prevents a rise in the level of parathyroid hormone in the blood, but the extent to which it can prevent the development of hyperplasia of the parathyroid glands has not yet been clarified.

Correction of anemia
Anemia is one of the most characteristic signs of CKD.
It usually forms when GFR decreases to 30 ml/min.
The leading pathogenetic factor of anemia in this situation is an absolute or, more often, relative deficiency of erythropoietin.
However, if anemia develops in the early stages of CKD, factors such as iron deficiency (low plasma ferritin levels), blood loss in the gastrointestinal tract due to the development of erosive uremic gastroenteropathy (the most common cause), protein-energy deficiency (as a consequence) should be taken into account in its genesis inadequate low-protein diet or due to dietary self-restraints of the patient in the presence of severe dyspeptic disorders), lack of folic acid (a rare cause), manifestations of the underlying pathology (SLE, myeloma, etc.).

Secondary causes of anemia in CKD must be excluded whenever low hemoglobin values ​​(7-8 g/dL) are recorded in patients with GFR above 40 ml/min. In all cases, basic therapy with iron supplements (oral or intravenous) is recommended.
Currently, a common point of view has emerged among nephrologists regarding the early initiation of erythropoietin therapy for anemia.
First, experimental and some clinical studies have provided evidence that correction of anemia in CKD with erythropoietin slows the rate of progression of PN.
Secondly, early use of erythropoietin inhibits the progression of LVH, which is an independent risk factor for sudden death in chronic renal failure (especially subsequently in patients on RRT).

Treatment of anemia begins with a dose of erythropoietin 1000 units subcutaneously once a week; It is first recommended to restore iron reserves in the body (see).
The effect should be expected within 6-8 weeks from the start of treatment.
Hemoglobin levels should be maintained between 10-11 g/dL. Failure to respond to treatment usually indicates iron deficiency or intercurrent infection.
Even with a slight improvement in red blood counts, patients, as a rule, significantly improve their overall health: appetite, physical and mental performance increase.
During this period, some caution should be exercised in the management of patients, since patients independently expand their diet and are less serious about maintaining the water and electrolyte regime (overhydration, hyperkalemia).

Among the side effects of treatment with erythropoietin, a possible increase in blood pressure should be noted, which requires increased antihypertensive therapy.
Currently, when using small doses of erythropoietin subcutaneously, hypertension rarely acquires a malignant course.

Correction of dyslipoproteinemia
Uremic dyslipoproteinemia (DLP) begins to form when GFR decreases below 50 ml/min.
Its main cause is a violation of the processes of VLDL catabolism. As a result, the concentration of VLDL and intermediate-density lipoproteins in the blood increases, and the concentration of the antiatherogenic fraction of lipoproteins - high-density lipoproteins (HDL) - decreases.
In practical work, to diagnose uremic DLP, it is enough to determine the levels of cholesterol, triglycerides, and a-cholesterol in the blood. Characteristic features of lipid metabolism disorders in CKD will be: normal or moderate hypercholesterolemia, hypertriglyceridemia and hypo-a-cholesterolemia.

Currently, there is an increasingly clear trend towards lipid-lowering therapy in patients with CKD.
This is explained by two reasons.
Firstly, lipid metabolism disorders in chronic renal failure are potentially atherogenic. And if we take into account that in CKD there are also other risk factors for the accelerated development of atherosclerosis (hypertension, impaired carbohydrate tolerance, LVH, endothelial dysfunction), the high mortality rate of patients with PN from cardiovascular diseases (including patients on hemodialysis) becomes understandable.
Secondly, DLP accelerates the rate of progression of renal failure in any renal pathology. Considering the nature of lipid disorders (hypertriglyceridemia, hypo-a-cholesterolemia), theoretically the drugs of choice should be fibrates (gemfibrozil).
However, their use in PN is fraught with the development of serious side effects in the form of rhabdomyolysis, since the drugs are excreted by the kidneys. Therefore, it is recommended to take small doses (no more than 20 mt/day) of 3-hydroxy-3-methylglutaryl reductase inhibitors - coenzyme A - statins, which are metabolized exclusively in the liver.
Moreover, statins also have a moderate hypotriglyceridemic effect.
The question of how lipid-lowering therapy can prevent the accelerated formation (development) of atherosclerosis in chronic renal failure remains open to this day.

