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Renal eclampsia is

Eclampsia renal

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Causes, symptoms Renal eclampsia is a syndrome that is manifested by loss of consciousness, convulsions, caused by spasm of cerebral arterioles and edema. Renal eclampsia is observed in patients with acute kidney disease; it can also occur with exacerbation of nephropathy in a pregnant woman. Renal eclampsia occurs during a period of increased blood pressure and pronounced edema. Its symptoms are increased intracranial pressure, swelling of brain tissue, and cerebral vasospasm. Attacks are provoked by unlimited fluid intake and the patient’s consumption of salty foods in large quantities. Clinical picture of an attack Almost always, an attack is preceded by drowsiness and lethargy. A strong one appears headache, dizziness may occur. The patient's consciousness becomes clouded, he may begin to delirium or see hallucinations, and sometimes there is a short-term loss of consciousness. Nausea appears, blood pressure rises quickly, and swelling increases. Vision is also upset: spots may flash before the patient’s eyes, a veil may appear, and sometimes vision simply drops sharply. Seizures always occur suddenly. They are strong tonic contractions, which are abruptly replaced by strong clonic convulsions. The patient's face becomes cyanotic, the neck veins swell, the tongue is bitten, and foam flows from the mouth. The eyes roll back or slant to the side, the pupils do not respond to light, and the eyeballs are hard. Blood pressure is elevated, as is the temperature, and the pulse is intense, but rare. Sometimes involuntary urination may occur. Such attacks usually last for several minutes, the number of seizures also varies - from 1-2 to 10 or more. After the attacks, the patient calms down and remains for some time in a state of stupor, stupor, or even coma. When he comes to, he doesn't remember anything. After a seizure, lethargy, difficulty speaking, and amaurosis remain for some time. True, such a clinical picture is not always present. Sometimes the patient may not even lose consciousness at all. Differential diagnosis and treatment Renal eclampsia is differentiated from seizures of other origins. Similar seizures are observed in epilepsy. True, with epilepsy, swelling does not occur, blood pressure does not increase, and attacks are observed for many years. Edema is also not expressed in hypertensive encephalopathy, with which renal eclampsia can be confused. Convulsions can also occur during uremic coma. True, in this case there is chronic kidney disease, slow development of seizures, signs of uremic intoxication. It is sometimes necessary to differentiate coma during eclampsia from hemorrhage in the brain. True, with a cerebral hemorrhage, the patient has no renal history, no edema is observed, but there is focal symptoms, which include paralysis and paresis. Diagnosis is carried out after the first medical care. The patient passes general tests blood, urine, biochemical analysis blood, does an ultrasound of the kidneys. The diagnosis of renal eclampsia is an indicator for hospitalization. Treatment is aimed at eliminating seizures, reducing swelling, and lowering blood pressure. The attack is blocked if the patient undergoes a spinal or suboccipital puncture and releases a certain amount of cerebrospinal fluid. At the same time, intracranial pressure decreases and the patient comes to his senses. Bloodletting and intravenous administration of magnesium sulfate help with attacks, which also lowers blood pressure and reduces swelling of the brain. After stopping the attack, the doctor prescribes the patient an achloride diet, and then a diet containing limited use sodium chloride up to 3-4 g and liquid up to 1 liter per day. Health Suggest news

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Renal eclampsia

Renal eclampsia is observed in acute nephritis, nephropathy of pregnancy and very rarely in chronic nephritis. In acute nephritis, it develops now rarely (no more than in 0.3% of all cases, according to M. Sarre, 1967), and in nephropathy of pregnant women - more often.

Pathogenesis renal eclampsia

Pathogenesis is associated with a significant increase in blood pressure, accompanied by spasm of cerebral vessels, leading to impaired blood supply to the brain, swelling, and increased intracranial and spinal pressure. Some clinicians attach great importance in the occurrence of renal eclampsia to increased blood pressure, vasospasm leading to cerebral ischemia, and others - to cerebral edema, but the importance of both of these factors in the occurrence of convulsive attacks is undoubted. Hypertension and vasospasm appear to precede the development of cerebral edema and increased intracranial pressure.

Renal eclampsia clinic

A convulsive attack may be preceded by prodromal symptoms: a significant increase in blood pressure, increased edema, proteinuria, severe headache, dizziness, tinnitus, decreased visual acuity (even loss), diplopia, decreased urine output, a feeling of pressure in the hypochondrium, vomiting. The prodromal period is usually very short (a few minutes) or absent altogether, and the seizure occurs suddenly. There are four phases of the attack: the 1st (about 30 s) is characterized by fibrillar twitching of the facial muscles, disappearance pupillary reflexes; 2nd (10-30 s) - phase of tonic convulsions skeletal muscles with a predominance of extensor tone (opisthotonus), with trismus (sometimes with tongue bite), loss of consciousness, dilated pupils, cyanosis; 3rd (30-120 s) - phase of clonic convulsions covering the whole body, breathing is labored, stridorous, the patient is tossing about, foamy liquid is released from the mouth; 4th - comatose; the patient is unconscious, breathing is noisy, attacks of clonic convulsions are repeated, urinary and fecal incontinence is possible. At this stage, in rare cases, death occurs from asphyxia, cerebral hemorrhage, or pulmonary edema. But usually the patient regains consciousness after a few minutes, a maximum of 30 minutes, the convulsions stop, but there remains a stuporous state or lethargy, stupor, difficulty speaking, amaurosis or hemianopsia, lasting several hours, then disappearing completely. Much less often, after the cessation of a convulsive attack, mental agitation and motor restlessness with attempts to escape and aggressiveness are observed for several hours. Patients, as with epilepsy, do not remember what happened to them. Seizures of renal eclampsia are rarely isolated; more often they are repeated several times during the day, then end as suddenly as they began. During seizures, the pulse is slow and blood pressure is high. There are signs of increased intracranial pressure: high tendon reflexes, positive symptom Babinsky, clonus of the foot, when examining the fundus - a picture of a congestive nipple, with a lumbar puncture - high cerebrospinal pressure (up to 800 mm water column).

However, such a typical picture of renal eclampsia is not always observed. The attack can occur with full consciousness or a very short-term loss of consciousness; against the background of increased blood pressure, only severe headache, amaurosis, lethargy, isolated twitching of the facial muscles, pyramidal signs, and congestive nipples are noted. The level of residual nitrogen, urea, and creatinine in the blood is usually not elevated in renal eclampsia. Severe anemia and electrolyte imbalance were not observed.

