Uremia is a syndrome of autointoxication that develops in the presence of severe renal failure as a result of disruption of acid-base, osmotic and water-salt homeostasis, retention of nitrogenous metabolites, as well as other toxic components in the body and is accompanied by general tissue degeneration, hormonal disorders, dysfunction of all systems and organs.
| ICD-10 | N19 |
|---|---|
| ICD-9 | 585-586, 788.9 |
| DiseasesDB | 26060 |
| eMedicine | med/2341 |
| MeSH | D014511 |
Classification
There are two forms of uremia:
- acute;
- chronic.
At acute uremia, which develops in the presence of an acute form of renal failure during oliguria, severe renal dysfunction occurs, as well as various disorders of the body. In the blood there is a sharp increase in the concentration of urea, creatinine, ammonia and other products of nitrogen metabolism, a change in the content of electrolytes, and an imbalance in the acid-base balance (chlorhydropenic uremia). As a result of changes in the activity of the cardiovascular system, tachycardia, hypertension, and arrhythmia occur. In acute uremia, neurological complications occur due to damage to the nervous system. Digestive system disorders such as anemia and pulmonary edema also develop. Typically, the acute form of uremia lasts about 5-10 days.
Chronic uremia results from most chronic kidney diseases. This form of uremia is accompanied by vascular damage, bone loss, a sharp increase in blood pressure, and the development of pericarditis. There is a low specific gravity of urine. As a result of an increase in the content of nitrogenous metabolic products, azotemic uremia develops. In case of chronic disease, conservative-curable and terminal stages of development are distinguished. The latter is characterized by a decrease in glomerular filtration, as well as a lack of ability to adapt to functional disorders of the kidneys.
Causes
The causes of acute uremia are the development of acute renal failure, which manifests itself as a result of circulatory disorders, frostbite, trauma, shock or frostbite. The causes of chronic uremia are irreversible processes of extinction of renal tissue functions. The following diseases can contribute to the development of the disease:
- pyelonephritis;
- congenital nephritis;
- glomerulonephritis;
- kidney stone disease;
- cysts in the kidneys.
Prostate adenomas and diabetes mellitus can also be causes of uremia.
Pathogenesis
The leading role in the pathogenesis of uremia is played by intoxication of the body with metabolic products, which under normal conditions are excreted in the urine. There is an accumulation of large amounts of organic matter. As a rule, these are products of protein metabolism that have toxic effects. In addition to urea, the level of ammonia, creatinine, uric acid, peptides, aromatic amine amino acids, phenols, acetone, oxalic acid, indole and other harmful substances increases.
Symptoms
Symptoms of uremia can appear gradually and intensify as the disease progresses. Signs of uremia are:
- drowsiness, lethargy, apathy;
- pallor of the facial skin, the appearance of a yellowish tint;
- brittleness and dryness of nails;
- sagging skin;
- manifestation of “uremic powder” (urea crystals that appear on the skin);
- hemorrhages in different parts of the body;
- muscle weakness in the back, pelvis and shoulders;
- bad breath (occurs due to the breakdown of urea in the oral cavity, resulting in the formation of ammonia);
Urea can accumulate in gastric juice, which leads to gastritis and colitis. As a result, uremia is accompanied by nausea, vomiting, and diarrhea with blood. Due to the increase in acids and nitrogenous metabolic products, an increase in the number of leukocytes can be detected in the patient. Leukocytosis with uremia is toxic.
With further development of the disease, disruptions in the functioning of the brain occur, which leads to disturbances in attention and sleep. Appetite decreases, patients may refuse food. Hallucinations and seizures may occur. If uremia is left untreated, the symptoms become so severe that they can lead to coma.
Diagnostics
Diagnosis of uremia is carried out on the basis of a laboratory test, the purpose of which is to determine nitrogen-containing products in the blood. With this disease, there is an increased level of these substances.
Treatment
For uremia, hemodialysis (removal of toxic products from the body, normalization of electrolyte and water balance) and renal transplantation are used. Blood transfusion for uremia allows you to remove a certain amount of harmful substances from the patient’s blood.
Uremia disease requires consideration of the issue related to replacement therapy. This is influenced by two circumstances. Firstly, many patients who have impaired differentiation of kidney tissue are characterized by a sharp deterioration in the functional state of the organs. It can occur after relative stabilization of functioning. In some cases, the cause of deterioration in the patient's condition with uremia is an intercurrent illness. But it is often not possible to establish what led to a sharp decrease in renal filtration capacity. Secondly, for renal dysplasia and chronic renal failure at the initial stage, organ transplantation is a fairly effective method of therapy. In this case, it is important to pre-prescribe hemodialysis, which will provide favorable conditions for transplantation.
In addition to the above methods, treatment of uremia involves following a strict diet, which will set a limit on the amount of protein consumed.
Forecast
Acute uremia is characterized by a progressive course and almost complete reversibility of the processes, subject to timely and correct treatment. If hemodialysis is not performed on time, the disease usually leads to death. When anuria drags on for a week or more, death usually occurs, caused by acidosis, hyperkalemia, and overhydration. When treating uremia with extrarenal cleansing methods, most patients manage to get rid of the disease (65−95%) and return to a full life.
In the conservative stage of chronic uremia, if treatment is not carried out, patients have different life expectancies. The prognosis is worsened by the presence of high arterial hypertension, pericarditis, and circulatory failure. When the terminal stage of uremia occurs, this means that death is imminent. At the same time, in order to prolong the patient’s life, regular dialysis is used for uremia.