Correction of metabolic acidosis
In CKD, the renal excretion of hydrogen ions, which are formed in the body as a result of the metabolism of proteins and partly phospholipids, is impaired, and the excretion of bicarbonate ions is increased.
A low-protein diet helps maintain ABS, so pronounced symptoms of metabolic acidosis occur in the later stages of CKD or in cases of non-compliance with the diet.
Typically, patients tolerate metabolic acidosis well until bicarbonate levels fall below 15-17 mmol/L.
In these cases, it is recommended to restore the bicarbonate capacity of the blood by administering sodium bicarbonate orally (1-3 g/day), and in case of severe acidosis, administering a 4% sodium bicarbonate solution intravenously.

Patients subjectively tolerate mild degrees of acidosis easily, so it is optimal to manage patients at the level of base deficiency (BE - 6-8).
With long-term oral administration of sodium bicarbonate, strict control over sodium metabolism in the body is necessary (hypertension, hypervolemia, and increased daily sodium excretion in urine are possible).
With acidosis, the mineral composition of bone tissue (bone buffer) is disrupted, and renal synthesis of 1,25(OH)2D3 is suppressed.
These factors may be important in the origin of renal osteodystrophy.

Stage III carrying out a complex of therapeutic measures in patients with CKD marks the immediate preparation of the patient for the start of renal replacement therapy.
NKF standards prescribe starting RRT when GFR is less than 15 ml/min, and in patients with diabetes it is advisable to start such treatment at higher levels of GFR, although the question of its optimal value in this situation is still a matter of debate.

Preparing patients to start RRT includes:
1. Psychological monitoring, training, information for relatives of patients, solving employment issues.
2. Formation of vascular access (during hemodialysis treatment) - an arteriovenous fistula with a GFR of 20 ml/min, and in patients with diabetes and/or with a poorly developed venous network - with a GFR of about 25 ml/min.
3. Vaccination against hepatitis B.

Naturally, the initiation of hemodialysis or peritoneal dialysis therapy is always a drama for patients and their family members.
In this regard, psychological preparation is of great importance for subsequent treatment results.
Clarification is needed regarding the principles of the upcoming treatment, its effectiveness in comparison with treatment methods in other areas of medicine (for example, in oncology), the possibility of a kidney transplant in the future, and so on.

From the standpoint of psychological training, group therapy and patient schools are rational.
The issue of employment of patients is significant, since many patients are able and willing to continue working.
Early creation of vascular access is preferable, since the formation of an arteriovenous fistula with satisfactory blood flow requires from 3 to 6 months.

According to modern requirements, vaccination against hepatitis B should be carried out before starting hemodialysis treatment.
Vaccines against the hepatitis B virus are usually administered three times, intramuscularly, with an interval of one month after the first administration, then six months after the start of vaccination (0-1 month schedule).
A faster immune response is achieved by administering the vaccine according to the 0-1-2 month schedule. The dose of HBsAg for an adult is 10-20 mcg per injection.
Post-vaccination AT persist for 5-7 years, but their concentration gradually decreases.
When the AT titer to the surface antigen of the hepatitis B virus decreases to a level of less than 10 IU/l, revaccination is necessary.

Kidney transplant
The most promising treatment method.
Kidney transplantation is a dramatic treatment.
In the long term, the patient is a healthy person if everything goes smoothly, if the kidney is transplanted according to all the rules.
In 1952, in Boston, at the transplant center, J. Murray and E. Thomas successfully transplanted a kidney from a twin, and 2 years later - from a corpse.
This success made the surgeons Nobel Prize laureates.
The same prize was awarded to A. Carrel for his work on transplantation.
The introduction of modern immunosuppressants into transplantation practice has ensured an exponential increase in the number of kidney transplants.
Today, kidney transplantation is the most common and most successfully developing type of internal organ transplantation.
If in the 50s. While we were talking about saving patients with GN, kidneys are currently being successfully transplanted into patients with diabetic nephropathy, amyloidosis, etc.
To date, more than 500,000 kidney transplants have been performed worldwide.

