Azotemia

One of the variants of nephrotoxic lesions is azotemia - this is a condition accompanied by impaired renal function against the background of excess nitrogen compounds in the bloodstream. If the course of such a pathology is severe, then the rapid development of acute renal failure is possible.

If we translate the name "azotemia" from Latin, it literally means "nitrogen in the bloodstream." Sometimes this condition is called uremia - that is, "urine in the bloodstream", but the concepts are not exactly the same: azotemia is usually the basis of uremia.

The essence of the pathology is that during the breakdown of protein, nitrogenous compounds such as uric acid, urea, creatinine, ammonia, purines and indican are released. The presence of such products in the blood is responsible for the development of azotemia.

Epidemiology

Interestingly, many aspects of azotemia are still unclear. With that said, azotemia is fairly common, accounting for 8% to 16% of hospital admissions and furthermore, it is associated with a significantly higher risk of death. [1]

Azotemia is the only reliable criterion for the development of renal failure, including its chronic form, in which serum creatinine values exceed 0.18 mmol / liter, and urea - 8 mmol / liter (the norm is 0.12 mmol / liter and 6 mmol / liter respectively). Uremia is spoken about when the mass of functioning nephrons decreases to less than 20-25% of the required amount, and with severe azotemia (creatinine level is more than 0.45 mmol / liter, with urea more than 25-30 mmol / liter).

The frequency of primary detection of azotemia is 5-20 cases per hundred population per year. Most often, pathology is diagnosed in patients 45-65 years old. [2]

Causes of the azotemia

The blood is continuously filtered by the kidneys, which is necessary for the elimination of waste products and maintenance of electrolyte balance in the circulatory system. When blood flow to the kidneys decreases, filtration is slowed down, which leads to an accumulation of products that must be excreted from the body. This condition can reach the level of intoxication.

The accumulation of nitrogenous compounds (for example, urea and creatinine) is typical for azotemia and can significantly complicate the body's work. Such a pathology is provoked by any disorders that impair renal blood circulation - including insufficient cardiac activity, shock, dehydration, severe blood loss, etc. [3]

In general, we are talking about the following causes of azotemia:

• disorder of renal circulation, decreased perfusion due to a drop in circulating blood volume, congestive cardiac function, weakening of systemic vascular resistance, a decrease in functional arterial volume, which can be caused by sepsis, hepatorenal syndrome, malfunctioning of the renal artery;
• acute or  chronic renal failure , damage to the glomeruli, tubules, capillaries;
• bilateral obstruction of the ureter with tumors or stones, retroperitoneal fibrosis,  neurogenic bladder , obstruction of the urinary neck due to an enlarged prostate gland or adenocarcinoma.

Azotemia can be combined and manifested against the background of other pathologies.

Risk factors

Dangerous factors that are important in the development of azotemia can be:

• traumatic shock;
• crash syndrome, damage and necrosis of muscle tissue;
• electrical injuries;
• thermal damage (frostbite, burns);
• severe blood loss;
• anaphylactic shock;
• peritonitis, pancreatitis, pancreatic necrosis, cholecystitis;
• dehydration, electrolyte imbalance, which may be associated with debilitating vomiting, diarrhea, etc.;
• severe course of infectious pathologies;
• bacterial shock;
• obstetrics pathology (sepsis, eclampsia, postpartum blood loss, nephropathy with premature placental abruption, etc.);
• cardiogenic shock;
• intensive loss of fluid during feverish conditions, physical overload, burns;
• intensive loss of fluid by the kidneys (with diabetes insipidus, therapy with diuretics, kidney disease with polyuria, decompensated diabetes mellitus, etc.);
• disturbed flow of fluid into the body.

The risk group for the development of azotemia includes patients with high blood pressure, diabetes mellitus, obesity, as well as persons over the age of 50, with various kidney diseases (including familial), and smokers. People at risk are advised to regularly visit a doctor for a routine examination and basic clinical tests. [4]

Pathogenesis

Urea is the final product of protein breakdown in the body, it is formed in the liver. In the course of excretion of urea by the kidneys, the residues of "excess" nitrogen are excreted. Partially excreted by the sweat glands (which causes the specific "aroma" of sweat).

