Azotemia

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

Azotemia, translated from Latin, literally means "nitrogen in the bloodstream." Sometimes this condition is called uremia, or "urine in the bloodstream," but these concepts are not quite the same: azotemia is usually the basis of uremia.

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

Epidemiology

Interestingly, many aspects of azotemia remain unclear. That said, azotemia is quite common, accounting for 8% to 16% of hospitalizations, and is furthermore 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 levels exceed 0.18 mmol/liter, and urea levels exceed 8 mmol/liter (the norm is 0.12 mmol/liter and 6 mmol/liter, respectively). Uremia is indicated by a decrease in the mass of functioning nephrons to less than 20-25% of the required amount, and by severe azotemia (creatinine levels greater than 0.45 mmol/liter, with urea greater than 25-30 mmol/liter).

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

Causes azotemia

Blood is continuously filtered by the kidneys, which is necessary to remove waste products and maintain electrolyte balance in the circulatory system. When the blood flow to the kidneys decreases, filtration slows down, which leads to the accumulation of products that should be removed from the body. This condition can reach the level of intoxication.

The accumulation of nitrogen compounds (for example, urea and creatinine) is typical for the state of azotemia and can significantly complicate the body's work. Such pathology is provoked by any disorders that worsen 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:

• renal circulatory disorder, decreased perfusion due to a decrease in circulating blood volume, congestive cardiac function, weakening of systemic vascular resistance, decreased functional arterial volume, which can be caused by sepsis, hepatorenal syndrome, and abnormal functioning of the renal artery;
• acute or chronic renal failure, damage to glomeruli, tubules, capillaries;
• Bilateral ureteral obstruction by tumors or stones, retroperitoneal fibrosis, neurogenic bladder, obstruction of the bladder neck due to prostatic enlargement 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 may include:

• traumatic shock state;
• crush syndrome, damage and death of muscle tissue;
• electrical injuries;
• thermal injuries (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;
• obstetric pathologies (sepsis, eclampsia, postpartum blood loss, nephropathy with premature placental abruption, etc.);
• cardiogenic shock;
• intense loss of fluid during feverish conditions, physical overload, burns;
• intensive loss of fluid by the kidneys (in diabetes insipidus, therapy with diuretics, kidney diseases with polyuria, decompensated diabetes mellitus, etc.);
• impaired fluid intake into the body.

Those at risk of developing azotemia include patients with high blood pressure, diabetes, obesity, as well as people over 50 years of age, with various kidney diseases (including familial ones), and smokers. People at risk are advised to regularly visit a doctor for preventive examinations and basic clinical tests. [ 4 ]

Pathogenesis

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

Urea helps to retain moisture in the body and normalizes mineral metabolism. However, 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 observed against the background of low-protein nutrition, starvation, as well as in liver pathologies, chemical intoxications (arsenic, phosphorus-containing substances), during pregnancy or hemodialysis.

Azotemia caused by the following reasons is considered clinically significant:

• kidney diseases in which the removal of urea from the circulatory system is impaired (pyelonephritis, glomerulonephritis, renal amyloidosis, acute renal failure, hydronephrosis);
• predominantly protein nutrition, dehydration, inflammatory pathologies accompanied by increased protein breakdown;
• mechanical blockage of urea excretion 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 of urea can lead to headaches, apathy, myasthenia, arthritis. With the development of chronic renal failure, the tubular-glomerular balance is disrupted, protein catabolism increases. [ 5 ]

Symptoms azotemia

The clinical picture of azotemia develops with increasing progression, depending on the damage to certain organs and systems, as well as on the 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, dry mucous membranes and skin;
• the appearance of various types of bleeding, hemorrhages, hematomas, etc.;
• the appearance of edema, up to generalized swelling of soft tissues;
• fluctuations in blood pressure;
• increased heart rate.

At the initial stage, patients complain of weakness, fatigue, apathy, and loss of appetite. Signs of anemia are noted early, caused by blood loss, iron deficiency, and decreased formation of erythropoietin. Over time, general weakness and drowsiness increase, apathy (uremic encephalopathy), weakening of muscles with convulsive twitching, itching of the skin, paresthesia, and bleeding occur. Pseudogout may develop. Symptoms may increase rapidly or gradually.