As a rule, the causes of death in patients with uremia disease are disorders of the cardiovascular system, hyperkalemia, concomitant infectious diseases, sepsis, uremic coma, and hemorrhagic disorders. Regular therapy will help prolong the life of patients with chronic uremia.
Prevention
Preventive measures for uremia include the prevention of kidney dysplasia. It is necessary to create the right conditions during pregnancy that will help protect the fetus from teratogenic influences. The search for markers of heterozygous pathology carriage is of great importance. If there is an increased risk, antenatal diagnosis of urinary tract malformations is recommended.
In chronic renal failure, the patient's body begins the process of self-poisoning. This condition is called uremia. And those who want to understand what uremia is should know that a malfunction in the body occurs against the background of impaired protein metabolism. In this case, all nitrogenous wastes settle in the patient’s body, while in a healthy person they are excreted through the kidneys along with urine. At the same time, along with disruption of protein metabolism, acid-base and osmotic balances are also disturbed.
Important: healthy kidneys function as a regulator of osmotic pressure, and also regulate water and electrolyte balance, control the composition of salts in the body and remove toxins. When, due to kidney disease, the kidneys cannot cope with their function, a high concentration of toxins that are not removed from the body changes the chemical composition of a person’s blood for the worse. The patient develops azotemic uremia.
Reasons for the development of uremia
If a person wants to know what uremia is, then it is necessary to initially understand the reasons for the development of the pathology. Azotemic uremia, as a rule, develops under the influence of such factors:
- Advanced renal pathologies (pyelonephritis, glomerulonephritis, etc.);
- Prostate adenoma in advanced forms;
- Stones in the kidneys or urinary tract;
- Urethral stricture.
With any of these pathologies, the outflow of urine is impaired. As a result, self-poisoning of the patient’s body develops with unresolved breakdown products of protein and other microelements. Potassium, magnesium, and phosphorus accumulate in excess in the body, which leads to an additional toxic load on all vital systems.
Important: if azotemic uremia develops against the background of the listed pathologies, then its course can last up to several years and not be diagnosed.
Symptoms
When uremia just begins, the symptoms are quite vague. First of all, the patient will show signs of mild intoxication, which are often attributed to the “modern tired person” syndrome. These are:
- Recurrent headache;
- Decreased performance;
- Increased fatigue;
- Feeling thirsty;
- Decreased appetite;
- Nausea.
Later, when the pathology takes on a large scale, the patient will experience the following clinical signs:
- Muscle cramps. This indicates damage to the central nervous system by toxins.
- Incessant vomiting and diarrhea. Indicate damage to the gastrointestinal tract.
- Development of tracheitis and stomatitis. These signs indicate that toxins and waste have begun to seek exit through the salivary glands.
- Pungent odor of urine from the mouth. It speaks of severe intoxication of the body.
- Uneven and noisy breathing. The penultimate stage of the pathology.
- Loss of consciousness. In this case, death occurs from uremic coma.
It is also worth remembering that under the influence of excess phosphorus during uremia, calcium is washed out of bone tissue. In this case, the patient develops osteoporosis. Patients have constantly high blood pressure. The level of platelets and hemoglobin decreases critically. Also, patients with uremia have decreased hearing and vision, a deteriorating sense of smell, and taste buds require unusual combinations.
Important: with all this, uremia can occur in a latent state (chronic) and the patient can feel familiar for a long time.
Types of uremia
A pathological toxic condition (uremia) can occur in two forms - acute and chronic. At the same time, the clinical picture and prognosis are completely different.
Acute uremia
This form of pathology lasts about 5-10 days and develops mainly against the background of severe renal failure (with inflammation of the kidneys or inflammation). This type of pathology develops after the onset of oliguria (decreased daily urine volume). So, if normally a person should excrete up to 1.5 liters of urine per day, then with oliguria its volume decreases to 0.5 liters. Accordingly, all wastes and toxins remain in the patient’s body. With well-chosen treatment tactics, the patient recovers in most cases, and complete recovery of the body takes about another six months to a year.
In acute uremia, the patient experiences the following symptoms:
- Arrhythmia and tachycardia;
- Increased blood pressure;
- Decreased hemoglobin;
- Disorders of the gastrointestinal tract;
- Pulmonary edema (worst case).
Important: it is worth remembering that if during acute uremia the patient’s blood is not dialyzed, then death occurs with a 99% probability.
Chronic uremia
The chronic course of the pathology occurs against the background of chronic advanced kidney diseases. Typically, untreated kidney disease leads to shrinkage of the kidneys, which causes uremia. A patient with chronic uremia has the following symptoms:
- Apathy, lethargy and poor sleep. All this indicates a disruption in the functioning of the nervous system.
- Frequent headaches. Here we are talking about damage to the vascular system.
- Constant itching of the skin. Sometimes the patient experiences very severe scratching in the chest area, on the body and on the back of the head.
- Formation of ulcers. As a rule, they form at the sites of infected scratches.
- White coating on the skin. It is localized on the face, wings of the nose and in the roots of the hair. This indicates an excess of salts in the body.
- Heart murmurs. As a rule, this indicates damage to the heart sac by salt crystals. In this case, the pericardium experiences severe friction. The patient may even feel pain in the chest area. Experts call such noises “the death knell,” which in most cases is a harbinger of death for the patient. Death occurs within 7-14 days.
