RENAL FAILURE — the syndrome which is developing as a result of disturbance of a renal blood-groove, glomerular filtering, a canalicular reabsorption and secretion, and also concentration ability of kidneys and characterized by an azotemia> disturbance of an electrolytic water balance and acid-base balance.
On a current distinguish acute and hron. Item of N. Acute P. of N arises suddenly owing to acute, most often reversible, damages of kidneys. Hron. The item of N develops gradually owing to the progressing irreversible loss of the functioning parenchyma of kidneys.
The acute renal failure
the Acute renal failure can arise at any age, but most often in 20 — 40 years.
disturbance of the general and renal hemodynamics, acute impact on kidneys of exogenous poisons, infectious agents, acute occlusion and damage of vessels of kidneys, obturation and a compression of uric ways, seldom an injury of kidneys are acute P.'s Reasons of N.
Etiol, factors of an acute renal failure can be united in groups. 1. Prerenalny factors — sharp reduction of volume of the circulating blood and decrease in the ABP at shock or bleeding, loss of a significant amount of water and electrolytes at a profuse diarrhea, long vomiting, burns, owing to use (especially long) diuretics. 2. Renal factors — exogenous poisoning with nephrotoxic poisons (salts of heavy metals, chlorinated hydrocarbons), alcohols, strong to-tami; poisons of a plant origin, napr, mushroom poison, snake poison, poison of insects; nek-ry medicines (at their overdose), and also damage of kidneys at occlusion of renal vessels (thromboembolism), at acute inflammatory diseases (an acute glomerulonephritis, acute pyelonephritis), nek-ry acute inf. diseases. 3. Prerenal factors — occlusion of uric ways a stone, a prelum of an ureter a tumor, a hematoma, a ligature, etc.
Acute P. of N can also arise after a bilateral nephrectomy according to vital indications and at traumatic loss of both kidneys (a so-called arenalny state).
Apprx. 90% of cases of acute P. of N it is connected with damage of kidneys owing to haemo circulator disturbances and poisonings with nephrotoxic poisons.
Necrotic changes of tubules at acute P. N are caused by the hypoxia developing as a result of hemodynamic disturbances or gistotoksichesky influences. Disturbance of a renal blood-groove and decrease in glomerular filtering — the most important mechanisms of acute P. of N. In an origin oligurias (see) or anuries (see) a significant role not selective absorption of a glomerular filtrate through a wall of the damaged renal tubule and hypostasis of an interstitium plays. A prelum of renal tubules and obstruction by their pigmental cylinders — only accessory factors of development of an oliguria. The big role in acute P.'s pathogeny of N belongs to humoral influences, especially from system a renin — angiotensin, (see. Angiotenzin ), capable to cause a vasospasm of kidneys and ischemia. There is an opinion that damage of tubules involves disturbance of a reabsorption of sodium and increase in its concentration in the field of a dense spot what the periarterial pad reacts increase in secretion to renin (see). High activity of a renin causes a spasm of the bringing glomerular arterioles (the bringing vessels) and decrease in glomerular filtering. In acute P.'s pathogeny of N such vasoactive substances as a histamine, serotonin, vasopressin, and also some steroids increasing sensitivity of fabrics to a hypoxia have a certain value. It is established that at this form of a disease shunting of a renal blood-groove is observed: blood, passing cortical substance of a kidney, comes to system of direct arterioles of marrow through balls of renal little bodies of yukstamedullyarny nephrons. Apparently, the spasm of interlobular arteries and ischemia of cortical substance of kidneys also possesses a certain role in a pathogeny of a cortical necrosis.