Urea allows you to maintain moisture in the body, normalizes mineral metabolism. However, an excess of this substance harms tissues and organs. Its level depends on the balance of the processes of production and excretion from the body. A decrease in concentration is noted against the background of low-protein nutrition, starvation, as well as with hepatic pathologies, chemical intoxication (arsenic, phosphorus-containing substances), during pregnancy or hemodialysis.

Azotemia caused by the following reasons is considered clinically significant:

• kidney disease, in which there is a violation of the excretion of urea from the circulatory system (pyelonephritis, glomerulonephritis, renal amyloidosis, acute renal failure, hydronephrosis);
• predominantly protein nutrition, dehydration, inflammatory pathologies, accompanied by increased protein breakdown;
• mechanical blocking of the excretion of urea by the kidneys (stone formation, tumors).

Azotemia causes an increase in the presence of urea, creatinine, uric acid, methylguanidine, phosphates, etc. In the bloodstream. Urea and creatinine are directly dependent on the degree of nephron dysfunction. There is no information on the toxic effects of creatinine, but an excess amount of urea can lead to headaches, apathy, myasthenia gravis, arthritis. With the development of chronic renal failure, the tubular-glomerular balance is disturbed, and protein catabolism increases. [5]

Symptoms of the azotemia

The clinical picture in azotemia develops in an increasing progression, depending on the damage to certain organs and systems, as well as on an increase in the level of nitrogenous compounds in the circulatory system.

The following are considered basic symptoms:

• a sharp decrease in the volume of urine excreted (oliguria), up to complete cessation (anuria);
• thirst, dryness of mucous membranes and skin;
• the appearance of various types of bleeding, bleeding, hematomas, etc.;
• the appearance of edema, up to generalized swelling of soft tissues;
• drops in blood pressure indicators;
• increased heart rate.

At the initial stage, patients complain of weakness, fatigue, apathy, and impaired appetite. Signs of anemia are noted early, due to blood loss, iron deficiency and low formation of erythropoietin. Over time, general weakness and drowsiness increase, apathy appears (uremic encephalopathy), muscle weakening with convulsive twitching, itching of the skin, paresthesia, bleeding. Development of pseudogout is possible. Symptoms can increase rapidly or gradually.

The picture of severe, irreversible on dialysis, azotemia includes pronounced dyspeptic symptoms (indomitable vomiting, diarrhea, anorexia), stomatogingivitis, cheilitis, pale and yellowing of the face, dry skin. Blood pressure rises significantly, cardiomegaly, reginopathy, and congestive heart failure are noted. The skeletal system is affected in the form of osteoporosis, osteomalacia. Neurological symptoms are represented by myopathy and encephalopathy.

In elderly patients, signs of coronary atherosclerosis are increasing .

First signs

The adequate amount of nitrogen in the bloodstream equates to 18-40 mg / liter. If this content rises for any reason, then they talk about the development of pathology, namely, about azotemia.

Doctors talk about the following main signs of the presence of nitrogen in the blood:

• Disorders related to the digestive tract: the smell of acid or ammonia from the mouth, intestinal disorders, nausea with vomiting, profuse diarrhea (sometimes with bloody streaks), signs of anemia.
• Disturbances in the work of the nervous system: trembling of the muscles of the arms and legs, emotional changes (apathy is replaced by a state of excessive excitement), drowsiness, shortness of breath.
• Other disorders (bleeding, dry skin, general itching).

These signs, as a rule, are combined with each other and speak of the development of renal failure. If treatment measures are not taken in a timely manner, then the picture is aggravated, and the chances of a cure are reduced.

Changes in the oral cavity with azotemia

At a doctor's appointment, when examining patients with azotemia, the following symptoms can be noted:

• general blanching of the skin ("anemic" complexion);
• darkening of the nails;
• abrasions on the skin, scratches associated with intense itching.

Patients complain of dryness in the mouth, pain in the gums, bleeding, changes in taste, the appearance of a metallic taste and an unpleasant odor. Some patients have pain in the tongue or the inside of the cheeks. The frequency of these pathological signs is variable. For example, dryness in the oral cavity is detected in 20-30% of cases, bleeding of the gums - in almost every second case, taste disturbances - in 25% of cases, and uremic breath odor can be observed in almost 80% of patients.