Diagnosis of pathology
To diagnose acute or chronic uremia, a series of laboratory blood tests should be performed. Urine tests are not particularly informative. So, the following analyzes are carried out:
- Biochemical blood test. With uremia, increased levels of creatine, urea, nitrogenous waste, and uric acid are detected in the blood. All these indicators will be critically increased if the patient has uremia. The concentration of magnesium, potassium and sodium, which are the main electrolytes, is also determined in the blood.
- Chemical blood test. Here, the concentration of blood protein, glucose and lipids is determined in the blood of sick people.
Treatment of pathology
Uremia requires urgent treatment. Because a person may experience a toxic coma and death. The main methods of treating this pathology are hemodialysis (blood purification through an “artificial kidney” device) or kidney transplantation.
- During hemodialysis, the machine is connected to the patient's body through a vein or artery. Blood from the patient’s body flows through a special membrane in which waste and nitrogenous compounds are deposited. The blood treated with the dialysis solution is returned back to the patient's body. A hemodialysis session can last 3-4 hours depending on the patient’s condition. Also, depending on the course of uremia, the patient is indicated from 10 to 50 hemodialysis sessions. To maintain the body during dialysis, you should follow a diet that involves increasing animal protein in the diet and limiting potassium, salt, smoked meats and marinades. A total of no more than 1 liter of liquid, including tea, soup, etc.
- Kidney transplantation is performed if dialysis does not provide the desired effect. In this case, it is necessary to save the patient's life only by organ transplantation. As a rule, kidney transplantation is indicated for patients in the age group of 15-45 years. A transplant is also indicated for young patients, since dialysis greatly inhibits the development of a young body and psyche as well. It is worth understanding that transplanting a diseased organ can prolong the patient’s life by 10-15 years. However, in women and men over 45 years of age, organ transplantation can cause side effects such as thrombosis, cerebral vasospasm, diabetes or heart attack.
Important: you will need to fight for the viability of the transplanted organ in addition by taking lifelong or very long-term immunosuppressive therapy.
Prevention of uremia
In order not to provoke intoxication of the body with toxins and protein breakdown products, it is necessary to treat all renal pathologies in a quality and timely manner, preventing them from becoming chronic. It is also necessary to promptly treat all cases of toxic damage to the body, which can lead to kidney failure. There are no other preventive measures to combat possible uremia.
Important: always pay close attention to your health and be happy.
Uremia is a severe intoxication of the body resulting from insufficient renal function. Uremia is caused by metabolic disorders, alkaline-acid balance, and the accumulation of toxic metabolic products in the blood, which disrupts the function of all organs and systems of the body.
There are acute and chronic uremia.
Acute uremia observed due to acute renal failure: in case of poisoning with barbiturates and some other poisons, with massive hemolysis as a result of transfusion of incompatible blood, with kidney injury, acute severe infections (typhoid, etc.), with various etiologies, burns, shock.
The course of acute uremia, like acute renal failure, is characterized by several stages (see, diseases).
The first signs of chronic uremia are lethargy, apathy, headaches,... When examining blood, an increased content of nitrogenous wastes is found in it: residual nitrogen (normal 20-40 mg%), urea (normal 20-40 mg%), creatinine (normal 1-2 mg%).
In a later period, urea and other nitrogen-containing substances accumulating in the blood begin to be intensively secreted by the skin, mucous and serous membranes, irritating them. As a result, symptoms of uremic (anorexia, ), colitis (), laryngotracheitis (usually already in the terminal period) appear.
Due to intoxication, the functions of the liver and bone marrow are impaired, anemia increases, a tendency to bleeding appears, and vision is impaired (uremic neuroretinitis). Subsequently, uremic coma develops - the patient loses consciousness, noisy deep breathing occurs (Kussmaul breathing), Cheyne-Stokes type breathing is less common (see Breathing, pathological), a strong odor of ammonia emanates from the patient, the pupils are constricted.
It is necessary to differentiate uremic coma from coma of another origin: chlorpenic, diabetic, hepatic, etc. (see Noma).
Serious, but chronic uremia, despite irreversible decline in kidney function, can sometimes last for years. Patients can be in a relatively satisfactory condition for a long time.
Rice. 1. Uremic “powder”. Rice. 2. Swelling of the entrance to the larynx with uremia. Rice. 3. Fibrinous focal pneumonia with uremia. Rice. 4. Fibrinous gastritis with uremia.
Speaking about uremia, we mainly mean poisoning of the body by urea and other nitrogenous wastes accumulated in the blood and tissues - indican, creatinine, uric acid.
Normally, the urea content in the blood is 20-35 mg%, and the residual nitrogen is 20-45 mg%; with uremia, their level increases to 200-300 mg% or even more. However, this circumstance is not the only factor that determines the clinical picture of uremia, since in some cases, with a high content of nitrogenous wastes in the blood, there are no signs of uremia, in others, they are observed with relatively low azotemia. Dehydration and acidosis play a major role in the uremic state.
In urological practice, uremia in most cases is associated with impaired renal function due to obstructed urine outflow. Prostate adenoma, urethral strictures, kidney and ureteral stones mostly disrupt the urinary process gradually, which explains the slow development of uremia in these diseases. Increased pressure in the urinary tract, caused by stagnation of urine, is then transmitted to the renal parenchyma, primarily to the tubular system. The tubular epithelium becomes flattened, its main function - water reabsorption - is disrupted, which entails an increase in diuresis from 1-1.5 to 2-3 liters of urine and a corresponding fluid deficit in the tissues. Dehydration of the body is compensated for a long time by increased fluid intake, so clinical symptoms of dehydration (dry tongue, thirst) appear only in the late stages of uremia, when the increased need for water can no longer be satisfied by drinking plenty of fluids.