Morfol, changes of kidneys at acute P. N depend on an etiology, the period of a disease, timeliness, character and volume to lay down. actions. Macro - and the microscopic picture of ischemic changes of kidneys, or a so-called shock kidney (blanching of cortical substance at a plethora of a yukstamedul-lyarny zone), is more often observed at traumatic shock, blood loss and is not characteristic of processes ekzo-and an endotoxic origin. At gistol, a research find focal defeats of an epithelium of tubules with dominance of gidro-pichesky dystrophy of nephrocytes (fig. 1). Electronic microscopic examination demonstrates the expressed and deep damage of renal tubules: vacuolations of cytoplasm owing to expansion of tanks of a cytoplasmic reticulum; hypostasis or swelling of mitochondrions with the advent of flocculent consolidations and fragmentation of cristas; focal destruction of a brush border with partial hypostasis and sequestration of apical departments of cytoplasm. Less often the widespread kollikvatsionny necrosis of nephrocytes of gyrose renal tubules of proximal and distal departments of nephron develops. All these damages are followed by fermental changes of nephrocytes. The rupture of renal tubules (tubulorrhexis) is considered typical at shock though some pathologists consider it an artifact. At the shock which is followed by hemolysis imiolizy, morfol changes in kidneys correspond to a hemoglobinuric and mioglobinuriyny nephrosis (see. Myoglobinuria ). After infusional therapy morfol, the picture of defeat of renal tubules can change: owing to an osmotic nephrosis there is vacuolation, pinotsitozny bubbles increase and there comes stretching of a brush border of nephrocytes. In balls of renal little bodies note an anemia, exfoliating of separate endotheliocytes with stripping of basal membranes, sometimes subendothelial deposits of fibrin.
Thrombosis of capillaries of balls as manifestation of the disseminated intravascular blood coagulation is observed more often at bacteriemic shock and patholologically the proceeding pregnancy. To manifestations of the disseminated intravascular blood coagulation with development of a generalized phenomenon of Shvarttsman — Sanarelli (see. Shvarttsmana phenomenon ) carry also symmetric cortical necrosis of kidneys (See. Hemorrhagic cortical necrosis of kidneys ). Distinguish total, sub-total, segmented and small forms of a necrosis. At a total form renal pyramids remain; at subtotal — in cortical substance islands of not struck fabric meet; at segmented — the centers of a necrosis have an appearance of the heart attacks surrounded with hemorrhages; small forms manage to be revealed only at microscopic examination. At prolonged acute P. of N nekrotizovanny cortical substance of a kidney becomes thinner. Poisoning with ethylene glycol involves the symmetric cortical necrosis of kidneys which is combined with a glycolic nephrosis, and at pathology of pregnancy — with an acute haemoglobinuria, an apoplexy and a necrosis of cortical substance of adrenal glands, a necrosis of a front share of a hypophysis. The coagulative necrosis of cortical substance of a kidney is histologically noted. In glomerular circulatory capillaries and arterioles find fibrinous blood clots (fig. 2, a). The zone of a necrosis is limited to a demarcation shaft from polymorphonuclear leukocytes. Argyrophil the framework is destroyed. In a further nekrotizirovanny sites are exposed to the organization, fibrosis and calcification.
The nature of damage of kidneys at poisoning with nek-ry chemical substances, pharmaceuticals, poisons of plant and animal origin (so-called ekzotoksiche-Skye a kidney) in many respects depends on properties of poisons and their metabolites. Nephrotoxic effect of poisons of thiol group (compound of heavy metals, etc.) in the form of a characteristic coagulative necrosis of an epithelium of renal tubules it is caused by blockade of sulphhydryl groups of fermental and structural proteins. The nekronef-rose is a classical example a so-called sublimate kidney. Characteristic for nee macro-II microscopic changes give at the beginning of the 1st week in connection with a sharp plethora of vessels a big red sublimate kidney; by the end of the 1st week — a small pale sublimate kidney with a widespread coagulative necrosis of an epithelium, rejection of sequesters and regeneration of nephrocytes of renal tubules; on the 2nd week — a big pale sublimate kidney (on a section wide pale gray cortical substance of a kidney contrasts with bright pink wet renal pyramids). It is histologically observed: expansion of renal tubules, regeneration of an epithelium (endoteliopodobny heterochromatic cells with ugly kernels, mitoses, amitotic divisions); formation of simplast; in renal pyramids — kruglokletochny infiltrates around cylinders.
At a glycolic nephrosis the kidney is increased, on a section wet; histologically balloon dystrophy of an epithelium of tubules of proximal and distal departments of nephron (fig. 2, b) decides on crystals of oxalates in their gleam and in cells. Electronic microscopic examination reveals vacuolation as a result of sharp expansion of tanks of a cytoplasmic reticulum. Nephrocytes in a condition of balloon dystrophy can is long not to be torn away, slowing down regeneration of tissue of kidney.
Damage of kidneys at poisonings with chlorinated hydrocarbons has some features. At poisoning with a dichloroethane fatty dystrophy of nephrocytes of renal tubules of proximal and distal departments of nephron is noted. Perchloromethane and chloroform cause gidropichesky dystrophy of nephrocytes of gyrose renal tubules with formation of large vacuoles owing to expansion of tanks of a cytoplasmic reticulum.