The picture of severe, irreversible with dialysis, azotemia includes pronounced dyspeptic phenomena (uncontrollable vomiting, diarrhea, anorexia), stomatogingivitis, cheilitis, paleness and yellowing of the face, dry skin. Arterial pressure increases significantly, cardiomegaly, reginopathy, 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 increase.

First signs

An adequate amount of nitrogen in the bloodstream is equal to 18-40 mg/liter. If this content increases for some reason, then we speak of the development of pathology, namely, 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 blood streaks), signs of anemia.
• Disturbances in the functioning of the nervous system: trembling of the muscles of the arms and legs, emotional swings (apathy gives way to a state of excessive excitement), drowsiness, difficulty breathing.
• Other disorders (bleeding, dry skin, general itching).

These symptoms usually combine with each other and indicate the development of renal failure. If treatment measures are not taken in a timely manner, the picture worsens and the chances of recovery decrease.

Changes in the oral cavity with azotemia

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

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

Patients complain of dry mouth, gum pain, bleeding, changes in taste, metallic taste and unpleasant odor. Some patients experience pain in the tongue or inside of the cheeks. The frequency of these pathological signs is inconsistent. For example, dry mouth is detected in 20-30% of cases, bleeding gums - in almost every second case, taste disturbance - in 25% of cases, and uremic odor from the mouth can be observed in almost 80% of patients.

A fairly common concomitant disease with azotemia is uremic stomatitis. The pathology develops when the urea in the serum increases by more than 150 mg/ml, but the full picture of the disorder's appearance has not yet been clarified. Pathological elements are most often found on the inner surface of the tongue and the oral mucosa. Stomatitis responds poorly to treatment until the urea level in the blood is normalized, after which it heals on its own within a few weeks.

Stages

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

The terminal stage is characterized by a marked decrease in glomerular filtration with a disruption of the adaptive mechanisms of the kidneys. The situation is worsened by high blood pressure, pericarditis, and circulatory disorders.

In the terminal stage, the risk of patient death increases sharply. Regular dialysis is used to prolong the patient's life. Fatal outcome can occur as a result of cardiovascular disorders, hyperkalemia, infectious complications, sepsis, hemorrhages, and also as a result of the development of uremic coma.

Forms

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

• Prerenal azotemia is caused by a decrease in cardiac output and develops as a result of renal blood supply deficiency. Such a disorder may occur as a result of shock, bleeding, decreased circulating blood volume, cardiac insufficiency, etc. The nitrogen/creatinine index in prerenal azotemia is more than 15. The reason is the filtration failure of nitrogen and creatinine. The glomerular filtration rate decreases as a result of hypoperfusion, which leads to an overall increase in nitrogen and creatinine content. However, due to nitrogen reabsorption in the proximal tubules, 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 parenzymatic lesions. The basic causes are glomerulonephritis, renal failure, acute tubular necrosis, etc. The index ratio of nitrogen / creatinine in renal azotemia is within the normal range. The glomerular filtration rate is reduced, and the levels of nitrogen and creatinine in the bloodstream are increased (although as a result of damage to the proximal tubules, nitrogen reabsorption is not observed). It turns out that nitrogen with creatinine are excreted with urine, which determines the normal index value. Renal retention azotemia is accompanied by insufficient excretion of urea with urine with normal entry into the bloodstream, which is associated with weak excretory renal function.
• Postrenal azotemia is explained by the appearance of an obstacle to adequate urinary outflow below the renal level. The cause of the disorder may be a congenital developmental defect (for example, vesicoureteral reflux), blockage of the ureter by a stone, enlargement of the uterus during pregnancy, a tumor process, an enlargement of the prostate gland. An increase in resistance to urinary flow can provoke the appearance of hydronephrosis. In postrenal azotemia, the nitrogen/creatinine index exceeds 15. Increased nephron pressure provokes an increase in nitrogen reabsorption, which increases its ratio in the index indicator.
• Productive azotemia (also known as adrenal azotemia) is characterized by excessive formation of slag substances, which becomes possible with excess intake of protein food into the body, with dehydration, inflammatory processes that are accompanied by severe protein destruction. In these situations, urea should be quickly excreted through the kidneys, but when the concentration reaches more than 8.3 mmol/liter, they speak of the development of renal failure.
• Subrenal azotemia is a consequence of mechanical blocking of urea excretion by the kidneys, as a result of which it is absorbed back into the bloodstream. The primary cause of the disorder may be stones, tumor processes (in particular, prostate adenoma).
• Transient, or transient azotemia, is a series of self-limiting disorders that can be provoked by a variety of factors that cause a temporary increase in the level of nitrogen in the blood. Transient azotemia can be functional (in a healthy person under the influence of temporary causes) and organic, caused by pathological conditions (acute intoxications, infections, digestive pathologies, taking certain medications, etc.).