The harmful effects of high blood pressure gradually affect the blood supply to the kidney. This is often accompanied by the destructive effect of urinary infection in the form of chronic pyelonephritis. All kidney functions are impaired, including ammonia synthesis. Instead, other alkaline ions, such as sodium and potassium, are attracted from the blood plasma to neutralize acidic metabolic products. A decrease in the alkaline valence of the blood leads to the fact that carbonic acid, which usually binds to sodium and is excreted in the urine in the form of Na 2 CO 3, remains free and causes a decrease in blood pH (acidosis).
Clinical symptoms uremia develops gradually. Initially, fatigue, lack of appetite, thirst, headaches, nausea are noted, which are later joined by some lethargy, muscle twitching - the result of deep intoxication of the central nervous system. In a later stage of uremia, persistent vomiting and diarrhea appear as manifestations of gastritis and enterocolitis, caused by the compensatory release of toxic urine ingredients through the gastrointestinal tract. The secretion of waste from the salivary glands and the mucous membrane of the trachea leads to persistent stomatitis and tracheitis (smell of urine from the mouth, hoarse voice). Intoxication of the respiratory center by free carbonic acid accumulated in the blood disrupts the breathing rhythm, it becomes deep, noisy, and with uneven pauses (Kussmaul breathing). Patients become unconscious and die from uremic coma.
Treatment uremia consists of removing obstacles to the outflow of urine, limiting protein foods, prescribing alkalis to combat acidosis, bloodletting with replacement blood transfusions, intravenous or subcutaneous administration of a 5% glucose solution or saline solution. Daily gastric lavage is important in order to remove excess amounts of toxins, compensatory secreted by the gastric mucosa. With regard to the intestines, siphon enemas are of the same importance.
Since the peritoneum has enormous absorption and excretory capacity, in order to remove toxins, the abdominal cavity is washed with weakly alkaline solutions - the so-called peritoneal dialysis.
Two drains are inserted into the peritoneal cavity through incisions on the anterior abdominal wall. One of them, the adductor, is connected to a vessel filled with a sterile liquid of a special composition, the second, the outlet, is connected to a device for suctioning the liquid.
To remove patients from the state of uremia, an “artificial kidney” device is also used (Fig. 8). Its operating principle is based on the ability of a number of low-molecular compounds found in the blood (electrolytes, urea, uric acid, creatinine and other nitrogenous compounds) to penetrate through the force of diffusion and osmosis through a semi-permeable membrane into a saline solution, thereby achieving the release of toxins from the blood. The main part of the artificial kidney is semi-permeable membranes made of cellophane and bakelite. Indications for the use of an artificial kidney are acute renal failure after blood transfusion, poisoning, severe burns, post-abortion sepsis.
Rice. 8. “Artificial kidney” device designed by NIIEKHAI.
Treatment acute uremia is the same as acute renal failure (see). Patients with chronic uremia are prescribed a fat-carbohydrate diet consisting of flour dishes, potatoes, rice, animal and vegetable fats, the amount of which is not limited. For nausea and vomiting, food is served in the form of purees, pastes, pureed soups, jellies, and jelly. Intake into the body is limited to 3-4 g per day and protein to 18-22.5 g per day. In the absence of a tendency to edema, drinking plenty of fluids is useful. Depending on the characteristics of the water-salt metabolism disorder, the doctor may prescribe an individual diet. It is supplemented with B vitamins (especially and) and ascorbic acid.
To suppress putrefaction processes in the intestines, oletethrin is prescribed in individual doses, as well as lactic acid products: kefir, yogurt, acidophilus. For uremic gastritis, colitis, as well as for additional cleansing of the body from nitrogen waste, the stomach and intestines are washed with a 1% solution of sodium bicarbonate. More effective methods of combating uremic intoxication are hemodialysis (see) and (see), however, in case of irreversible chronic kidney damage, these methods, without eliminating the cause of uremia, can only slightly prolong the life of patients.
Patients with uremia must also undergo symptomatic therapy: for high blood pressure, iron supplements and red blood cell transfusions for severe anemia. The underlying disease (nephritis, pyelonephritis, etc.) is treated if its exacerbation is observed. Treatment of heart failure with uremia (drugs in strictly individual doses) should be carried out with extreme caution, taking into account the impaired excretion of these drugs by the affected kidneys.
To the question “what is uremia in humans?” you can answer knowing the etymology of this word. The term uremia consists of two Greek words, uron - urine and hamia - blood, which literally means urine-blood. Its synonym is renal failure.
This syndrome is characterized by a violation of the filtration function of the kidney, difficulty in removing protein metabolic products, nitrogenous substances and other toxic substances from the blood, as a result of which they accumulate in the blood, azotemia develops, and self-poisoning of the body occurs.
- Acute uremia develops as a result of injuries, for example, large burns, frostbite, after prolonged compression syndrome, after which detritus of damaged tissue rushes into the renal capillaries and clogs them.
- The development of uremia is possible after massive hemolysis, shock, severe hemodynamic disturbances, acute inflammatory kidney diseases, acute glomerulonephritis.
- It is also possible to develop uremia for urolithiasis, in case of acute urinary retention, ureteral obstruction and hydronephrosis, and the development can be both acute and chronic. According to pathological anatomy, with prolonged hydronephrosis, the parenchyma stretches and thins under the pressure of accumulated urine in the renal pelvis, the number of functional elements in it becomes smaller, sometimes the parenchyma is reduced almost completely.