Differential diagnosis of renal eclampsia

Differential diagnosis is difficult only if an attack of renal eclampsia is the first manifestation of acute nephritis or nephropathy in pregnancy (which is rare) or if it happened outside the hospital or outside the home, which is also a rare exception, since patients with acute nephritis and nephropathy in pregnancy must comply bed rest and are under medical supervision. In these cases, it is most difficult for a doctor to distinguish renal eclampsia from epilepsy. But with the latter, there is no swelling, a pronounced increase in blood pressure, bradycardia, and scars from old bites are often visible on the tongue. Epileptiform convulsions, observed during atrioventricular blockade, are characterized by pronounced bradycardia (less than 30 beats per minute), often normal or slightly increased value only systolic pressure, absence of swelling on the face, a cannon tone can be heard on auscultation, and there are no signs of increased intracranial pressure. In difficult cases, they resort to an ECG. In abortive forms of renal eclampsia, the thought of hypertensive encephalopathy may arise, but in the latter, edema is not expressed. When questioning patients, it is possible to establish a history of acute nephritis or nephropathy in pregnancy. In cases that are difficult to diagnose, it is necessary to perform a urine test (in acute nephritis - severe albuminuria, cylindruria, erythrocyturia, in hypertension- absence (or in small quantities) of protein in the urine, red blood cells, casts). Sometimes it is necessary to differentiate between coma due to eclampsia and cerebral hemorrhage. But in the latter case, there is no “renal” history, edema, pallor of the face, the prodromal symptoms described above (the comatose state occurs suddenly), changes in the urine, and on the other hand, there are focal symptoms (paresis, paralysis).

It is easy to differentiate between renal eclampsia and uremic coma, since the latter is the outcome of chronic nephritis, in which renal encephalopathy is rarely observed. Cases of a significant increase in azotemia in acute nephritis are rare, as a rule, only when it is complicated by acute renal failure (anuria). The latter is usually short-term (3-4 days) and occurs without loss of consciousness or convulsions.

Treatment of renal eclampsia

If during an attack of renal eclampsia the patient was not in the hospital, he must be immediately hospitalized (in the case of acute nephritis in the therapeutic or nephrological department, and in the case of nephropathy in pregnant women - in the obstetric department). In this case, it is necessary to prevent the tongue from biting and retracting (insert a spatula or spoon wrapped in a thick layer of gauze between the teeth and push it forward lower jaw), damage to the head and other parts of the body (support the head, place a pillow or blanket).

Immediately using the venipuncture method (if it fails, then using the venesection method), it is necessary to perform a fairly massive bloodletting (300-500 ml) to lower blood pressure and reduce cerebral edema. At the same time, 40-60 ml of a 40% glucose solution and 10-15 ml of a 25% magnesium sulfate solution are administered intravenously (slowly, over 3-4 minutes). The latter has a vasodilatory effect, anticonvulsant effect, and also, along with hypertonic solutions glucose, reduces cerebral edema. Along with intravenous administration, intramuscular administration of 15-20 ml of a 25% solution of magnesium sulfate is also used. If an attack of eclampsia does not stop, after 1-2 hours you need to repeat the intravenous infusion of glucose and magnesium sulfate in the same doses. It must be remembered that in large doses, magnesium sulfate can have a depressing effect on respiratory center. In such cases, a magnesium antagonist, calcium, is administered (10 ml of 10% calcium chloride solution intravenously). Additionally, to relieve frequently recurring convulsive attacks, 1 ml of a 2.5% solution of aminazine is administered intravenously, 1 ml of a 1% solution of morphine hydrochloride is administered subcutaneously, 50 ml of a 3-5% solution of chloral hydrate is administered as an enema, if necessary, up to 7 g of chloral hydrate and 0.025- 0.03 g of morphine hydrochloride per day. If cerebral edema is combined with general edema, left ventricular failure, 60 mg of furosemide (Lasix) should also be administered slowly intravenously, continuing if necessary. intravenous administration drip method. For renal eclampsia, dibazol (3-4 ml of 1% solution or 6-8 ml of 0.5% solution intravenously), aminophylline (10 ml of 2.4% solution intravenously repeatedly) are also used.

In most cases, with the help of the measures listed above, an attack of renal eclampsia is stopped. It is relatively rare to resort to lumbar puncture, which is usually performed in a hospital setting. The release of cerebrospinal fluid should be done slowly and not sharply reduce intracerebral pressure. After spinal tap intracranial pressure decreases and eclamptic seizures stop. After stopping the attack, the patient needs hospital treatment. In the first days, he needs to be prescribed an achloride diet, and then a diet limiting sodium chloride to 3-4 g per day and liquid to 1 liter per day (in the first 1-2 days, you can carry out classical treatment with hunger and thirst). For high blood pressure, antihypertensive drugs (reserpine, dibazole, aldomet or dopegit, clonidine, etc.) are prescribed in appropriate doses. For severe edema, diuretics are indicated; for heart failure, cardiac glycosides are indicated.

Forecast. Attacks of renal eclampsia usually do not worsen the prognosis in acute nephritis. On the contrary, it seems that if acute nephritis is accompanied by attacks, it usually does not develop into chronic nephritis. Death during an attack of renal eclampsia is rare. Its causes are cerebral hemorrhage and heart failure.

Prevention of attacks of renal eclampsia includes: early diagnosis, timely hospitalization and proper treatment of patients with acute nephritis and nephropathy in pregnant women. To eliminate hypertension, edema, and heart failure, first of all, a diet with limited water and sodium chloride, bed rest, and appropriate medications are prescribed.

Emergency conditions in the clinic of internal diseases. Gritsyuk A.I., 1985

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Renal eclampsia

Renal eclampsia occurs during acute nephritis, and in very rare cases - during exacerbations of chronic nephritis. It is based on spasm of cerebral vessels with the development of cerebral edema and increased intracranial pressure (angiospastic encephalopathy).

Symptoms of renal eclampsia

Eclampsia usually occurs at the peak of acute nephritis, most often in patients with significant edema. Sometimes attacks of renal eclampsia appear during the period of reduction of edema. The incorrect dietary regimen of patients with acute nephritis (taking significant amounts of fluid, table salt).

The attack is preceded by a period of precursors (preeclampsia), which usually lasts 2 days. The harbingers are; increased headaches (sometimes meningeal symptoms appear), vomiting, visual disturbances (fog before the eyes, flickering dark spots, sometimes transient hemianopsia or amaurosis), general excitement or, on the contrary, drowsiness, a state of stupor. At the same time, there is a significant increase in blood pressure compared to the initial level (superhypertension) and bradycardia.

Against the background of the described condition, a deep loss of consciousness (eclamptic coma) may suddenly occur simultaneously with an attack of convulsions. At first, the convulsions are tonic in nature, then clonic. There is a sharp cyanosis of the face, hoarse breathing, dilated pupils, the tongue is often bitten, and there may be involuntary discharge of urine and feces. The attack most often lasts several minutes, then the patient remains in stupor. Often seizures are repeated (most often one, two or three seizures, but sometimes up to 30-40 seizures occur per day - eclamptic status).

After recovery from a coma with renal eclampsia, there is often loss of vision (amaurosis) or hemianopia associated with central brain changes. Visual disturbances are temporary and usually disappear completely soon.