Uremic stomatitis becomes a fairly common concomitant disease with azotemia. Pathology develops with an increase in serum urea by more than 150 mg / ml, but the full picture of the appearance of the disorder has not yet been clarified. Pathological elements are more often found on the inner surface of the tongue and the oral mucosa. Stomatitis does not respond well to treatment until the blood urea level is normalized, after which it heals on its own for several weeks.

Stages

The course of chronic azotemia is subdivided into curable and terminal stages. The curable stage is completely reversible with the timely appointment of treatment and the elimination of the cause of the pathology. If we are talking about a severe case, when the period of anuria lasts for several days, then a fatal outcome can occur as a result of hyperkalemia , acidosis, and disturbances in water and electrolyte metabolism .

The terminal stage is characterized by a pronounced decrease in glomerular filtration with impaired renal adaptive mechanisms. The situation is aggravated by high blood pressure, pericarditis, and circulatory disorders.

In the terminal stage, the risk of death of the patient increases sharply. To prolong the patient's life, regular dialysis is used. Death can occur as a result of cardiovascular disorders, hyperkalemia, infectious complications, sepsis, hemorrhages, as well as due to the development of uremic coma .

Forms

Azotemia has several classifications, depending on the causative factor of the onset of the disorder. However, all types of azotemia in renal failure share several common characteristics: they typically have a decrease in renal glomerular filtration rate and an increase in blood urea nitrogen and serum creatinine levels. The index of the ratio of urea nitrogen to creatinine is used: this indicator is necessary to assess the type of azotemia. The normal index is <15.

• Prerenal azotemia is triggered by a decrease in cardiac output and develops as a result of a deficiency in the renal blood supply. Such a violation can occur due to shock, bleeding, decreased circulating blood volume, cardiac insufficiency, etc. The nitrogen / creatinine index in the prerenal form of azotemia is more than 15. The reason lies in the filtration failure of nitrogen and creatinine. Glomerular filtration rate decreases as a result of hypoperfusion, which leads to an overall increase in nitrogen and creatinine. However, due to nitrogenous reabsorption in the proximal tubule, the concentration of nitrogen in the bloodstream increases rapidly.
• Renal azotemia, renal azotemia in most cases causes the development of uremia. This pathology occurs with various disorders of renal function, with any parenzymal lesions. The basic causes are glomerulonephritis, renal failure, acute tubular necrosis, etc. The nitrogen / creatinine index ratio in renal azotemia is within normal limits. Glomerular filtration rate is decreased, and blood nitrogen and creatinine levels are increased (although nitrogenous reabsorption is not observed as a result of damage to the proximal tubules). It turns out that nitrogen with creatinine is excreted with urinary fluid, which determines the normal index of the index. Renal retention azotemia is accompanied by insufficient excretion of urea with urinary fluid with normal entry into the bloodstream, which is associated with weak renal excretory function.
• Postrenal azotemia is explained by the appearance of an obstruction to adequate urinary flow below the renal level. The cause of the violation may be a congenital developmental defect (for example, vesicoureteral reflux), blockage of the ureter with a stone, an increase in the uterus during pregnancy, a tumor process, an enlargement of the prostate gland. Increased resistance to urinary flow can trigger hydronephrosis. In postrenal azotemia, the nitrogen / creatinine index exceeds 15. Increased nephron pressure provokes an increase in nitrogenous reabsorption, which increases its ratio in the index.
• Production azotemia (it is also adrenal) is characterized by excessive formation of slag substances, which becomes possible with an excess of protein intake in the body, with dehydration, inflammatory processes, which are accompanied by strong protein destruction. In these situations, urea should be rapidly excreted through the kidneys, however, when a concentration of more than 8.3 mmol / liter is reached, one speaks of the development of renal failure.
• Subrenal azotemia results from the mechanical blocking of the excretion of urea by the kidneys, as a result of which it is absorbed back into the bloodstream. The root cause of the violation can be stones, tumor processes (in particular, prostate adenoma).
• Transient, or transient azotemia, is a series of spontaneously passing disorders that can be triggered by a variety of factors that cause a temporary increase in the level of nitrogen in the blood. The transient form of azotemia can be functional (in a healthy person under the influence of temporary reasons) and organic, due to pathological conditions (acute intoxication, infections, digestive pathologies, taking certain medications, etc.).