Graft survival has reached unprecedented levels.
According to the United Network for Organ Allocation (UNOS) kidney registry, the 1-year and 5-year survival rates of cadaveric kidney transplants are 89.4% and 64.7%, respectively.
Similar figures for transplants from living donors are 94.5% and 78.4%.
The survival rate of patients at the same time with cadaveric transplants was 95% and 82% in 2000.
It is slightly higher in patients with kidneys transplanted from living donors - 98% and 91%.

The steady development of immunosuppression techniques has led to a significant increase in the half-life of transplants (almost 2 times).
This period is 14 and 22 years for cadaveric and living donor kidneys, respectively.
According to the Freiburg University Hospital, which summarized the results of 1086 kidney transplantations, 20 years after the operation, the survival rate of recipients was 84%, the graft functioned in 55% of those operated on.
The survival rate of grafts decreases noticeably, mainly in the first 4-6 years after surgery and especially significantly during the first year. After 6 years, the number of graft losses is negligible, so over the next 15 years the number of transplanted kidneys that maintain function remains almost unchanged.

The spread of this promising method of treating patients with end-stage CKD is hampered primarily by the shortage of donor kidneys.
A big problem in transplantation is the issue of providing donor organs.
Finding a donor is very difficult, since there are diseases that can prevent the donation of a kidney (tumors, infections, changes in the functional state of the kidneys).
It is mandatory to select a recipient based on blood type and histocompatibility antigens.
This achieves improved long-term functioning of the transplanted kidney.
This circumstance led to a significant increase in the waiting time for surgery.
Despite the high cost of immunosuppressive therapy in the postoperative period, kidney transplantation is more cost-effective than other methods of RRT.

In developed country settings, successful surgery can result in savings of approximately $100,000 over 5 years compared to a patient receiving dialysis treatment.
Despite the enormous successes of this treatment method, many issues still require further solutions.

A complex problem is the indications and contraindications for kidney transplantation.
When establishing indications for surgery, it is assumed that the course of chronic renal failure has many individual characteristics: the level of creatininemia, the rate of its increase, the effectiveness of other treatment methods, as well as complications of chronic renal failure.

A generally accepted indication for kidney transplantation is the condition of patients when the developing complications of chronic renal failure are still reversible.
Contraindications to kidney transplantation are: age over 75 years, severe pathology of the heart, blood vessels, lungs, liver, malignant neoplasms, active infection, active vasculitis or glomerulonephritis, severe degrees of obesity, primary oxalosis, uncorrectable pathology of the lower urinary tract with obstruction of urine outflow, drug or alcohol addiction, severe psychosocial problems.

Without dwelling on the purely technical details of the operation, we will say right away that the postoperative period occupies a special place in the problem of kidney transplantation, since at this time the future fate of the patient is determined.

The most important are immunosuppressive therapy, as well as the prevention and treatment of complications.
In terms of immunosuppressive therapy, the leading place belongs to “triple therapy” - GCS, cyclosporine-A (tacrolimus), mycophenolate mofetil (sirolimus).
To monitor the adequacy of immunosuppression when using cyclosporine-A and to monitor complications of treatment, the concentration of this drug in the blood should be monitored.
Starting from the 2nd month after transplantation, it is necessary to maintain the level of CSA in the blood within 100-200 μg/l.

In recent years, the antibiotic rapamycin has entered clinical practice, preventing the rejection of transplanted organs, including kidneys. Of interest is the fact that rapamycin reduces the likelihood of secondary narrowing of blood vessels after balloon angioplasty. Moreover, this medicine prevents the metastasis of certain cancers and suppresses their growth.