If the patient comes under the supervision of a doctor already in a state of coma or eclamptic status, there is a need to differentiate from epilepsy. Renal eclampsia is characterized by the phenomenon arterial hypertension, edema is often observed, changes typical of nephritis are found in the urine, and bradycardia occurs.

Treatment of renal eclampsia

During the preeclamptic period, rest, limiting the amount of fluid and salt. Fasting days are recommended (500 g of milk per day or 500 ml of compote or jelly). Massive bloodletting (300-500 ml), administration of magnesium sulfate, intravenous infusions of glucose, dibazole, reserpine, natriuretics (hypothiazide, fonurit, lasix). Eufillin is administered 0.24 g intravenously. In case of severe arterial hypertension - drip infusion of arfonade. Distraction procedures (foot baths, mustard plasters).

In a state of eclamptic attack - immediate reduction in pressure, administration of 40% glucose, administration of 25% magnesium sulfate intravenously (slowly, over 3 minutes or intramuscularly. The hypotensive effect of magnesium sulfate can be enhanced by the administration of dibazole, aminophylline (0.24 g) intravenously or aminazine intramuscularly. To relieve seizures, chloral hydrate is prescribed as an enema.

In most cases, these measures are sufficient; if there is no effect, it is necessary to perform a spinal puncture.

After recovering from renal eclampsia, the patient must remain in bed, the amount of fluid and salt is limited for several days, active antihypertensive drugs are prescribed - magnesium sulfate (intramuscular), glucose (intravenous), dibazole, reserpine, hypothiazide; in case of persistent and significant hypertension (and the absence of massive hematuria), diathermy is performed lumbar region.

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Renal eclampsia

Consequently, in a number of kidney diseases, renal hypertension syndrome can come to the fore in the clinical picture of the disease and determine its course and outcome.

Eclampsia (from the Greek eclampsis - outbreak, convulsions) is most often observed with acute diffuse glomerulonephritis, but can also occur during exacerbation chronic glomerulonephritis, nephropathy in pregnant women. In the pathogenesis of eclampsia, the main significance is given to increased intracranial pressure, swelling of brain tissue and cerebral vasospasm. In all of these diseases, eclampsia usually occurs during a period of severe edema and increased blood pressure.

Attacks are provoked by patients taking salty foods and unlimited fluid intake.

The first signs of approaching eclampsia are often unusual lethargy and drowsiness. Then a severe headache, vomiting, short-term loss of consciousness (amaurosis), speech, transient paralysis, confusion, and a rapid increase in blood pressure appear. Convulsions occur suddenly, sometimes after a cry or a noisy deep breath. At first, these are strong tonic contractions, which then, after 1/2 - 1 1/2, are replaced by strong clonic convulsions (less often, only isolated convulsive twitchings of one or another muscle group are noted). The patient's face becomes cyanotic, the neck veins swell, the eyes squint to the side or roll upward, the tongue is bitten, and foam flows from the mouth. The pupils are dilated and do not react to light, the eyeballs are hard. The pulse is intense, rare, blood pressure is increased; with frequent attacks, body temperature rises. Involuntary urination and defecation are often observed.

Attacks of renal eclampsia usually last several minutes, rarely longer. In many cases, there are two or three consecutive attacks, then the patient calms down and remains in a state of stupor, deep stupor or coma for some time, and then comes to his senses. Sometimes amaurosis (blindness of central origin) and aphasia (speech disorder) persist for some time after awakening.

This is the classic picture of an eclamptic attack. However, it should be borne in mind that in some cases attacks occur atypically, without loss of consciousness or in an erased form - in the form of transient aphasia, amaurosis, mild convulsive twitching.

Renal eclampsia must be differentiated from seizures of other origins. Convulsions of a similar nature are observed in epilepsy, a neurological disease of congenital or post-traumatic origin. However, with epilepsy there is no swelling or other signs of kidney disease, and seizures are usually observed for many years. Convulsions also occur during uremic coma, but in this case there is a typical medical history (the presence of chronic kidney disease), signs of uremic intoxication, and a slow development of a convulsive state over a number of days; The very nature of the seizures is also different: they occur in the form of small fibrillary twitches.

Currently developed effective methods combating an attack of renal eclampsia. The attack ends almost immediately if the patient undergoes a suboccipital or spinal puncture and releases a certain amount of cerebrospinal fluid. Intracranial pressure decreases, the patient regains consciousness. The striking effect of spinal puncture confirms the importance of increased intracranial pressure in the pathogenesis of attacks of renal eclampsia. Bloodletting and intravenous administration of magnesium sulfate (10 ml of 25% solution), which lower blood pressure and reduce cerebral edema, also help to stop attacks of eclampsia.

Kidney failure (insufficientia renalis) - pathological condition, characterized by impaired renal function with a delay in the excretion of nitrogen metabolism products from the body and a disorder of water, electrolyte, osmotic and acid-base balance.

Acute renal failure (insufficientia renalis acuta) is sudden renal failure caused by acute lesion kidney tissue, for example, in shock, poisoning, infectious diseases; in most cases, reverse development is possible.

In the pathogenesis of acute renal failure and acute uremia, great importance is given to shock and the accompanying circulatory disorders, primarily in the kidneys. As a result of the anoxia that develops, dystrophic changes occur in the renal glomeruli and tubules. In other cases, when acute renal failure occurs as a result of poisoning or a severe infectious disease, its pathogenesis is largely due to the direct effect of toxic substances and toxins on the renal parenchyma. In both cases, the filtration of urine in the renal glomeruli is disrupted, the excretion of urine by the kidneys is reduced - oliguria occurs, in severe cases up to anuria. Potassium, sodium, phosphorus salts, nitrogenous products and some other substances are retained in the body.

Acute renal failure grows quickly and is manifested by a severe general condition, vomiting, confusion, impaired breathing and cardiac activity. Due to ischemia of the renal glomeruli, blood pressure may increase, and edema develops with anuria. If anuria and azotemia cannot be eliminated within a few days, death occurs. With a favorable course, diuresis increases in the future, but the concentrating ability of the kidneys remains insufficient for some time; Gradually, kidney function normalizes and recovery occurs.

The clinical picture of acute renal failure varies somewhat depending on the nature of the disease that caused it. In many cases, acute renal failure occurs with a number of common symptoms, which makes it possible to distinguish this syndrome. There are 4 stages of acute renal failure: 1) initial stage lasting from several hours to 1-2 days, clinically manifested mainly by symptoms of one disease (traumatic or transfusion shock, severe acute infectious disease, intoxication, etc.); 2) oligoanuric stage, manifested by changes in diuresis (to complete anuria), uremic intoxication, and water-electrolyte disturbances. When examining urine, proteinuria, cylindruria, and erythrocyturia are determined. The oligoanuric stage may end in the death of the patient or his recovery; 3) in the latter case - polyuric stage - there is a sudden or gradual increase in diuresis with low relative density of urine, a decrease in the content of residual products of protein metabolism in the blood, normalization of water-electrolyte balance, disappearance pathological changes in urine; 4) the recovery stage begins from the day of normalization of the content of residual nitrogen, urea and creatinine in the blood and lasts from 3 to 12 months.