Hypercalcemia and azotemia

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

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

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

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

Complications and consequences

Regardless of how acutely the state of azotemia develops, the 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, may 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 hyperazotemia as a result of impaired renal excretory function and increased protein catabolism. The content of magnesium and potassium in the circulatory system increases, while the level of calcium and sodium decreases. Such disorders are manifested by abnormal heart rhythms, general weakness, drowsiness, and impaired consciousness. Cardiac activity is severely depressed, and consciousness may be completely lost, which may be due to an increase in the concentration of magnesium in the blood serum or a decrease in the sodium level.

In chronic renal failure, a comatose state develops against the background of severe oliguria (anuria), azotemia, ammonemia, and metabolic acidosis. In azotemia, renal nitrogen excretion is impaired, which leads to increased excretion of urea through the skin, pleura, and digestive organs. Excretion of urea through the intestines entails the formation of toxic ammonium derivatives, which is considered especially dangerous. Severe intoxication is noted, the signs of which are depression of consciousness, thirst, nausea, and vomiting. The skin becomes dry, gray, covered with small hemorrhagic rashes and seems to be 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. Breathing becomes difficult. Toxic pneumonia and hepatitis may develop.

Diagnostics azotemia

Early diagnosis of azotemia may cause certain difficulties. Firstly, asymptomatic course of early stages of azotemia in chronic renal failure is not excluded, which is typical for patients with chronic pyelonephritis, latent nephritis, polycystic disease. Secondly, due to polymorphism of damage to internal organs, non-specific signs may come to the fore: anemia, hypertension, asthenia, gout, osteopathy.

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

The following analyses are performed:

• general blood test;
• general urine analysis;
• blood urea nitrogen (BUN) test;
• creatinine level test or daily urine analysis.

The main indicators of kidney function are creatinine and urea. Creatinine is formed in the muscles, after which it enters the bloodstream. Creatinine is involved in energy intra-tissue processes. It is excreted by the kidneys, so the indicator of the presence of this product in the blood is important in diagnostic terms. [ 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. Urea accumulation occurs in pathologies - primarily of the urinary system.

In azotemia, urine analysis shows low sodium, high urine creatinine to serum creatinine ratio, high urine urea to serum urea ratio, and increased urinary concentration (osmolarity and specific gravity). However, 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 to detect an increase in renal volume, stones in the renal pelvis or urinary tract, tumor processes);
• radioisotope renal scanning (helps assess renal perfusion, identify obstruction);
• computed tomography and magnetic resonance imaging;
• chest X-ray (to rule out fluid accumulation in the pleural cavity, pulmonary edema);
• excretory urography (if obstruction of the renal venous vessels is suspected);
• renal angiography (to exclude vascular causes of pathology - for example, renal artery stenosis, dissection of an abdominal aortic aneurysm, ascending thrombosis of the inferior vena cava), nephrobiopsy (in case of unclear etiology of the disease, in case of prolonged anuria, in difficult diagnostic cases);
• electrocardiography, electroencephalography, ultrasound of the heart;
• fundus examination.

Differential diagnosis

Differential diagnostics are performed with uremic coma, diabetic and hepatic coma. The following specialist consultations are indicated:

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

Azotemia should also be differentiated from the following diseases:

• kidney stone disease;
• tuberculosis of the kidneys;
• 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 azotemia increase 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 experiences muscle twitching, drowsiness, depression of consciousness, shortness of breath associated with nephrogenic pulmonary edema and renal acidosis. The composition of the plasma changes:

• levels of creatinine, urea, residual nitrogen, phosphates, sulfates, potassium, and 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 azotemia is discussed in acute renal failure or in the early stages of chronic pathology, then uremia corresponds to the terminal stage of CRF.