The results of new animal experiments at the American Mayo Clinic suggest that rapamycin increases the effectiveness of radiation treatment of malignant brain tumors.
These materials were presented by Dr. Sarkario and his colleagues in November 2002 to participants in an oncology symposium in Frankfurt.
In the early postoperative period, in addition to rejection crises, patients are threatened with infection, as well as necrosis and fistula of the bladder wall, bleeding, and the development of a steroid gastric ulcer.

In the late postoperative period, there remains a risk of infectious complications, development of graft artery stenosis, and relapse of the underlying disease in the graft (GN).
One of the pressing problems of modern transplantology is maintaining the viability of the transplanted organ.
The chances of restoring graft function are sharply reduced if the period of renal ischemia exceeds 1 hour.
Preservation of a cadaveric kidney is achieved by non-perfusion preservation in a hypothermic solution resembling intracellular fluid.

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The main task that we must solve is to simply and clearly talk about the mechanisms of development, symptoms and principles of treatment of both acute and chronic renal failure in women and men. The difficulty is that while the processes are undoubtedly similar, there is a significant difference between acute and chronic renal failure.

There are no differences between female kidney failure and male kidney failure. The kidneys, as an organ, do not have gender differences in structure and function. Therefore, women may have special reasons its occurrences, which do not occur in men.

For example, during pregnancy, the uterus “pinches” the ureter, dilatation of the renal collecting system occurs, and development. But pregnancy is a short period, and, as a rule, kidney failure simply does not have time to develop.

Very roughly, but true, a chronic disease state can be compared to a slightly forgetful, but quite “adequate” patient with cerebral atherosclerosis, and acute renal failure can be compared to a stroke, or stroke. In this case, everything will be different here - the treatment is calculated by the hour, all the principles and protocols for managing the patient will be special. And it would seem that just chronic disorders turned into acute ones.

The difficulty is that acute renal failure, or acute renal failure, is a condition that may not be related to the kidneys at all, and may occur against the background of their complete health.

Why this condition arises and develops will be explained below, but first we should talk very briefly about how a normal kidney works so that the course of further presentation is clear.

A little physiology

Get used to the idea that urine is former blood, its liquid part, and it was blood quite recently. Urine formation occurs in several stages:

• In the cortical layer of the kidney, in the glomeruli of nephrons (this is the structural and functional unit of the kidney), constant primary filtration of blood occurs.

Its normal speed is 120 ml/min. But a person does not have the luxury of excreting primary urine, since its volume would be about 200 liters per day. According to the losses, a person would have to constantly replenish the same amount.

It is clear that humanity would have no time for anything other than drinking and urinating, and we wouldn’t even get out of the sea onto land. Therefore, urine needs to be concentrated - in other parts of the nephron, urine is concentrated 100 times, and in this form it enters the ureter.

Of course, in addition to concentration, very important processes occur, for example, reabsorption or reverse absorption from the primary filtrate into the blood of many important compounds, for example, glucose, which simply passed through the primary filter. Concentrating urine requires a lot of energy.

Thus, the kidneys are organs that maintain homeostasis, that is, the constancy of the internal environment of the body. In addition to participating in water and salt metabolism, the kidneys decide the fate of hundreds of different compounds, and also participate in the production of various substances (for example, erythropoietins, which stimulate hematopoiesis).

We end up with normal urine that excretes everything it shouldn't and doesn't miss any "deficiencies" like protein. But in kidney failure, these mechanisms are disrupted, and the urine of a patient with kidney failure resembles a border where drugs and contraband have been established, and unplanned infiltrations occur. What is kidney failure?

Differences between acute and chronic renal failure

AKI (acute renal failure) and CRF (chronic renal failure) are called disorders of the homeostatic function of the kidneys. In the case of acute renal failure, it sometimes develops in a few hours or days, and in the case of chronic renal failure, it can progress for years.

• The most important difference between these conditions is the fact that in acute renal failure, the kidneys are most often “not to blame” - they are taken by surprise by an emergency situation, and they do not cope with the function, simply, “like everyone else,” participating in a whole cascade of metabolic disorders.