Chronic renal failure (insufficientia renalis chronica) is a gradually developing irreversible renal failure caused by slowly increasing changes in the kidneys due to abnormalities of their development, metabolic diseases, chronic inflammation, etc.

The occurrence of chronic renal failure is caused by progressive nephrosclerosis. There is a latent period of chronic renal failure, when renal dysfunction is not clinically manifested and

are detected only by special laboratory methods, and there is a clear period manifested by the clinical picture of uremia.

In the latent period, the initial phenomena of renal dysfunction can be judged by conducting tests for concentration, dry eating and Zimnitsky tests; in this case, a tendency is revealed for patients to excrete urine of a lower (below 1.017) and monotonous relative density - isohyposthenuria. Cleansing tests (“clearance”) allow us to identify initial disturbances in reabsorption by the renal tubules and filtration in the glomeruli. Minor violations Kidney functions are also detected by radioisotope nephrography. It is believed that the first signs of renal failure in patients with chronic diseases kidneys appear only when the mass of functioning renal parenchyma decreases to at least 1/4 of its original value.

As renal failure progresses, changes in the daily rhythm of urination occur: isuria or nocturia is observed. Concentration and dilution tests reveal a significant impairment in the concentrating ability of the kidneys

Severe isohyposthenuria (the relative density of all urine portions ranges from 1.009 to 1.011, i.e., approaches the relative density of plasma ultrafiltrate

Primary urine); more pronounced reabsorption disorders and glomerular filtration determined using purification tests and radioisotope nephrography. There is a gradual increase in the content of nitrogenous waste in the blood, and the content of residual nitrogen increases several times (normally 20-40 mg%). Laboratory research allows you to determine the increase in blood levels various products protein breakdown: urea (normally 20-40 mg%, and in case of renal failure increases to 200 mg% or more), creatinine (normally 1-2 mg%), indican (normally 0.02-0.08 mg%). It is important to note that an increase in the level of indican in the blood is often the first and most reliable sign of chronic renal failure, since its level in the blood does not depend on the protein content in food and does not accumulate in tissues.

A moderate increase in the content of nitrogen breakdown products in the blood (azotemia) may not affect the patient’s well-being until a certain time. However, then a number of external changes appear, on the basis of which uremia can be clinically diagnosed. Some of the signs of uremia are due to the fact that insufficiency of kidney function is partially compensated by a more active participation in the excretory processes of the skin, mucous membranes, digestive glands. The decomposition of urea secreted by the mucous membranes of the respiratory tract and mouth, under the influence of bacteria in them, to ammonia causes the appearance of a characteristic uremic odor from the mouth; in more severe cases, this smell can be detected when already approaching the patient’s bed. It is believed that a uremic odor can be detected when the concentration of residual nitrogen in the blood exceeds 100 mg% (i.e., more than 70 mmol/l).

Nitrogenous products, and primarily urea, are secreted by the gastric mucosa and decompose to form ammonia salts. These salts irritate the mucous membrane of the stomach and intestines - nausea, vomiting (uremic gastritis), diarrhea (uremic colitis) occur. Irritation of the mucous membrane of the respiratory tract by secreted products leads to laryngitis, tracheitis, and bronchitis. Severe stomatogingivitis develops. Due to irritation, necrosis and ulceration form on the mucous membranes. On the patient's skin, one can often see the deposition of urea crystals in the form of a white thread, especially at the mouth of the sweat glands (at the base of the hair). An excruciating itching occurs, which forces patients to endlessly scratch the skin. Accumulating in the blood toxic substances are also secreted by serous membranes; Uremic pericarditis is especially characteristic, which is determined by listening to the heart with a stethoscope by the characteristic rough friction noise of the pericardium. This noise is usually

appears in the terminal period and indicates near death sick. According to the figurative expression of old doctors, the pericardial friction rub is the “death knell of the uremic.”

Due to general intoxication, memory and sleep are disrupted, fatigue and a dull headache appear, then drowsiness and apathy develop, and vision is impaired. When examining the fundus, narrowed arteries and dilated veins, swelling of the optic nerve head, and in places whitish lesions (neuroretinitis) are visible. The development of neuroretinitis is primarily explained by trophic disorders due to spasm of the fundus vessels (as it is observed in the absence of uremia); However, uremic intoxication, which aggravates these changes, is also of certain importance. The pupils are constricted (different from eclampsia).

Metabolism is sharply disrupted: patients become cachetic; due to dystrophy, the functions of the liver and bone marrow change; toxic uremic anemia occurs, usually accompanied by leukocytosis, and thrombocytopenia. Due to a decrease in the number of platelets in the blood, disorders in the blood coagulation system and increased capillary permeability as a result of toxicosis, there is a tendency to bleeding (from the nose, gastrointestinal tract, urinary tract, uterus), and skin hemorrhages occur. Body temperature decreases slightly.

Subsequently, intoxication increases, the patient’s consciousness is lost, he falls into a coma (uremic coma), periods of severe lethargy alternate with periods of excitement, hallucinations; noisy, rare breathing occurs with very deep breaths (Kussmaul breathing); less often, peculiar breathing with variable increase and decrease is observed breathing movements(Cheyne-Stokes breathing). In the final stage, the patient is in a deep coma, occasional muscle twitching occurs, and after some time death occurs.

There is currently no generally accepted classification of chronic renal failure. A. P. Peleshchuk et al. (1974) distinguish 3 stages of it: initial (1) with a slight increase in the content of residual nitrogen (up to 60 mg%) and creatinine (up to 1.5-3.0 mg% in the blood) and a moderate decrease in glomerular filtration; pronounced (2A and 2B) with more significant azotemia and electrolyte disturbances and terminal (3), manifested by a clear clinical picture of uremia.

Uremia (from the Greek urina - urine and haima - blood) - urinary bleeding - severe

intoxication of the body due to total failure of kidney function. Acute uremia occurs due to poisoning with nephrotoxic poisons (compounds of mercury, lead, carbon tetrachloride, barbiturates, etc.), transfusion of incompatible blood and massive hemolysis, shock states. Chronic uremia develops in the final stage of many chronic kidney diseases ending in nephrosclerosis: chronic glomerulonephritis, pyelonephritis, renal vascular lesions, etc.

The pathogenesis of uremia is not well understood. It has been established that with uremia, protein breakdown products accumulate in the blood - nitrogenous wastes: urea, uric acid, creatinine. The content of indican, phenol and other aromatic compounds that are formed in the intestines during decay and through intestinal wall enter the blood. Normally, these substances are excreted from the blood by the kidneys. Various compounds of sulfur, phosphorus, magnesium and other substances accumulate; ionic balance is disrupted. Due to the accumulation of acidic foods in the body and the disruption of the kidneys' production of ammonia, which neutralizes acids, acidosis develops. Uremia is accompanied by severe liver damage and metabolic disorders.