Hypercalcemia and azotemia

Hypercalcemia  is an excess of blood calcium levels of more than 2.5 mmol / liter. Common causes of this condition are tumors (of the respiratory system, mammary glands), endocrinopathies, acute renal failure, taking certain medications (retinol, thiazides, calcium supplements), sarcoidosis, prolonged immobilization, hereditary pathologies.

In acute renal failure, the early diuretic phase of hypercalcemia develops as a result of resorption of calcium deposits in soft tissues and accelerated production of the vitamin D metabolite by the renal tissue.

Hypercalcemia leads to spasm of afferent arterioles, slows down the renal circulation (mainly in the cortex), inhibits the glomerular filtration and reabsorption in the tubules of magnesium, potassium and sodium, enhances the reabsorption of bicarbonate and the excretion of calcium and hydrogen ions.

With a prolonged course of hypercalcemia in the kidneys, signs of interstitial fibrosis and minimal glomerular changes are found. Since the intrarenal calcium level increases from the cortex to the papilla, with this disorder, calcium crystals fall out mainly in the medulla, which leads to nephrocalcinosis and nephrolithiasis . Among other clinical manifestations, urinary syndrome is usually noted in the form of moderate proteinuria, erythrocyturia, as well as prerenal azotemia due to dehydration, acute renal failure, or chronic renal failure, which developed against the background of obstructive pyelonephritis.

Complications and consequences

Regardless of how acutely the state of azotemia develops, pathology adversely affects all organs and systems of the body. First of all, complications affect the brain, the central nervous system, and the digestive organs also suffer.

The terminal condition, which is a consequence of both acute and chronic azotemia, can be azotemic (uremic) coma. Its development is explained, first of all, by the accumulation of a large amount of nitrogen metabolism products in the bloodstream, which causes an increase in intoxication.

Acute renal failure leads to the appearance of hyperazotemia as a result of impaired renal excretory function and increased protein catabolism. In the circulatory system, the content of magnesium and potassium increases, the level of calcium and sodium decreases. Such violations are manifested by a violation of the heart rhythm, general weakness, drowsiness, and disturbance of consciousness. Cardiac activity is strongly inhibited, consciousness can be completely lost, which may be associated with an increase in the concentration of magnesium in the blood serum, or with a decrease in the level of sodium.

In chronic renal failure, a  coma  develops against the background of severe oliguria (anuria), azotemia, ammonia, metabolic acidosis. With azotemia, renal nitrogen excretion is disturbed, which leads to increased excretion of urea through the skin, pleura, and digestive organs. Excretion of urea through the intestine entails the formation of toxic ammonium derivatives, which is considered particularly dangerous. Severe intoxication is noted, the signs of which are depression of consciousness, thirst, nausea, vomiting. The skin becomes dry, gray, covered with small hemorrhagic rashes and, as it were, powdered, which is associated with the deposition of urea crystals on it. The mucous membrane of the oral cavity is damaged by ulcerative necrotic foci. Difficulty breathing. Possible development of toxic pneumonia and hepatitis.

Diagnostics of the azotemia

Early diagnosis of azotemia can be challenging. First, the asymptomatic course of the early stages of azotemia in chronic renal failure is not excluded, which is typical for patients with chronic pyelonephritis, latent nephritis, and polycystic disease. Secondly, because of the polymorphism of damage to internal organs, nonspecific signs can come to the first position: anemia, hypertension, asthenia, gout, osteopathy.

The doctor should be alerted by the combination of normochromic anemia with impaired urination, arterial hypertension. However, early diagnosis is based mainly on laboratory and biochemical studies.

The following analyzes are performed:

• general blood analysis;
• general urine analysis;
• study of  blood urea nitrogen  (AMK);
• study of  creatinine levels  or 24-hour urine analysis.

The main indicators of kidney functionality are creatinine and urea. The formation of creatinine occurs in the muscles, after which it enters the bloodstream. Creatinine takes part in energy interstitial processes. Its excretion is carried out by the kidneys, therefore, the indicator of the presence of this product in the blood is important in the diagnostic plan. [6]

Urea is a waste product of the body. It is formed as a result of protein breakdown in the liver and is excreted from the bloodstream by the kidneys. The accumulation of urea occurs in pathologies - primarily of the urinary system.