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

Treatment azotemia

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

It is extremely important to follow a low-protein diet and control renal hypertension to eliminate azotemia.

With properly adjusted nutrition, a significant decrease in the intensity of azotemia, improvement in mineral metabolism indicators, and preservation of residual renal functionality are observed. The effectiveness of the diet is assessed as signs of azotemic intoxication decrease, phosphate and urea levels in the blood decrease, and pH and serum bicarbonate levels stabilize.

At the early stage 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 hemodynamic disorders, anti-shock measures are carried out - for example, blood transfusion, drip administration of 0.2% norepinephrine (1 ml per 200 ml of saline). If the primary 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 the patient's weight). Further treatment is aimed at regulating homeostasis.

Intramuscular injection of testosterone propionate is performed at 50 mg per day, or retabolil at 100 mg per week. If antibiotic therapy is indicated, the dosage of antibiotics is reduced by half, which is associated with limited excretory function of the kidneys. In case of azotemia, the administration of ototoxic agents is undesirable - in particular, streptomycin, monomycin, neomycin.

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

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

Indications for hemodialysis:

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

Contraindications to hemodialysis:

• cerebral hemorrhages;
• internal bleeding;
• severe form of hemodynamic disturbances, accompanied by collapse.

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

Antiazotemic drugs have the property of increasing the excretion of urea. One of the most common drugs in this group is Hofitol - a purified plant extract of artichoke, produced in the form of tablets and ampoules for intravenous and intramuscular injections. A similar antiazotemic effect is possessed by the drug Lespenefril, the plant basis of which is Lespedeza capitata. Lespenefril is usually taken orally, 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. The following medications may be prescribed:

• Furosemide 40 mg in the morning, under control of daily urine output, up to three times a week. Possible side effects: decreased blood pressure, tachyarrhythmia, dizziness, headache, tinnitus.
• Adsorbix 1 capsule three times a day, under the control of creatinine levels. Possible side effects: constipation, nausea, diarrhea, dysbacteriosis.
• As a potassium antagonist, calcium chloride or gluconate 10% 20 ml is used intravenously over 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-acting) 50 IU intravenously by drip, 15-30 IU every three hours for two days, until the potassium content in the bloodstream stabilizes.
• Sodium bicarbonate 5% intravenously by drip. It is important to consider that with prolonged use of the drug, alkalosis may develop, which is accompanied by loss of appetite, nausea, stomach pain, flatulence.
• Dextrose 5% 500 ml intravenously by drip until the lack of circulating blood volume is replenished. More complete and accelerated absorption of dextrose occurs against the background of insulin administration (3 U per 1 g of dry preparation).
• Furosemide 200 mg intravenously under control of hourly urine output.
• Dopamine in the amount of 3 mg/kilogram/minute intravenously by 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, tremor, motor restlessness, a feeling of anxiety, as well as local reactions.

The following may be prescribed as additional medications:

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

As emergency treatment, it is possible to use medications 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;
• therapeutic mud;
• ozokerite;
• electromagnetic field, electric current, laser, etc.

In case of azotemia, mechanical, electromagnetic, and thermal effects are used, which promote pain relief, stimulation of metabolic processes, trophism, blood circulation, and high-quality urine excretion.

Magnetic therapy has a sedative, antihypertensive, anti-inflammatory, anti-edematous, analgesic, trophic-regenerative effect, activates cellular and humoral immunity.

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

Herbal treatment

Azotemia is a rather serious pathological condition, in which it hardly makes sense to hope for folk treatment. It is important to listen to the doctor's recommendations and follow them, as well as adhere to a strict diet.

Medicinal plants can be used as a supplement if the attending physician does not object.