However, none of the listed processes can be considered the main one in the pathogenesis of uremia. Thus, intravenous administration of urea in large doses does not lead to uremia, but only increases urine output, and therefore urea preparations at one time

Renal eclampsia is an acute condition with a number of characteristic features, which are based on disorders of the brain (encephalopathy with swelling of brain tissue as a result of a sharp and prolonged spasm of arterioles). This syndrome is different:

convulsions (clonic and tonic);
clouding or loss of consciousness (coma);
an increase in blood pressure to critical levels;
pronounced metabolic disorders in the body.

Renal eclampsia is quite rare, but very dangerous disease. As a rule, it manifests itself in pregnant women as a complication in the last trimester, as well as in people with chronic renal pathologies. In the early childhood the pathology practically does not occur; it is diagnosed sporadically in junior and senior schoolchildren and adolescents, that is, only in isolated cases in acute forms of nephritis.

Reasons

Nephropathy in pregnant women (impaired kidney function).
Chronic nephritis.

Factors that provoke renal eclampsia include:

consumption by pregnant women and sick people of significant amounts of salty, spicy, spicy foods or large volumes of liquid;
disturbances in the functioning of the endocrine system;
neuropsychic overexcitation, stress;
changes in the composition of the blood (increase in its viscosity, release of a large number of platelets, intensification of their coagulation processes).

Development mechanism

The syndrome develops against the background of vascular spasm and tissue swelling in the brain. This occurs due to sodium retention in the body's cells, accumulation and long-term retention of water in them. This process triggers mechanisms for raising arterial and intracranial pressure, brain hypoxia, and ischemia of its tissues. Therefore, the work of the brain structures (both the brain and the spinal cord) is disrupted, a significant narrowing of its functions occurs, and everyone suffers greatly. internal organs(heart, lungs, liver).

Renal eclampsia is characterized by:

increased tissue permeability in the body, which is expressed in the formation of internal and external edema;
metabolic disorders - accumulation of harmful substances resulting from decay reactions (acidosis);
lack of normal filling of blood vessels, decrease in blood volume in them;
increased loss of fibrin and its sedimentation in the cells of the body, which changes the normal process of blood clotting;
hemorrhages (single and multiple petechial) in the brain and (or) internal organs.

Clinic, symptoms of renal eclampsia

In medicine, there is such a thing as preeclampsia (a triad of signs signaling the danger of a crisis) - this is:

increased blood pressure;
the appearance of severe swelling;
protein in urine.

Any doctor who discovers a combination of these symptoms is obliged to “sound the alarm” and immediately begin treatment measures. The main thing is to prevent an impending attack or provide emergency assistance in a timely manner (preferably at the very beginning). Delay in this case can lead to the death of the patient, and in pregnant women, the fetus.

Prodromal (preceding) signs of renal eclampsia, in addition to the main ones, include:

double vision or a white veil in front of them;
dizziness and migraine-like pain;
lethargy and confusion;
the occurrence of delirium, hallucinations, fainting;
decreased desire to urinate;
nausea, vomiting, heaviness in the epigastrium.

At chronic pathologies in the renal system, preeclampsia can last up to 4 days, in other cases the attack develops rapidly within a few hours. After a sharp rise in pressure, patients develop convulsions according to a certain “scenario”:

twitching of individual muscles (1-3 min);
trismus of the whole body with further loss of consciousness, with pronounced blue discoloration of the skin (cyanosis), dilated pupils (up to 30 seconds);
clonic contraction of the entire body muscles, with signs of respiratory and heart failure (up to 2 minutes);
involuntary urination and bowel movements, return to consciousness; with irreversible changes in the body, patients die during this period from suffocation, cardiac arrest, and extensive hemorrhages in the brain.

The number of convulsive seizures can range from 1 to 10 or more.

In the recovery phase, patients are left with a foggy consciousness, speech and coordination disorders are observed, they do not remember their feelings during attacks, they are disoriented in space and perception of the world.

Objective symptoms of eclampsia are characterized by:

slow heart rate;
high tendon reflexes;
congestion in the fundus;
When cerebrospinal fluid is taken (puncture), an increase in pressure in it is diagnosed.

Atypical and mild, renal eclampsia can occur in people with chronic nephritis, without pronounced convulsions and “turning off” consciousness (it leaves patients for seconds). In urine tests, such patients do not have a large number of protein fractions, although blood pressure is significantly increased and there may be edema.

Diagnostics

It is important to distinguish seizures in eclampsia from seizures in epilepsy. The distinctive signs of eclampsia are:

decreased heart rate;
swelling on the body;
increase in blood pressure.

With epilepsy, the pulse is normal or rapid, there is no swelling or hypertension, and visible marks on the tongue from previous attacks may remain.

To differentiate from traumatic coma or stroke, urine analysis is used; in the latter cases, protein is not detected in it, and observations also show the presence of paresis and (or) paralysis in patients. In eclampsia they are not present.

Distinctive feature this state from uremic coma is the absence of organic changes in the kidneys (wrinkling, reduction), as well as dystrophy and hypertrophy of the myocardium.

Main laboratory method Determining the development of renal eclampsia is to study urine (for protein, for creatinine) and blood (biochemistry, for electrolytes, for pH balance, for urea, for platelet levels, etc.).

Instrumental examinations include: ultrasound, CT, X-ray, MRI of the kidneys and other organs.

Treatment

Attacks of renal eclampsia can only be stopped in a hospital; if there is any suspicion of them, patients are urgently hospitalized. Therapeutic procedures include:

application anticonvulsants(Droperidol, Seduxen, Sodium oxybutyrate), antihypertensive drugs(Magnesium sulfate);
bleeding up to 400 ml.;
taking diuretics (Furosemide, Lasix).

The diet is salt-free in the first weeks, and then with limited sodium chloride intake.
Antihypertensive drugs as prescribed by a doctor.
Decongestants, including folk ones. You can drink kidney tea (Orthosiphon stamen), the regimen will be prescribed by a specialist.

Romanovskaya Tatyana Vladimirovna

The concept of “eclampsia” is usually used to characterize the most complex form of gestosis in pregnant women - a condition with convulsive syndrome, pressure surges and severe disorders in the body. But the disease renal eclampsia occurs not only in pregnant women, but also in other categories of the population.

Renal eclampsia

Renal eclampsia is understood as an encephalopathic syndrome accompanied by convulsions, loss of consciousness against the background of spasm of cerebral arterioles and swelling of brain tissue. Is rare disease, in most cases becomes a complication of renal pathologies.

In acute forms of nephritis, the disease occurs only in 0.3% of cases. Most often, renal eclampsia is recorded in pregnant women during latest dates. It almost never occurs in children aged 1-3 years; in childhood it is more typical for schoolchildren. It is necessary to distinguish eclampsia from azotemic uremia, which is a consequence severe forms chronic nephritis.