Chronic renal failure is a condition in which the kidneys are to blame and a “test of reserves” occurs. With chronic renal failure, its slow development makes it possible to compensate, develop temporary measures, adapt, and ultimately maintain kidney function at a decent level for a long time, without a threat to life.

Thus, it is known that there are 2 million nephrons in the kidneys. Even if half die (which is equivalent to losing one kidney), there may be no signs of disease. And only when only 30% of nephrons remain in the kidneys, and the filtration rate drops threefold, to 40 ml/min, do clinical signs of chronic renal failure appear.

• A mortal threat to life occurs when 90% of nephrons die.

Acute renal failure - what is it?

Acute renal failure syndrome occurs in one patient in 5000 cases. This is not much, given the spontaneous nature of its occurrence. But, on the other hand, in a large regional or regional center with a population of 1 million people there will already be about 200 patients within a year, and this is a lot.

From the history of the issue, it can be established that in 90% of cases, acute renal failure occurred in the middle of the twentieth century, as a complication of criminal abortion. Currently, acute renal failure occurs in various fields of medicine, and is most often a manifestation of multiple organ failure syndrome. There are:

• Prerenal acute renal failure (i.e. prerenal) – 50%.

Prerenal acute renal failure occurs with completely preserved renal function. But arrhythmias, various shocks, pulmonary embolism and heart failure simply cannot provide “pressure supply” to the kidney system.

Also, acute renal failure develops with vasodilation (with allergic shock, or anaphylaxis, with sepsis). Of course, if a significant amount of fluid has disappeared from the body (bleeding, severe diarrhea), then this will also lead to an elementary lack of filtration volume.

• Renal (acute nephron damage);

According to statistics, almost all renal acute renal failure is caused by either ischemia or intoxication of nephrons. Almost always, with this disorder, acute tubular necrosis occurs, that is, “death” of the urine concentration apparatus. For example, this type of acute renal failure occurs when there is a massive release of muscle breakdown products (myoglobin) into the blood during prolonged crush syndrome, or crash syndrome, shortly after improper removal of compression.

It is also caused by certain medications (antibiotics - aminoglycosides), NSAIDs, X-ray contrast agents, captopril.

In 1998, a case was described in which, after a single administration of cefuroxime (an antibiotic from the cephalosporin group), the patient developed acute bilateral necrosis. As a result, she lived on hemodialysis for 1.5 years, and her condition improved only after a kidney transplant.

• Postrenal (postrenal, urine outflow is disrupted) – 5%.

This type of acute renal failure is rare and can occur in unconscious, elderly and mentally ill patients. Accompanied by anuria (less than 50 ml per day). The reason is stones, adenoma, cancer and other obstacles to the passage of urine leading to obstruction at any level, from the urethra to the pelvis.

Symptoms of acute renal failure

ARF develops in stages. With a favorable outcome, this is: the initial, oliguric stage, restoration of diuresis and recovery.
There are no specific symptoms of acute renal failure. The following general features can be identified:

• collapse, or decrease in blood pressure;
• oliguria (decreased amount of urine);
• nausea, diarrhea, bloating, refusal to eat;
• anemia;
• hyperkalemia;
• development of acidosis and “acidification” of the blood, the appearance of noisy Kussmaul breathing.

The clinical picture of acute renal failure is very variable. Thus, hyperkalemia occurs with extensive burns, anemia - with severe hemolysis, convulsions and fever, sweating - with septic shock. Thus, acute renal failure occurs under the guise of the cause that caused it.

Its main indicators will be an increase in blood urea against the background of a sharp decrease in the amount of urine.

Treatment of acute renal failure

It is known that various shocks (cardiogenic, burn, pain, infectious-toxic, anaphylactic) are the cause of acute renal failure in 90% of cases.

Therefore, the fight against shock allows one to resolve acute renal failure. To do this, they replenish the volume of circulating blood, limit the intake of potassium, carry out blood transfusions, and provide a protein-free diet. For severe disorders, hemodialysis is used.