- Kidney failure may be caused by infection, for example, HFRS (hemorrhagic fever with renal syndrome) is a viral disease accompanied by azotemic uremia.
The causes of uremia can be very different. Uremia can be caused by kidney disease, and can also be extrarenal, when azotemia develops due to extrarenal causes, prerenal and postrenal.
Chronic renal failure develops over a long period of time:
- against the background of chronic kidney diseases;
- with pyelonephritis; toxic nephritis;
- with damage to the kidney parenchyma due to systemic diseases, diabetes mellitus, amyloidosis;
- for chronic diseases of the cardiovascular system.
Uremia can be complicated by urosepsis, which develops against the background of secondary immunodeficiency caused by renal failure and is associated with the addition of a bacterial infection.
What disability group is given for uremia?
Group I disability is given to a patient with uremia in the terminal stage, if the patient cannot care for himself and needs outside help.
Group II given to the patient in case of disruption of the functioning of vital organs and systems.
III group is prescribed to patients with minor disorders of organs and systems with uremia and the presence of contraindications for certain types of activities.
Uremia according to ICD 10
Uremia in ICD 10 is noted in two sections, in the group of kidney diseases called acute renal failure, chronic renal failure and unspecified renal failure. (N17-19).
Renal failure with hypertension belongs to the group of cardiovascular diseases, code I12. Extrarenal uremia belongs to group R - symptoms and signs not classified in other groups.
Uremia disease symptoms, signs and pathogenesis
Acute uremia occurs rapidly and begins immediately after exposure to a damaging factor.
Chronic renal failure divided into three types - l attentive, azotemic uremia (retention) and uremic terminal stage. The extreme degree of severity of both acute and chronic forms is uremic coma.
Uremic coma must be differentiated from chlorhydropenic coma, which develops in adrenal insufficiency, and from diabetic or ketoacidotic coma in diabetes mellitus.
The starting point in the mechanism of development of pathological changes is violation of the filtration function of the glomerular apparatus due to any reason.
In uremia syndrome, the pathogenesis consists of several links:
- First, toxic substances, urea, accumulate in the blood, and a change in laboratory parameters of the acid balance of the blood towards acidosis and azotemia is observed. At the same time, the specific gravity of urine is reduced.
- The increased content of metabolites has a toxic effect on the organs and systems of the body, and the main symptoms of the clinical picture of uremia are associated with this.
The pathophysiology of intoxication by protein metabolism products includes a vicious circle of stimulation of protein catabolism in the presence of acidosis in the blood, while protein synthesis is not affected by acidosis. As a result, a negative nitrogen balance develops and is maintained; urea, ammonia, creatinine, uric acid, polyamines, indole, phenols, acetone, glucuronic and oxalic acid accumulate in the blood, and this is not a complete list of metabolic products that are usually excreted in the urine.
With uremia, symptoms increase according to the level and rate of accumulation of toxic substances.
- Urea in an aqueous solution, it partially dissociates to cyanate, which is associated with signs of intoxication characteristic of the disease uremia. Protein breakdown products have a toxic effect on the myocardium by disrupting membrane permeability.
- High content ammonia in the blood causes depression of the central nervous system. Patients note weakness, drowsiness, lethargy, speech disorder, confusion, manifestations of toxic damage can be attacks of excitement, convulsions. Signs of polyneuritis may appear.
- Increased content creatinine associated with depression, apathy, lethargy, stomach and intestinal problems. Clinical manifestations of azotemic gastritis may include nausea, loss of appetite, vomiting, and thirst. Negative effect on peristalsis up to intestinal atony and intestinal obstruction.
The disease uremia itself affects the hematopoietic system, von Willebrand factor, which affects thrombocytopoiesis, is inhibited, and consequently bleeding develops. Hematuria, due to damage to the renal parenchyma, and anemia are also observed.
In severe condition and with high levels of uric and other acids in the disease uremia, pathogenesis includes the deposition of salts in physiological cavities, and the development of pericarditis is possible. Uremia clinics are also characterized by a specific odor from the patient’s mouth and skin, and dehydration.
In addition, uremia has a toxic effect on the immune system and contributes to the development of secondary immunodeficiency, which can lead to the development of urosepsis.
Causes of uremia and its treatment
Diagnosis of renal failure is carried out on the basis of medical history, clinical symptoms, and laboratory tests.
First of all, if this disease is suspected, a biochemical blood test is performed to determine the level of urea and creatinine. Normally, the urea content in the blood is 20-35 mg%, and the residual nitrogen content is 20-45 mg%; with uremia, their level increases to 200-300 mg% or even more.
After this, it is necessary to conduct a thorough examination of the body to identify the causes of this condition. First of all, a general urine test and a general blood test are performed. Blood tests for sugar, bacteriological studies, immunological and other diagnostic methods are also indicated. Ultrasound diagnostics is mandatory.
Etiological treatment is carried out if causes characteristic of this disease are identified in the state of uremia. Renal etiology requires treatment of the underlying kidney disease.
If prerenal and postrenal uremia are identified, treatment will differ.
- Postrenal uremia suggests the presence of an obstruction to the outflow of urine, and the main therapeutic measures should be aimed at eliminating the obstacles and restoring normal outflow. In the case of nephrolith, this may include surgery, removal of stones, puncture of the ureter, catheterization of the bladder.
- Prerenal uremia in case of massive injuries, it requires measures to prevent and eliminate blockage of the renal capillaries.
In case of acute uremia, treatment should begin immediately, with hospitalization and emergency measures and intensive care.