Reasons

Diseases against which such a complication may develop are the following:

Nephropathy of pregnancy;
Toxicosis of the second half of pregnancy;
Spicy ;
Exacerbation of chronic nephritis.

As a rule, the development of pathology occurs during severe swelling and a sharp increase in blood pressure. In pregnant women, eclampsia occurs even after swelling decreases. Convulsions can be provoked by the abuse of salty foods and the consumption of large amounts of liquid.

Pathogenesis

The development of eclampsia comes from two equivalent factors - cerebral circulatory disorders against the background of cerebral edema and impaired blood microcirculation with vasospasm. In the acute form of kidney damage, sodium and water molecules are retained in the brain tissue. Intracranial pressure increases, as does the pressure in the cerebral vessels.

Due to an increase in blood pressure and spasm of the walls of blood vessels, ischemia (oxygen starvation) of brain tissue is observed, leading to significant disorders brain functions. In parallel, acute renal (sometimes liver) failure develops, and spinal cord dysfunction occurs.

In pregnant women, renal eclampsia is often associated with an increase in blood viscosity and the development of disseminated intravascular coagulation - with the massive appearance of blood clots. Blood flow is disrupted both in the brain and in vital organs, so the consequences for the body are extremely serious.

Etiology and pathogenesis of renal eclampsia

Clinical picture

The main manifestation of renal eclampsia does not always occur - often the patient experiences attacks in full consciousness, or short-term loss of consciousness. And yet, more often than not, the development of eclampsia is “standard” - it is preceded by sudden lethargy, drowsiness, headaches against the background of acute nephritis. An attack can last for several minutes (prolonged attacks are not typical), often followed by a whole series of attacks. Between them, the patient seems to be in a stunned state, cannot come to his senses, or (in a severe form of the disease) falls into a coma. The total duration of the pathology without treatment can be a day or more.

Main symptoms acute attack renal eclampsia are:

Severe headache;
Nausea and vomiting;
Fainting;
Visual impairment, speech impairment;
Paresis and paralysis (reversible);
Increasing pressure to high numbers;
Swelling of the veins in the neck;
Rolling eyes upward;
Tongue biting;
Foaming at the mouth;
Pale skin;
Irregularity, intermittency of breathing.

Seizures are an important symptom of renal eclampsia. They develop at the height of an attack during a sigh or a cry. The seizures may be weak at first (tonic) but then become stronger (clonic). In some patients, instead of typical cramps, individual muscles twitch. During convulsions, involuntary urination and defecation often occur. In severe cases, the pupils do not react to light and the eyes harden.

A patient with renal eclampsia necessarily has edema - this distinguishes the pathology from epileptic attacks, which occur with a similar clinical picture.

The development of symptoms of an attack occurs in four periods:

The first, or precursor. Duration – up to a minute.
The second, or the period of tonic convulsions. Duration – up to 30 seconds.
Third, or period of clonic convulsions. Duration – up to 2 minutes.
Fourth, or permissive. The patient comes to his senses.

Diagnostics

In patients hospitalized for treatment of acute nephritis, diagnosis usually does not cause difficulties.

But in those patients who are admitted to the department during the development of renal eclampsia, differential diagnosis is required:

With epilepsy - absent, the disease has a long history, there may be scars on the tongue from previously occurring attacks.
With azotemic - occurs only in patients with chronic nephritis, is characterized by slow development, urine has a low specific gravity, the smell of urine is present in the exhaled air, there is anemia in the blood, and residual nitrogen is increased.
C – no convulsions, the face is not pale, but red, hyperemic, symptoms of paralysis are rapidly increasing, coma is developing acutely.

To facilitate the diagnosis, collecting anamnesis from the words of the patient or his relatives, in particular, indicating a sharp increase in pressure and the appearance of edema before attacks. Distinctive signs of renal eclampsia according to tests are a high specific gravity of urine, the presence of blood in the urine, and in pregnant women - an increase in blood platelets.

Video of an attack of renal eclampsia:

First aid

The tasks of loved ones and the arriving ambulance team are to stop the current attack and prevent the development of a new one, eliminate existing acute disorders, and bring down the pressure to normal levels.

At home urgent Care is this:

Place the person on the bed, sofa, floor (without a pillow).
Tilt your head to the side, fix your tongue so that it does not sink in - insert a spoon wrapped in gauze into your mouth.
Open the window and provide air access.
Remove all squeezing clothing from the neck.
If necessary, perform mouth-to-mouth breathing manipulations.
Give the person a Nitroglycerin tablet if he is conscious.

Ambulance specialists use oxygen masks to restore spontaneous breathing; in the absence of breathing, they install constant mechanical ventilation. In case of cardiac arrest indirect massage. Treatment of renal eclampsia is more effective under anesthesia, so the patient is often given general anesthesia while still in the ambulance.

Treatment

To relieve seizures, anticonvulsant therapy is performed in the hospital - solutions of Seduxen, Droperidol, Promedol, Fentanyl with glucose are administered. At the same time, arterial hypertension is treated with Clonidine, Dibazol, Eufillin, etc.

Bloodletting with taking up to 400 ml of blood and subsequent administration of a glucose solution has proven itself well in the treatment of renal eclampsia. Another method of treating cerebral edema and reducing pressure is the administration of the drug Magnesium sulfate, which quickly relieves spasm of cerebral vessels and normalizes intracranial pressure.

Severe seizures are blocked using a spinal puncture - as small portions of fluid leak out, brain edema decreases in intensity due to a decrease in intracranial pressure. This treatment method is used only if the first two indicated methods are ineffective.

After acute renal eclampsia has resolved, the patient should remain in the department for treatment of nephritis. A strict diet with limited salt and liquid is recommended. Fasting days on milk are mandatory, fermented milk products, jelly. Treatment with diuretics, Prednisolone, and drugs for arterial hypertension is used, and diathermy of the lumbar region is prescribed.

Complications

Thanks to the development of medicine, deaths from this type of eclampsia are rare. Nevertheless, death from acute renal or heart failure, from massive cerebral hemorrhage is still possible. The prognosis becomes more difficult when other forms of eclampsia – cerebral, hepatic – are added. In pregnant women, death is possible from disseminated intravascular coagulation. Typically, renal eclampsia does not further complicate the course of acute nephritis - on the contrary, the pathology after attacks often does not become chronic.

Complications of renal eclampsia

Renal eclampsia is a relatively rare complication of acute nephritis. It should not be confused with azotemic uremia, a terminal complication of chronic nephritis.

Pathogenesis

The development of an attack of renal eclampsia in acute nephritis is explained by an increase in intracranial pressure associated with cerebral edema and insufficient blood supply(ischemia) of the latter due to spasm of cerebral vessels. Upon examination, the patient shows signs of increased intracranial and spinal pressure: stiffness of the head, clonus of the feet, increased tendon reflexes. During a lumbar puncture, cerebrospinal fluid flows out under high pressure.