For infections and sepsis, dialysis is combined with hemosorption and ultraviolet irradiation of the blood. For blood diseases that lead to anemia, plasmapheresis is used.

Treating acute renal failure is an art because doctors are constantly limited in what they can do. Thus, in case of infectious-toxic shock, which led to acute renal failure, the infection must be dealt with as quickly as possible, but the use of effective drugs is limited, since renal function is reduced and the possibility of toxic damage to the glomeruli must be taken into account.

Forecast

As a rule, with isolated renal failure, mortality does not exceed 10-15%, but it rapidly increases to 70% in old age, against the background of acute heart or liver failure, reaching 100% in the case of “all failures”, or multiple organ failure.

For those who survive, kidney function is completely restored, according to various sources, in 30-40% of cases. If we talk about long-term complications, the most common occurrence is pyelonephritis associated with stagnation of urine during acute renal failure.

Chronic renal failure - what is it?

Let us now turn to slowly emerging chronic renal failure, the outcome of which is uremic coma, with the “death knell of the uremic” as the symptom immediately preceding the coma. This is the name given to a rough, shuffling pericardial friction noise that occurs in patients with end-stage chronic renal failure.

It arose because urea, which was formed as a result of protein breakdown, was not excreted by the kidneys and was deposited in the form of inorganic crystals throughout the body, including in the pericardial cavity.

Of course, at present such symptoms, and especially those detected for the first time, practically do not occur - but chronic renal failure can lead to this. What causes chronic renal failure?

Causes of chronic renal failure

The main diseases leading to chronic renal failure affect the glomeruli of the kidneys, which filter primary urine, and the tubules. The connective tissue of the kidneys, or interstitium, in which the nephrons are embedded, may also be affected.

Chronic renal failure is also caused by rheumatic diseases that affect connective tissue, metabolic diseases and congenital kidney abnormalities. Vascular lesions and conditions that occur with obstruction of the urinary tract make their contribution. Here are some of these diseases:

• glomerulonephritis, chronic pyelonephritis, interstitial nephritis;
• systemic scleroderma, hemorrhagic vasculitis;
• diabetes, amyloidosis;
• polycystic kidney disease, congenital hypoplasia;
• malignant renal hypertension, renal artery stenosis;

The basis of nephron damage in chronic renal failure, regardless of the cause, is glomerulosclerosis. The glomerulus becomes empty and is replaced by connective tissue. Uremia occurs in the blood, that is, roughly speaking, “urinary bleeding.”

Circulating uremic toxins (urea, creatinine, parathyroid hormone, beta microglobulin) poison the body, accumulating in organs and tissues.

Symptoms of chronic renal failure

Symptoms of chronic renal failure in women and men are the same, and begin with disorders of water-salt metabolism.

During chronic renal failure there are four stages:

1) Latent, which corresponds to the onset of water-salt disorders.

It all starts in the early stages of chronic renal failure:

• Isosthenuria and hyposthenuria. The kidneys cannot concentrate urine. Urine “reaches” only a density of 1010-1012, and with hyposthenuria, in general, up to 1008.
• Nocturia, or the predominance of nighttime urine volume over daytime. Healthy nephrons become overloaded and work the night shift. This occurs, for example, because at night the spasm of the kidney vessels is eliminated;
• Polyuria. The amount of urine increases, compensating for the lack of “quality”. In the terminal stage of renal failure, the amount of urine decreases to 600-800 ml per day, which is an indication for dialysis.

2) Compensated, in which the kidneys are still coping and there is no oliguria.

All this leads to salt depletion - weakness and decreased blood pressure occur. But in some patients, sodium retention, on the contrary, causes an increase in blood pressure. Sleep is also disturbed and appetite decreases.

Fatigue, headache, itching, dizziness, and depression occur. Body temperature decreases and bleeding occurs. Potassium and magnesium retention leads to muscle weakness, cardiac dysfunction, and drowsiness.

3) Intermittent (oscillating), when periods of oliguria occur and the accumulation of ions in the plasma increases.