With azotemia, urine analysis shows a low sodium content, a high ratio of urine creatinine and serum creatinine, a high ratio of urinary fluid urea and blood serum urea, an increase in urinary concentration (osmolarity and specific gravity indicators). But these values are of little help in diagnosis: prerenal and postrenal forms can be determined based on the nitrogen / creatinine index.

Instrumental diagnostics includes the following studies:

• ultrasound examination of the kidneys and abdominal organs (allows you to detect an increase in renal volume, calculi in the renal pelvis or urinary tract, tumor processes);
• radioisotope renal scan (helps assess renal perfusion, identify obstruction);
• computed and magnetic resonance imaging;
• chest x-ray (to exclude the accumulation of fluid in the pleural cavity, pulmonary edema);
• excretory urography (with suspicion of obstruction of the renal venous vessels);
• renal angiography (to exclude vascular causes of pathology - for example, stenosis of the renal artery, dissection of the abdominal aortic aneurysm, ascending thrombosis of the inferior vena cava), nephrobiopsy (with an unclear etiology of the disease, with prolonged anuria, in difficult diagnostic cases);
• electrocardiography, electroencephalography, ultrasound of the heart;
• fundus examination.

Differential diagnosis

Differential diagnosis is carried out with uremic coma, diabetic and hepatic coma. The following expert consultations are shown:

• rheumatologist (with symptoms of systemic pathology);
• hematologist (to exclude blood diseases);
• toxicologist (with severe intoxication);
• resuscitator (for shock, emergency conditions);
• ophthalmologist (to determine changes in the fundus);
• cardiologist (with a pronounced increase in blood pressure, ECG abnormalities);
• infectious disease specialist (with viral hepatitis and other infectious pathologies).

Also, azotemia should be differentiated from such diseases:

• kidney stone disease;
• kidney tuberculosis ;
• renal colic ;
• polycystic kidney disease ;
• pyelitis, pyelonephritis ;
• hydronephrosis , amyloidosis.

Differences between uremia and azotemia

Azotemia is a cardiac sign of  acute renal failure , which determines the severity of its course. For an acute process (not chronic), an increased rate of increase in azotemia is typical: an increase in the level of creatinine in the blood can be 5 mg / liter / day, and urea nitrogen - 100 mg / liter / day. During the aggravation of azotemia, acidosis, electrolyte metabolism disorders, the patient has muscle twitching, drowsiness, depression of consciousness, shortness of breath associated with nephrogenic pulmonary edema and renal acidosis. Plasma composition changes:

• the levels of creatinine, urea, residual nitrogen, phosphates, sulfates, potassium, magnesium increase;
• the content of calcium, chlorine and sodium decreases.

Azotemia is the basis of uremia, a specific clinical syndrome of renal failure progression. If they talk about azotemia in acute insufficient renal function, or in the early stages of chronic pathology, then uremia corresponds to the terminal stage of chronic renal failure.

Both azotemia and uremia are not separate pathologies, but only a consequence of kidney damage, a complication of other diseases.

Treatment of the azotemia

Conservative treatment for azotemia involves stopping the progression of the pathological process, eliminating factors that can aggravate the course of azotemia (infections, imbalance in water and electrolyte balance, drug nephrotoxicity, etc.), correction of metabolic and hormonal disorders. [7]

It is imperative to follow a low-protein diet and control renal blood pressure elevation to eliminate azotemia.

Against the background of a well-adjusted diet, there is a significant decrease in the intensity of azotemia, an improvement in mineral metabolism, and the preservation of residual renal functionality. The effectiveness of the diet is assessed as the signs of azotemic intoxication decrease, the levels of phosphates and urea in the blood decrease, and the pH and serum bicarbonate levels stabilize.