Clinic

An attack of renal eclampsia most often occurs unexpectedly when acute nephritis is at its height. By carefully observing the patient, you can detect a number of signs that precede an attack. In addition to headaches, there is stupor, frequent vomiting, and neck rigidity. Before an attack of eclampsia (the word eclampsia in Greek means convulsions), blood pressure rises sharply, and the protein content in the urine increases. In other cases, attacks coincide with an increase in swelling.

The attack itself begins with sudden tonic convulsions, which are quickly replaced by clonic convulsions of the whole body.

The patient’s skin is pale before the attack (has an appearance characteristic of acute nephritis), and during it becomes cyanotic. Cyanosis extends to the neck. The veins in the neck swell. The eyes are squinted to the side. The teeth are clenched, but foamy saliva, often stained with blood, is released through them, as the patient bites his tongue. During an attack, the patient loses consciousness (is in a coma). Breathing is erratic, sometimes intermittent, sometimes snoring (stertorous), associated with convulsions. The attacks last several minutes and repeat after 1/2-1 hour. Eclamptic attacks in acute nephritis can last for a day or more. In addition to blood pressure, intracranial pressure also increases.

After an attack of eclampsia, the patient, as a rule, plunges into deep sleep, and if he sometimes wakes up, he finds it difficult to navigate his surroundings. Only after the attack is it possible to establish that the patient has experienced complete blindness or partial loss of vision - hemianopsia, which is associated with damage to the visual centers in the brain. With the cessation of attacks of eclampsia in the next 2 days, it goes away.

Diagnosis

When recognizing the disease that caused a coma (an attack of eclampsia), difficulties may occur. They occur if the patient is under the supervision of a doctor or paramedic not from the onset of kidney disease (acute nephritis), but only during an eclamptic attack. The diagnosis is made easier if the medical history is known and it can be established that the disease began with the characteristic signs of acute nephritis: rapidly developing edema, hypertension and hematuria. These symptoms make it possible to distinguish renal eclampsia from an epileptic seizure.

Symptoms of renal eclampsia and epileptic seizures similar. In both cases, the attack occurs suddenly. In both cases, tongue biting, involuntary urination, total loss consciousness. Anamnestic data, the presence of arterial hypertension, and edema allow one to diagnose eclampsia in acute nephritis. Epilepsy is characterized by scarring on the tongue, indicating previous seizures.

Sometimes, with renal eclampsia, azotemic uremia is mistakenly diagnosed. Differential diagnosis for these two syndromes is not difficult. The main disease in the first case is acute nephritis, while azotemic uremia develops in a patient with chronic nephritis. With eclampsia, the attack occurs quickly and violently, while uremia is characterized by a long and slow development. A low specific gravity is constantly detected in the urine of a patient with uremia. In eclampsia, the excretory function of the kidneys is not impaired and the urine has a high specific gravity.

In addition, it is not difficult to detect signs of azotemic intoxication in uremia: the smell of urine in the exhaled air, excretory gastritis and colitis, anemia. With eclampsia, these signs are absent. In the blood with uremia, increased residual nitrogen is always detected. With eclampsia, the content of residual blood nitrogen is not increased, and if there is an increase, it is for a short time. Azotemia in renal eclampsia occurs when urination stops (anuria), but this is a short-term phenomenon. With improvement in urine output, azotemia in eclampsia disappears.

If eclampsia develops in old age, a cerebral hemorrhage may be suspected. In this disease, the symptoms common to eclampsia are: suddenly developing unconsciousness, the presence meningeal symptoms(stiffness of the muscles of the neck and limbs, decreased pulse, etc.). Distinctive are following symptoms. In eclamptic coma, unconscious comatose state preceded by an attack of convulsions, reminiscent of an epileptic seizure. Pallor and often swelling of the face are noteworthy.

Renal eclampsia is observed more often at a young age. With cerebral hemorrhage, patients do not experience seizures. Coma develops acutely within a few seconds; the patient's face is not pale, but, on the contrary, red and hyperemic. The emerging signs of hemiplegia (one-sided paralysis) quickly increase, whereas with renal eclampsia, signs of paralysis rarely appear and soon disappear. Cerebral hemorrhage at a young age is very rare. In the vast majority of cases, it develops in older people.

Treatment

A patient diagnosed with an attack of renal eclampsia should be immediately hospitalized. Serious condition cannot serve as a basis for keeping a sick person at home. Rapid hospitalization and appropriate treatment measures applied in a hospital setting provide favorable outcome. Meanwhile, at home without proper medical care, the patient may die during an attack.

If transportation of the patient is impossible or delayed, then it is necessary to begin treatment at home, which is used in a hospital. In the future, at the first opportunity, the patient should be sent to the hospital.

First urgent therapeutic measure in a patient with renal eclampsia, bloodletting is performed, and at least 400-500 ml of blood should be released.

If even after bloodletting the patient cannot be hospitalized (not for health reasons, but for other reasons), then he needs to be administered intravenously 30-40 ml of a 40% glucose solution. Both phlebotomy and glucose administration help reduce cerebral edema.

For renal eclampsia, it is advisable to treat with a solution of magnesium sulfate. The purpose of this salt is its vasodilating effect. We have already indicated that one of the causes of an eclamptic seizure is a spasm of cerebral vessels. This served as the basis for designating eclampsia as “angiospastic encephalopathy.”

Besides vasodilator effect, magnesium sulfate in concentrated solutions acts as a means of causing tissue dehydration (hence its role in lowering intracranial pressure). Magnesium sulfate is used intravenously or intramuscularly. For intravenous infusion, a 10% solution in an amount of 10-15 ml is used. 20-25 ml of a 25% solution of magnesium sulfate is injected intramuscularly.

Rp. Sol. Magnesii sulfuric! 25% 20.0
D.t. d. N. 10 in amp.
S. 20 ml intramuscularly every 6 hours

It is advisable to continue the administration of glucose and magnesium sulfate, begun during an attack, for several days.

Bloodletting, treatment with glucose and magnesium sulfate, as a rule, ensure success, and the attacks stop. If the patient remains in a deep coma or, despite treatment, continues seizures, it is necessary to resort to a measure that reliably and quickly reduces intracranial pressure - a spinal puncture. The flow of cerebrospinal fluid in a trickle indicates a sharp increase in cerebrospinal pressure, and therefore intracranial pressure.

A decrease in cerebrospinal pressure is also determined by the nature of the flow of cerebrospinal fluid. If the fluid stops flowing out in a stream or frequent drops and is released in more rare drops, then the intracranial pressure has decreased. After this manipulation, convulsions occur. patients stop, the state of stunning decreases. Spinal puncture is resorted to in cases where bloodletting, administration of glucose and magnesium sulfate do not have an effect. This event must be remembered when making a diagnosis of renal eclampsia.