- Intensive symptomatic therapy is aimed primarily at detoxification and rehydration of the body. Intravenous infusions of infusion drugs are carried out: saline solution, glucose, rheopolyglucin in significant volumes, taking into account the patient’s condition.
- Also held drug therapy and instrumental methods, aimed at maintaining the functions of the cardiovascular and respiratory systems of the body.
- Gives the best effect for massive injuries and necrosis hemodialysis, which allows you to remove circulating tissue breakdown products from the blood, bypassing the kidneys.
In late pregnancy, signs of impaired urine outflow and renal failure may occur due to compression of the ureter by the enlarged uterus. In such cases, a stent is placed in the ureter, restoring the lumen of the ureter and allowing pregnancy to be carried to term. The stent is removed after childbirth and uterine contraction.
All patients with chronic renal failure are prescribed a diet with limited protein and salt, which is similar in composition to the diet for glomerulonephritis. In the absence of edema, drinking plenty of fluids is recommended. Also, the diet should contain a sufficient amount of vitamins and lactic acid products. Severe forms of chronic renal failure require periodic hemodialysis sessions.
Attention
For uremia in the terminal stage of chronic renal failure, peritoneal dialysis may be the method of choice to reduce the severity of intoxication.
Main complications of uremia
Renal failure itself is a complication of renal and extrarenal diseases. However, it can lead to more severe conditions, uremic coma, urosepsis, uremic pericarditis, uremic peritonitis.
- Uremic coma increases gradually, with symptoms of renal encephalopathy. A picture of toxic brain damage is observed - hand tremors, headache, loss of consciousness, forgetfulness, intellectual and mental disorders.
- Further progression of intoxication is accompanied by confusion, lethargy and leads to stupor. If the patient is not helped at this stage, the coma progresses, which is accompanied by disruption of the vasomotor and respiratory centers. With uremic coma, the risk of death is high; after recovery from the comatose state, disturbances in intellectual and mental activity are expected.
Acute renal failure goes away after eliminating the cause, if this elimination is possible, without serious consequences for the body.
In the chronic course of renal failure, it is possible to achieve stable long-term remission. In the stage of remission and in consultation with a doctor, it is allowed to use folk remedies.
- Great importance is given to proper nutrition with limited protein and salt; patients are recommended to eat a carbohydrate diet. Cereals, vegetables and fruits in any quantity are recommended as main courses.
- Patients are recommended to drink alkaline mineral waters in moderation. Collections of medicinal herbs that have diuretic, anti-inflammatory, antiseptic, and antipyretic effects are also indicated.
- Chamomile, lingonberry leaves, rose hips, parsley, juniper, birch leaves and other medicinal herbs have a good effect.
It is worth noting
During the period of exacerbation of uremia, pre-medical care in the form of wraps and baths is recommended to alleviate the patient’s condition. The bath water should be hot, at least 40 degrees Celsius. The wraps are carried out with a wet sheet, a blanket is wrapped over the patient, and the legs should be warm.
It is acceptable to use an enema with a weak vinegar solution and take laxatives. You also need to pay special attention to the drinking regime; you can drink iced tea, water, whey.
For severe nausea, you can use ice, biting it into pieces. For severe headaches, applying ice or a cold wet towel is recommended.
Treatment of kidney failure, according to patient reviews and medical data, is expensive, lengthy and not the most pleasant. A stay in the intensive care unit in a coma and on artificial ventilation costs in Moscow from 2.5 to 20 thousand rubles per day.
In order to prevent renal failure, careful sanitation of foci of infection, correct and timely treatment of infectious kidney diseases, a rational work and rest regime, avoidance of traumatic situations, as well as treatment of chronic and systemic diseases of the urinary system and other systems and organs are recommended.
According to the Latin terminology adopted in medicine, “uremia” is not a disease, but a clinical syndrome that develops with complete “failure” of kidney function, accumulation of waste substances in the blood and poisoning of one’s own body.
What substances lead to disaster?
As a result of biological life support processes, unnecessary waste substances appear in the blood. Most of them are protein in nature, since they come from decaying old cells and dying tissues.
Nitrogenous organic compounds include:
- urea;
- ammonia;
- guanidines;
- cyanate;
- amino acids;
- creatinine;
- uric acid;
- globulins;
- glucoproteins;
- amines;
- pyridine derivatives;
- indole;
- mannitol;
- phenols.
Peptides have an average molecular weight. In healthy kidneys, they pass through the glomerular membrane and are excreted into the urine.
In addition, the “set” of slag substances includes:
- acetone;
- glucuronic acid;
- oxalic acid;
- lipochromes;
- some hormones;
- cyclic adenosine monophosphate;
- unnecessary enzymes and pigments.
The development of uremia is caused by the toxic effect of these substances on the cells of the brain, myocardium, and liver.
Mechanisms of self-poisoning of the body
In the cells of the main vital organs:
- all types of metabolism stop;
- becomes disordered in water-salt and acid-base metabolism;
- osmotic pressure is not controlled;
- secondary hormonal disorders occur;
- dystrophy increases.
What is happening leads to disruption of the functions of all organs and human life support systems. The clinical course can be called self-poisoning of the body.
What causes acute uremia?
The causes leading to uremia can occur suddenly or act gradually. Therefore, the division into 2 types is accepted.
Acute uremia – most often occurs due to impaired renal blood flow with:
- shock states;
- massive hemolysis of red blood cells;
- the entry into the blood of products of crushing muscle tissue (long-term compression syndrome);
- a severe allergic reaction with the destruction of its cells by autoantibodies.