At an early stage of the onset of azotemia, pathogenetic therapy is carried out, the features of which are determined, depending on the cause of the disorder. Plasmapheresis is prescribed, based on the patient's condition and the degree of intoxication. The removed plasma is replaced with albumin or fresh frozen plasma. In case of violations of hemodynamic processes, anti-shock measures are carried out - for example, blood transfusion, drip injection of 0.2% norepinephrine (1 ml per 200 ml of saline). If the root cause of azotemia is bacterial shock, then in addition to anti-shock measures, antibiotic therapy is prescribed. [8]

The initial stage of the disease involves intravenous administration of furosemide (200 mg 4 times a day), or 10% mannitol (1 g per kilogram of patient weight). Further treatment is aimed at regulating homeostasis.

Intramuscular administration of testosterone propionate 50 mg per day, or retabolil 100 mg per week is performed. If antibiotic therapy is indicated, then the dosage of antibiotics is reduced by half, which is associated with limited renal excretory function. It is undesirable for azotemia to prescribe ototoxic agents - in particular, streptomycin, monomycin, neomycin.

Acidosis is eliminated by intravenous injection of 100-200 ml of 5% sodium bicarbonate solution.

If oliguria continues, signs of uremia increase, then the patient is transferred to the hemodialysis unit for extracorporeal cleansing using an artificial kidney or  peritoneal dialysis .

Indications for  hemodialysis :

• increasing level of azotemia with impaired diuresis;
• the indicator of plasma urea is more than 2 g / liter, potassium - 6.5 mmol / liter;
• uncompensated metabolic acidosis;
• signs of developing acute uremia.

Contraindications to hemodialysis:

• cerebral hemorrhage;
• internal bleeding;
• severe form of hemodynamic disorders, accompanied by collapse.

Sorbent preparations are used in combination with dietary food. Such agents adsorb ammonia and other toxic substances in the digestive system onto their surface. Adsorbix, Enterodez, Karbolen can be used as sorbents. [9]

Anti-azotemic drugs tend to increase the excretion of urea. One of the most common medicines in this group is Hofitol - a purified herbal extract of artichoke, available in the form of tablets and ampoules for intravenous and intramuscular injections. A similar anti-azotemic effect is possessed by the drug Lespenephril, the plant basis of which is Lespedeza capitate. Lespenephril is taken more often by mouth, starting with a couple of teaspoons per day. In addition, intravenous or intramuscular administration of the drug is possible. 

Medicines

Medicines are prescribed by a doctor, depending on the severity of azotemia, the severity of clinical manifestations and the presence of other pathological symptoms. Perhaps the appointment of such medications:

• Furosemide 40 mg in the morning, under the control of daily urination, up to three times a week. Possible side effects: lowering blood pressure, tachyarrhythmias, dizziness, headache, tinnitus.
• Adsorbix 1 capsule three times a day, under the control of creatinine levels. Possible side effects: constipation, nausea, diarrhea, dysbiosis.
• As a potassium antagonist, calcium chloride or gluconate 10% 20 ml is used intravenously for 3 minutes with repeated administration of the same dosage if there are no changes in the electrocardiogram.
• Glucose 20% 500 ml in combination with insulin (soluble human short effect) 50 IU intravenously, 15-30 IU every three hours for two days, until the potassium content in the bloodstream stabilizes.
• Sodium bicarbonate 5% intravenously. It is important to take into account that with prolonged use of the drug, alkalosis can develop, which is accompanied by loss of appetite, nausea, stomach pain, flatulence.
• Dextrose 5% 500 ml intravenously drip to fill the lack of circulating blood volume. A more complete and accelerated assimilation of dextrose occurs against the background of the introduction of insulin (3 IU per 1 g of dry preparation).
• Furosemide 200 mg intravenously under the control of the hourly amount of urine.
• Dopamine in the amount of 3 mg / kg / minute intravenously drip for six hours, under the control of blood pressure and heart rate. Side effects from the introduction of a cardiotonic drug: changes in blood pressure and heart rate, vasospasm, bronchospasm, tremors, motor restlessness, anxiety, as well as local reactions.

As additional drugs, it is possible to prescribe:

• norepinephrine, mesotone, infesol, albumin, colloidal and crystalline solutions, fresh frozen plasma, antibiotics, blood transfusion drugs, etc.;
• methylprednisolone (4 or 16 mg tablets);
• cyclophosphamide (intravenous);
• torasemide (tablets of 5, 10 or 20 mg);
• rituximab (intravenous infusion 100 mg, 500 mg);
• normal human immunoglobulin (10% solution, 100 ml).