During an attack, it is advisable to administer 40-50 ml of a 3% solution of chloral hydrate as an enema. In addition, the patient must be completely at rest. It is necessary to protect it from bruises. To protect the tongue from biting, a spatula (wrapped in gauze) or a spoon is inserted between the teeth.

With the disappearance of the attacks, the patient’s treatment does not stop: he must be left in the hospital and treated for acute nephritis.

Renal eclampsia is a complication of acute nephritis. It is known that in a hospital setting it is observed much less frequently than in cases where patients with acute nephritis remain at home. Timely hospitalization of such patients and appropriate treatment serve as measures to prevent life-threatening attacks of eclampsia.

Basic clinical syndromes for kidney diseases:

Edema syndrome

The mechanism of occurrence of renal edema is complex, therefore it is not correct to explain their occurrence only by a decrease in plasma oncotic pressure due to the loss of protein in the urine. According to their origin, renal edema is nephritic and nephrotic. The first are observed in patients with glomerulonephritis in acute and chronic stages disease, but without the presence of

They are due to the following factors:

primary retention of sodium and water due to damage to the glomeruli;
increased capillary permeability in glomerilonephritis due to activation of autoimmune processes and damage to the main substance connective tissue, increasing hyaluronidase activity;
increase in hydrostatic pressure;
activation of the renin-angiotensin-aldosterone system. Increased production of aldosterone by the adrenal glands further increases the retention of sodium ions in the body, and this automatically leads to water retention in the bloodstream and tissues;
overproduction of antidiuretic hormone by the posterior lobe of the pituitary gland.

Nephrotic edema most often develops with inflammatory or degenerative damage to the tubules. It is in nephrotic syndrome that the leading mechanism for the development of edema is severe hypoproteinemia due to massive loss of protein in the urine. The result is a decrease in oncotic pressure in the bloodstream and the release of fluid into the surrounding tissues. Particularly persistent swelling occurs when several mechanisms are activated simultaneously.

Renal edema in the classic version is localized on the face and appears in the morning. The skin over them is pale, their consistency is soft, loose, and mobile. With large edema, they spread throughout the body and are often cavitary.

Arterial hypertension syndrome (hypertensive syndrome)

With kidney disease, secondary arterial hypertension, so-called renal hypertension, can develop. Hypertensive syndrome occurs:

as a result of damage to the kidney parenchyma (with glomerulonephritis or pyelonephritis, nephrosclerosis) - this is renoparenchymal, or truly nephrogenic hypertension;
in case of pathology of the vessels supplying the kidneys, this is renovascular (renovascular) hypertension;
in case of disturbances in the outflow of urine, this is reflux hypertension.

The mechanism of development of renal hypertension, especially renoparenchymal hypertension, is complex. Some differences have been established depending on the morphological form of glomerulonephritis. Regardless of the damaging factor (damage to the vessel or inflammatory process in the area of the glomeruli), ischemia of the renal parenchyma occurs, including the juxta-glomerular apparatus of the kidney, located in the glomeruli.

As a result, the production of renin is activated, thereby increasing the activity of angiotensin-converting enzyme, leading to increased production of angiotensin-2, a powerful pressor factor. Angiotensin-2 increases arteriolar spasm, which sharply increases peripheral resistance. The production of aldosterone by the adrenal glands and antidiuretic hormone is activated, which leads to sodium and water retention.

The selective accumulation of sodium ions in the walls of blood vessels, which also attracts water, has been proven. The resulting swelling of the vascular wall leads to a significant and persistent increase in peripheral resistance, which automatically sharply increases blood pressure. At the same time, a decrease in the production of depressor factors (kallikrein, prostaglandins, antirenin, angiotensinase, bradykinin, etc.) has been proven. Clinical manifestations of renal hypertension are generally the same as with primary (essential) arterial hypertension.

Features of renal hypertension:

There is always a clinical picture of kidney damage (glomerulonephritis, pyelonephritis, amyloidosis, nephrosclerosis, congenital or acquired stenosis renal artery etc.).
In 20% of cases, there is a rapid, malignant course that is difficult to treat.
Mainly increases diastolic pressure due to pronounced spasm of peripheral vessels.
Specific changes in the fundus: spasm of retinal arterioles and exudative changes in the form of numerous flocculent spots; retina with a grayish background, disc swelling optic nerves; small and large hemorrhages at the posterior pole of the eyeball, a “star” figure in the area of the visual spot.

Renal eclampsia syndrome

Eclampsia is most often observed in acute diffuse glomerulonephritis and nephropathy of pregnancy. In the pathogenesis of eclampsia, the main importance is given to:

increased intracranial pressure;
swelling of brain tissue;
vasospasm of cerebral vessels.

Attacks of eclampsia usually occur during periods of severe edema and increased blood pressure. Attacks are triggered by eating salty foods and drinking large amounts of liquid.

The first signs of an approaching attack of eclampsia are unusual lethargy and drowsiness. Then there appears a severe headache, vomiting, short-term loss of vision (amaurosis), speech (aphasia), transient paralysis, clouding of consciousness, increased blood pressure, and decreased pulse. Then frequent (every 30 seconds - 1 minute) tonic and clonic convulsions appear.

During an attack, the patient's face becomes cyanotic, the neck veins swell, the eyes roll upward, the tongue is bitten, and foam flows from the mouth. The pupils are dilated and do not react to light, the eyeballs are hard. Involuntary defecation and urination are often observed.

Attacks of renal eclampsia usually last several minutes. Patients often die from cerebral edema or cerebral hemorrhage.

Renal colic syndrome

Renal colic most often develops with, less often with kinking of the ureter, nephroptosis, or kidney tumor. Pathogenesis: reflex spasm of the ureter due to irritation of its wall with a stone and stretching renal pelvis, which is caused by a violation of the outflow of urine from it.

Renal colic has a characteristic clinical picture. Suddenly, usually after walking or jolting, severe, cramping pain appears, localized in the half of the lumbar region where the stone is located. The pain spreads down the ureter, into the groin area, and into the genitals. They are sharp in nature.

During an attack, the patient is extremely restless, screams, moans, and cannot find a place for himself. Renal colic is accompanied by nausea, repeated vomiting that does not bring relief, a feeling of fullness in the abdomen, bloating, and symptoms of functional intestinal obstruction.

Along with the pain, the following phenomena develop: frequent urination, pain and difficulty urinating. The amount of urine excreted is reduced, and at the end of the attack it is increased.

Changes in the urine are detected: single fresh red blood cells, and sometimes severe hematuria. “Urine sand” and small stones can be found in the urine. But during an attack it may not contain pathological impurities if there is a complete blockage of the ureter. The duration of the attack ranges from several minutes to 2-3 or more hours.

When examining the patient, the body temperature is normal, sharp pain is detected when palpating the lumbar region and a positive Pasternatsky sign. The diagnosis of renal colic in urolithiasis is usually confirmed by the typical clinical picture of the disease, changes in urinary sediment and X-ray and ultrasound data.