Mass admission of patients in a state of shock with uremia accompanies terrorist attacks and earthquakes
Shock is caused by:
- severe intoxication due to infectious diseases;
- significant blood loss and dehydration;
- poisoning with toxic substances and toxins.
The damage level is defined as:
- prerenal (extrarenal) – independent of the kidneys, associated with pathology of other organs;
- renal – the main role is played by the filtration mechanism of the kidneys;
- postrenal - caused by sudden obstruction of the underlying urinary tract, a large volume of urine accumulates in the pelvis, parenchymal tissue stretches and thins, and the disappearance of nephrons is noted, up to the complete loss of organ function.
According to the International Classification ICD-10, the uremic condition is registered in two categories:
- as a consequence of kidney disease (acute or chronic renal failure) with code N17–19;
- in cases of extrarenal pathology - in section R.
In the acute form of uremia, the kidneys often suffer secondarily.
At the renal level, uremia develops when:
- acute glomerulonephritis;
- interstitial nephritis;
- pyelonephritis;
- poisoning with nephrotoxic poison;
- renal artery thromboembolism.
Acute glomerulonephritis is one of the causes of uremia
Features of the development of chronic uremia
Chronic uremia– caused by long-term diseases:
- amyloidosis;
- glomerulonephritis;
- pyelonephritis;
- polycystic disease;
- diabetes mellitus;
- prostate adenoma;
- kidney stone disease.
The morphological basis of chronic uremia is nephrosclerosis or replacement of renal tissue with scars with loss of nephrons. The main diseases leading to this outcome are:
- chronic glomerulonephritis;
- diabetic nephropathy;
- urolithiasis disease.
Kidney function is gradually impaired. This course gives the patient more chances to choose treatment. A chronic form of renal failure develops. Some of the tissue is replaced by scar tissue, and the nephrons die.
Nephrologists argue that when the glomerular filtration rate decreases below 25 ml/min, the development of terminal uremia is inevitable, regardless of the presence or absence of activity of the underlying disease. This observation confirms that, to a certain extent, nephrosclerosis depends on some nonspecific mechanisms.
These include hemodynamic and metabolic factors.
- Hemodynamic– associated with blood circulation within the renal glomeruli. Their number has already been reduced; in the remaining ones, intracapillary pressure increases. It causes increased protein excretion in the urine, activation of cytokines and accumulation of extracellular substances.
- Metabolic disorders– due to increased levels of fats, calcium, phosphates, glucose, and uric acid in the blood, low-density lipoproteins are deposited in the kidney tissue, parenchyma grows, and nephrosclerosis eventually progresses.
After a period of latent progression, at first all changes are compensated by healthy tissues. Then comes decompensation. The final stage of renal failure is azotemic, which is accompanied by all the signs of impaired metabolism and organ damage.
What are the symptoms of uremia?
By analogy with chronic renal failure, some authors consider it possible to distinguish three stages in uremia:
- latent (hidden course), symptoms of only the underlying disease;
- azotemic or retention – confirmed by laboratory and pronounced clinical signs;
- uremic or terminal - with extreme severity of symptoms and cessation of filtration activity of the kidneys.
Dry skin cracks occur in areas of physical activity
The initial symptoms of uremia appear gradually. The patient is concerned about:
- headache;
- nausea;
- insomnia;
- thirst;
- dry skin with painful cracks;
- loss of appetite.
People around notice memory impairment and indifference to the situation. When measuring body temperature, the indicator is usually low (35 degrees). Sometimes there are random twitches in the muscles.
Symptoms of severe uremia
The further course of the uremic state shows damage to internal organs by toxins:
- the nervous system reacts with lethargy, periodic hallucinations, convulsions, speech disorders;
- from the gastrointestinal tract - due to the release of nitrogenous waste through the mucous membranes, excessive irritation, uremic gastritis, enterocolitis occurs, frequent vomiting and diarrhea appear;
- the effect on the upper respiratory tract and pleural layers contributes to the manifestations of laryngitis, tracheitis, accumulation of fluid in the pleural cavity, the patient suffers from a constant barking cough, the voice becomes hoarse, shortness of breath appears, pain in the chest when breathing;
- the accumulation and secretion of waste through the salivary glands leads to severe stomatitis, painful ulcers appear on the oral mucosa, the gums swell and bleed, the tongue is dry, and the smell of urine spreads from the mouth;
- disruption of the liver is expressed in a decrease in coagulation and bleeding, in addition, intoxication of bone marrow cells is expressed in the suppression of hematopoiesis, anemia appears, and the number of platelets in the blood decreases significantly;
- due to the impact on the optic nerve, vision is significantly weakened, to the point of complete blindness, the pupils become narrow and do not respond to light.
"Uraemic frost" is clearly visible in black patients
Manifestations of the final stage of the disease
The terminal stage is accompanied by:
- an inhibited state that turns into a complete coma, a person does not respond to external stimuli due to the death of nerve cells in the brain;
- nitrogenous substances are released through the skin, so a fine white powder consisting of crystalline urea is noticed on the skin (on the nose, chin), it is called “uremic frost”;
- the heart muscle weakens sharply, fluid and waste substances accumulate between the leaves of the heart sac, salts are deposited, evidence of pericarditis is a typical friction noise heard over the heart area, it is called the “death knell”;
- damage to the respiratory and vascular centers of the medulla oblongata is expressed in rare noisy breathing (Kussmaul type), sometimes in the form of Cheyne-Stokes, blood pressure drops.