As drugs for emergency care, it is possible to use medicines to eliminate pulmonary edema, anticonvulsants and antihypertensive drugs.

Physiotherapy treatment

Physiotherapy is a specialized area of clinical medicine that uses natural and artificial effects on the body:

• climatotherapy;
• fresh and mineral waters;
• healing mud;
• ozokerite;
• electromagnetic field, electric current, laser, etc.

With azotemia, mechanical, electromagnetic, thermal effects are used, which contribute to anesthesia, stimulation of metabolic processes, trophism, blood circulation, and high-quality urine excretion.

Magnetotherapy has a sedative, antihypertensive, anti-inflammatory, decongestant, analgesic, trophic-regenerating effect, activates cellular and humoral immunity.

Laser treatment helps to optimize microcirculation, launch recovery processes, and stimulate the glucocorticoid function of the adrenal glands.

Herbal treatment

Azotemia is a serious enough pathological condition in which it hardly makes sense to hope for an alternative treatment. It is important to listen to your doctor's advice and follow them, as well as stick to a strict diet.

As a supplement, you can use medicinal plants, if the attending doctor does not object to this.

• Flaxseed normalizes renal blood flow and increases the elasticity of the vascular walls, which has a positive effect on the functionality of the kidneys. It is recommended to consume about 25-30 g of seed daily - in the form of a decoction, infusion, or add to salads, cereals, jelly.
• Lingonberry leaves have antibacterial properties, prevent the development of bacterial infection in the kidneys, and prevent stone formation. It is optimal to use the infusion (tea) from the leaves, with the addition of a small amount of honey.
• Elderberries strengthen blood vessels, have an antibacterial and diuretic effect, enhance the protection of the urinary system, and increase resistance to infection. The berries are ground with honey and consumed daily for 2 tbsp. L. As a supplement, you can drink an infusion of plant flowers.
• Rosehip fruits are famous for their anti-inflammatory, diuretic, antispasmodic properties. They cleanse the kidneys, facilitate their function. A decoction with honey is prepared from rose hips, which is consumed during the day instead of tea.

In addition to the listed medicinal plants, the herbal pharmacy collection Fitonefrol has a good healing effect, containing a bearberry leaf, calendula flowers, dill seeds, eleutherococcus root, mint leaf. This collection improves urination, eliminates spasms and inhibits the development of the inflammatory process. In order to avoid complications, alternative treatment can be taken only after examination and consultation with a doctor.

Diet

The diet for azotemia should include about five meals in fractional portions.

In the early days of illness (at least three days), meals should be practically salt-free. Optimally arrange contrasting days (apple, banana, watermelon, pumpkin, etc.). Further, from the fourth day, a diet is prescribed with a restriction of protein products to 20-40 g / day, depending on the degree of renal failure (0.6-1 g per kilogram of body weight). It is equally important to provide the body with the necessary amino acids and vitamins.

It is necessary to correctly calculate the daily calorie content of the diet: approximately 35 kcal / kg of body weight.

The diet for azotemia should include foods that are low in protein and sufficient in calories. In addition, you need to limit foods containing a large amount of potassium (raisins and potatoes, dried apricots, etc.), phosphates (dairy products), magnesium (fish and cottage cheese). Excludes alcohol, coffee and tea, chocolate and cocoa. Table salt is minimized to 3 g per day. Spicy condiments, sorrel and spinach, smoked foods are also excluded.

Dishes are steamed, boiled or baked. The volume of free liquid can be 1.5-2 liters.

Recommended products for azotemia:

• protein-free or bran bread (no salt);
• eggs (no more than one per day);
• butter or vegetable oil;
• cabbage, carrots, beets, onions and green onions;
• green peas, radishes, fresh cucumbers;
• parsley;
• tomato paste;
• pumpkin, watermelon, melon;
• sago;
• corn starch.

Natural fruit and vegetable juices, rosehip decoction are used as drinks.