The most common symptoms are thirst, nausea, vomiting, bad taste in the mouth, stomatitis and ammonia odor on the breath. The skin is pale, dry and flabby. There is a slight tremor of the fingers.

At the advanced stage of chronic renal failure, anemia often occurs because the kidneys produce a substance that affects the synthesis of red blood cells. The clinical picture reflects azotemia, that is, the accumulation of protein metabolic products in the body.

4) Terminal.

Encephalopathy occurs. Memory is impaired and insomnia occurs. Muscle weakness appears, climbing stairs is difficult. Then painful skin itching, paresthesia appears, subcutaneous bleeding increases, and nosebleeds appear.

In severe cases, due to water retention and “water poisoning,” pulmonary edema, chronic heart failure occurs, and myocardial dystrophy develops. Progresses (“pins and needles”, numbness, pain), sense of smell and taste worsen or disappear.

The retina is affected, which can lead to complete blindness, stunning and uremic coma develop. A strong smell of ammonia emanates from patients.

Treatment of chronic renal failure + diet

Since chronic renal failure lasts a long time, all measures must be taken at the initial stages: diet, regimen, the possibility of dialysis and other measures. Patients should be spared physical activity (protein catabolism increases), and exposure to fresh air is recommended. The basis of treatment is proper diet.

Diet

Treatment of chronic renal failure begins with properly selected nutrition:

• meals are fractional, 4-5 times a day;
• it is required to limit protein to 50-70 grams per day;
• meet energy needs from fats and carbohydrates;
• regulation of salt metabolism (limiting table salt).

In clinical nutrition for chronic renal failure there is. In the initial stage, diet No. 7 is sufficient, and in case of severe disorders, diets No. 7a or 7b are used (20 and 40 grams of protein per day).

In nutrition, it is advisable to arrange fasting days: rice - compote, carbohydrate apple - sugar, potato. Potatoes are cut raw and soaked to reduce potassium levels.

In this case, 50% of the daily dose of protein should be easily digestible protein (curd or egg). But meat, fish, poultry, legumes, nuts and chocolate should be completely excluded. Marshmallows, marshmallows, honey and caramel are not prohibited. Dried fruits (except soaked ones) are contraindicated, as they contain excess potassium.

Fat is given in the form of vegetable oils. The amount of table salt is strictly taken into account and does not exceed 8 g per day. The amount of liquid in food and drinks depends on the patient's diuresis and should not exceed it.

Drugs for the treatment of chronic renal failure

Drugs for the treatment of renal failure are symptomatic. We will not consider the treatment of diseases that led to chronic renal failure. For this, patients may be prescribed serious medications, for example, hormones and cytostatics. As for taking medications to correct chronic renal failure itself, these include:

• antihypertensive drugs in the presence of malignant hypertension;
• diuretics and cardiac glycosides in case of impaired cardiac pumping function and the development of congestive heart failure;
• sodium bicarbonate to relieve acidosis,
• iron supplements for anemia;
• antiemetics for nausea and vomiting (“Cerucal”);
• enterosorbents to reduce azotemia (Enteros-gel);
• colon lavage, enemas.

In the treatment of chronic renal failure, extracorporeal detoxification methods are currently the “salvation”: hemosorption, plasmapheresis, as auxiliary methods, and chronic hemodialysis, or an “artificial kidney” device. This allows you to save the life and activity of patients, and wait for a kidney transplant, if indicated.

But science does not stand still. In 2010, a prototype of an implantable artificial kidney was created, and the time is not far when it will be possible to create a human kidney anew, using its stem cells, as well as its connective tissue base.

Forecast

We have outlined only the surface issues related to the causes, symptoms and treatment of chronic renal failure. The main thing to remember is that chronic renal failure is a nonspecific syndrome that develops in many diseases.

Only the opportunity to reverse the course of the underlying disease provides a chance to stabilize the patient’s condition. In addition, it is necessary to take into account age, concomitant pathology, the possibility of dialysis and the prospects for a kidney transplant.