The outcome of uremic coma is the inevitable death of the patient.
In acute uremia, the above symptoms develop rapidly, and death occurs after a few days or weeks. If the chronic form develops, the condition lasts for years; patients do not feel signs of uremia for a long time.
Uremia is accompanied by suppression of the immune system, so infection may be complicated by sepsis due to renal failure. Its course is extremely severe.
Diagnostic criteria for uremia
To date, it remains unknown which specific substances from the list of slags cause intoxication. Among them, the main culprits suspected are:
- amino acids;
- hormones;
- nucleotides;
- polypeptides.
A nephrologist is a qualified specialist who takes care of a patient with uremia
Researchers are trying to separate the molecular structure and find the main toxic components. However, in clinical practice, it is most convenient to carry out a biochemical study with the determination of nitrogen-containing substances (residual nitrogen, urea, creatinine, uric acid, indican), since their standards are known to doctors.
Residual nitrogen is 14.3-26.8 mmol/l. Signs of uremia are accompanied by an increase of 10 times or more.
The level of urea in the blood with good filtration capacity is kept within the range of 2.5-8.3 mmol/l. It, unlike other slags (ammonia, cyanate, acetone, phenols), is not toxic. Easily penetrates through all barriers, pulls water with it, causes “bloating” of cells and loss of performance.
In diagnosis, it is important to notice not only the total amount of change in nitrogenous substances, but also their structure or percentage. So, if in full health urea makes up half of all nitrogenous substances, then with uremia its level reaches 80–90%.
An indicator such as creatinine depends more on a person’s muscle mass. It normally ranges from 53 to 115 µmol/l, slightly less in women than in men. It is studied together with total protein and other nitrogenous substances in the blood.
The classification of Soviet urologists N.A. Lopatkin and I.N. Kuchinsky suggests distinguishing four periods during the terminal stage. They are determined by nitrogen-containing substances, electrolyte changes, glomerular filtration rate of urine, and clinical symptoms.
Stage I - filtration decreases to 10-14 ml/min (normal value 90-130) and the level of urea in the urine drops significantly, but total diuresis remains within a liter.
IIa – urine output decreases to oliguria, residual nitrogen in the blood increases, a shift in acid-base balance towards acidosis appears, changes in the heart muscle, liver and other organs are still reversible.
IIb – in addition to IIa, pronounced signs of damage to internal organs appear.
III - characterized by increasing intoxication, an increase in creatinine to 2.0 mmol/l, urea - up to 66 mmol/l and higher, potassium content - more than 7 mmol/l. Clinically, cardiac decompensation and liver dysfunction due to cell degeneration are determined. It is practically impossible to get rid of or reduce intoxication even with the help of hemodialysis.
IV – a pronounced clinical picture appears, the content of nitrogenous substances in the blood increases significantly, the protein content is sharply reduced, especially albumin. The activity of all organs and systems is disrupted.
If the etiology of the coma is unclear, differential diagnosis of uremia with diabetic coma and adrenal insufficiency is carried out.
With uremia, urea is deposited on the leaves of the pericardium and cardiac sac, the characteristic noise is of diagnostic value
How can you help the patient?
Patients are treated in a hospital. The diet represents a version of table No. 7 with a limitation of salt, protein, dairy products, and pureed fruit.
Treatment of uremia is impossible without hemodialysis. The method provides replacement of kidney function. It is prescribed for:
- creatinine values more than 700 µmol/l;
- hyperkalemia.
Imitation of the functioning of the renal membrane is achieved by the composition of the dialysate fluid and the presence of a filter that retains toxins and nitrogenous wastes. The operation of the device is controlled by biochemical parameters and electrolyte composition of the blood.
Peritoneal dialysis may be the treatment of choice. The abdominal cavity is pierced with special trocars and catheters are inserted, through which up to 50 liters of liquid are injected with its simultaneous removal.
Etiological treatment (directed at the main cause) is possible in the initial stages of the disease. Anti-inflammatory therapy, the use of immunosuppressants, and anticoagulants for nephritis are important. Surgical interventions are possible to improve urine flow if blockage is detected at some level. For example, during pregnancy a stent is placed in the ureter.
To maintain water-electrolyte balance and combat acidosis, small volumes of alkaline solutions, Hemodez, and Reopoliglucin are infused, taking into account compensation of cardiac activity.
Progressive uremia, even with the use of hemodialysis, can only prolong the patient’s life, but not cure the underlying disease. There is only one option left - kidney transplantation. The problem is difficult to solve; donor selection is delayed; tissue incompatibility is possible, despite a successful operation.
How to care for a patient with uremia at home?
Given the unfavorable prognosis, relatives often prefer to care for the patient themselves.
Gastric lavage should be done every other day
Caring for a patient with uremia requires a lot of patience on the part of loved ones. The patient needs:
- daily hygienic baths to cleanse the skin of released toxins and prevent suppuration;
- frequent change of bed linen;
- wiping the face several times a day with a swab moistened with a soda solution to remove crystalline uric acid salts;
- if the patient is conscious, then gastric lavage is recommended using a rubber tube or by drinking a liter of water and then pressing on the root of the tongue;
- rinsing the mouth with a warm chamomile decoction, soda solution for stomatitis;
- cleansing enemas with sodium bicarbonate solution;
- feeding pureed dishes from milk porridges, vegetables, fruits.
Uremia - despite numerous studies in this area, is still an inaccessible area of therapy. The development of new hemodialysis machines provides hope for longer survival for patients.