Sample menu for the day:

• First breakfast: baked apples, toast, apricot juice.
• Second breakfast: berries, yogurt.
• Lunch: vegetable soup, cabbage and carrot salad, pumpkin casserole, jelly.
• Afternoon snack: rosehip broth, toast.
• Dinner: vegetable pilaf, cucumber and green onion salad with vegetable oil.

Signs of azotemia disappear faster with diet # 7A. As the condition of the patients improves, they are transferred to the dietary table No. 7B. Diet No. 7A is used for no more than 20-25 days, since against the background of such nutrition, the emaciation of patients, an increase in hunger are often noted. Periodic alternation of the indicated treatment tables is possible.

Surgery

Modern medicine involves the use of three methods of active treatment of severe azotemia and uremia. We are talking about hemodialysis, peritoneal dialysis and kidney transplantation.

Hemodialysis is performed by connecting an arteriovenous fistula to an "artificial kidney" apparatus. Electrolytes and nitrogenous slags penetrate through a semi-permeable membrane, and moisture is removed under the influence of hydrostatic blood pressure (ultrafiltration). The standard type of hemodialysis is performed intermittently every other day (dialysis term 12 to 15 hours per week) with an acetate or bicarbonate buffer.

Peritoneal dialysis is performed by catheterization and the introduction of a special solution for dialysis into the abdominal cavity. A semi-permeable membrane that retains nitrogenous toxins and electrolytes, in this situation, is represented by the peritoneal mesothelium. Removal of moisture in the form of ultrafiltration is carried out under the influence of an osmotic pressure gradient, which is achieved by using liquids with a high glucose content (dextrose).

A kidney transplant is a surgical procedure in which a healthy kidney from another person is transplanted to a patient with chronic renal failure. A kidney transplant is usually obtained from a living donor (often a relative) or from a deceased person.

Prevention

Azotemia is sometimes very insidious, proceeding asymptomatically until the moment when the pathology becomes severe. Preventive diagnostics and routine blood and urine tests can help to timely detect disorders of renal function and begin treatment even before the development of irreversible consequences for the body. A number of basic prevention rules are known, the observance of which will help prevent the development of azotemia.

1. Activity, moderate physical activity can stabilize blood pressure, optimize blood circulation and reduce the burden on the urinary system. Regular gymnastics helps to avoid stagnation of blood in the small pelvis and the appearance of inflammatory reactions in the genitourinary organs.
2. A healthy balanced diet and maintaining a normal weight is one of the important preventive measures to prevent the development of diabetes mellitus, cardiovascular pathologies, and chronic kidney disease. For normal kidney function, it is important not to overload the organs, therefore, it is necessary to adjust both the diet and the drinking regime. Food should enter the digestive system evenly, without overeating and starvation. Food may contain only minimal amounts of salt and seasonings. Drinking water should be clean: carbonated drinks and store juices should be limited.
3. Smoking and drinking alcohol impairs blood flow to the kidney area, which can interfere with kidney function. Passive smokers are also at risk.
4. A preventive visit to a doctor always plays an important role, especially if a person is at risk of developing kidney disease.
5. Blood pressure control is another important preventive step to prevent both azotemia and other genitourinary and cardiovascular pathologies.

Forecast

If the cause of azotemia is eliminated quickly and completely, then the short-term prognosis of the disorder for patients who do not suffer from other diseases can be called favorable. The serum creatinine content in most cases normalizes (or almost normalizes) within 1-3 weeks. For patients with concomitant pathologies, even against the background of a mild course of acute renal failure, the prognosis worsens. [10]

The outcome of azotemia is more favorable for patients whose condition does not require intensive care measures. Mortality rates are increasing significantly:

• with the development of anuria or severe oliguria;
• with severe concomitant pathologies.

Patients who survived severe azotemia and acute renal failure are at increased risk of developing chronic kidney damage.

High-quality treatment of the underlying disease, which led to the appearance of azotemia, has a positive effect on the prognosis. Elimination of inflammatory processes in the urinary system reduces the severity of signs of renal failure.

In order to avoid negative consequences, patients need to avoid hypothermia, excessive physical and stressful stress. Patients need lightweight living and professional conditions. Prolonged rest may be beneficial after treatment. 

With late seeking medical care, in the absence of treatment, azotemia has a poor prognosis. The disease progresses, acquires a chronic course, and later complications join.