• Flaxseed normalizes renal blood flow and increases the elasticity of vascular walls, which has a positive effect on kidney function. It is recommended to consume about 25-30 g of seeds daily - in the form of a decoction, infusion, or add to salads, porridge, jelly.
• Lingonberry leaves have antibacterial properties, prevent the development of bacterial infection in the kidneys, and prevent stone formation. It is best to use an infusion (tea) from the leaves, with the addition of a small amount of honey.
• Elderberries strengthen blood vessels, have antibacterial and diuretic effects, strengthen the protection of the urinary system, and increase resistance to infectious lesions. The berries are ground with honey and consumed daily, 2 tablespoons. As a supplement, you can drink an infusion of the plant's flowers.
• Rose hips are famous for their anti-inflammatory, diuretic, antispasmodic properties. They cleanse the kidneys, facilitating their function. Rose hips are used to make a decoction with honey, which is consumed during the day instead of tea.

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

Diet

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

In the initial days of the disease (at least three days), meals should practically exclude salt. It is optimal to arrange contrast days (apple, banana, watermelon, pumpkin, etc.). Then, from the fourth day, a diet is prescribed with a limitation 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 ensure the intake of essential amino acids and vitamins.

It is necessary to correctly calculate the daily caloric intake: approximately 35 kcal/kg of weight.

The diet for azotemia should include products with a low amount of protein and sufficient caloric value. In addition, it is necessary to limit products containing a large amount of potassium (raisins and potatoes, dried apricots, etc.), phosphates (dairy products), magnesium (fish and cottage cheese). Alcohol, coffee and tea, chocolate and cocoa are excluded. Table salt is minimized to 3 g per day. Hot spices, sorrel and spinach, smoked products 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 (without 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;
• cornstarch.

Natural fruit and vegetable juices and rosehip infusion 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 infusion, toast.
• Dinner: vegetable pilaf, cucumber and green onion salad with vegetable oil.

Signs of azotemia disappear faster when using diet No. 7A. As the patients' condition improves, they are transferred to diet table No. 7B. Diet No. 7A is used for no more than 20-25 days, since such a diet often causes weight loss in patients and an increase in hunger. Periodic alternation of the above-mentioned treatment tables is possible.

Surgical treatment

Modern medicine suggests the use of three methods of active treatment of severe azotemia and uremia. These are hemodialysis, peritoneal dialysis and kidney transplantation.

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

Peritoneal dialysis is performed by catheterization and introduction of a special dialysis solution into the abdominal cavity. The semi-permeable membrane that retains nitrogenous waste and electrolytes is represented in this situation by the peritoneal mesothelium. Moisture is removed in the form of ultrafiltration under the influence of an osmotic pressure gradient, which is achieved by using fluids with an increased glucose content (dextrose).

A kidney transplant is a surgical procedure in which a healthy kidney, removed from another person, is transplanted into a patient with chronic kidney failure. The kidney transplant usually comes from a living donor (often a relative) or from a deceased person.

Prevention

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

1. Activity and moderate physical exercise help stabilize blood pressure, optimize blood circulation, and reduce the load on the urinary system. Regular exercise helps avoid blood stagnation in the pelvis and the appearance of inflammatory reactions in the genitourinary organs.
2. Healthy balanced nutrition and maintaining normal weight are important preventive measures that prevent the development of diabetes, cardiovascular pathologies, and chronic kidney diseases. For normal kidney function, it is important not to overload the organs, so it is necessary to adjust both the diet and drinking regime. Food should enter the digestive system evenly, without overeating or starvation. Products may contain only a minimal amount of salt and seasonings. Drinking water should be clean: carbonated drinks and store-bought juices should be limited.
3. Smoking and drinking alcohol worsen blood flow in the kidney area, which causes disruption of their functioning. Passive smokers are also at risk.
4. Visiting a doctor for preventive purposes always plays an important role, especially if a person is at risk of developing kidney disease.
5. Controlling blood pressure 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, the short-term prognosis for patients who do not suffer from other diseases can be called favorable. Serum creatinine levels in most cases normalize (or almost normalize) 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 increase significantly:

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

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

A positive effect on the prognosis is exerted by high-quality treatment of the underlying disease that led to the development of azotemia. Elimination of inflammatory processes in the urinary system reduces the severity of signs of renal failure.

To avoid negative consequences, patients should avoid hypothermia, excessive physical and stressful loads. Patients need easier living and professional conditions. After treatment, a long rest may be advisable.

If medical help is sought late, and if there is no treatment, azotemia has an unfavorable prognosis. The disease progresses, becomes chronic, and complications later occur.