The acute hemoglobinuric nephrosis develops at poisoning with hemolitic poisons (acetic to - that, hydrogen arsenide, a copper vitriol, amino compounds, nitro compounds, etc.). At the same time morfol, changes reflect transport of hemoglobin on system of nephron; the black-brown radial striation of renal pyramids caused by existence of pigmental cylinders (fig. 3) giving positive reaction of Lepene is typical for a gross appearance (see. Lepene way ) with benzidine. At poisoning acetic to - that the defeat of an epithelium of tubules of proximal departments of nephron caused by a reabsorption of hemoglobin which comes to light in a look benzidine - positive granules in cytoplasm histologically is found; at electronic microscopic examination the resorption of hemoglobin in vacuoles of cells with a partial necrosis of the apical departments «overloaded» with a pigment is found, process is followed by a rupture of tubules of distal departments of nephron with an exit in a stroma of contents of a tubule, inflammatory reaction around it and the subsequent its obliteration. Poisoning with hemolitic poisons of thiol group (hydrogen arsenide, compounds of copper, etc.) it is shown by an acute hemoglobinuric nephrosis in combination with a coagulative necrosis of nephrocytes.
A clinical picture
During acute P. N distinguish four periods: initial action etiol, factor, oliguria or anury, recovery of a diuresis, recovery.
During initial action etiol, a factor the manifestations caused by a specific etiology are observed; e.g., at the incomplete infected abortion anaerobic sepsis, bacteriemic shock, an intravascular hemolysis and acute P. of N develops. General symptoms of a disease: a fever, temperature increase, decrease in the ABP, pallor and cyanosis of integuments in combination with quickly accruing jaundice; urine gains dark color, in it appear protein, erythrocytes, leukocytes, cylinders, a blood pigment and a detritis. Irrespective of acute P.'s reason for N in this period changes of a hemodynamics, sometimes with considerable falling of the ABP always prevail; only after removal from shock (collapse) signs of disturbance of functions of kidneys begin to prevail.
The period of an oliguria or anury is characterized by decrease in a diuresis (less than 500 ml per day) and disturbance of renal functions — in blood the level of products of proteinaceous metabolism, nonvolatile to - t increases, the water and electrolytic balance changes. Patients complain of weakness, loss of appetite, a headache, become apathetic, sleepy. Nausea accrues, vomiting develops. In process of increase in level of urea, creatinine, uric to - you increase concentration of sulfates, phosphates, the hyperpotassemia is observed, concentration of sodium, chlorine and calcium in plasma decreases. The these shifts are more expressed, the signs are shown more clearly uraemias (see). There are symptoms of defeat of a nervous system: anisocoria, nystagmus, decrease corneal, tendon and periosteal jerks, anizorefleksiya, patol, reflexes, adynamia, decrease in memory, sometimes excitement, spasms, paralyzes. Drowsiness can be replaced by coma.
In this period there can be mental disorders which have preferential character of reactions of exogenous type (see. Bongeffera exogenous types of reactions ), is more often in the form of various delirious states. The delirium has usually fantastic contents (see. Delirious syndrome ). Meets less often amental syndrome (see), devocalization, development to-rykh demonstrates weighting of an acute renal failure. Epileptic seizures can take place (single or serial) up to development of the epileptic status.
Disturbances of functions of cardiovascular system and a hemodynamics are various, but tachycardia, expansion of borders of heart to the left, a systolic apex murmur are almost always observed. High the ABP — a non-constant symptom, but significantly influencing the current of this period; it can be the cause of emergence of pains in heart, heart failure, an attack eclampsias (see). Sometimes arises pericardis (see), at the same time the patient notes pains in heart, the pericardial rub appears; in process of increase of an exudate in his cavity the friction murmur decreases, but accrue simpto Toma of heart failure, borders of heart extend, the picture develops characteristic of a pericardis rentgenol. It is especially dangerous possible at acute P. by N the hyperpotassemia breaking electric activity of a myocardium. Depending on degree of a hyperpotassemia on an ECG the expressed delay of atrioventricular and intra ventricular conductivity, increase in amplitude and a sharp-pointed form of a tooth of T, decrease in potential of a tooth of R comes to light in various measure.
Increase of breath is often connected with acidosis (see); at heavy acidosis (acidemia) breath becomes noisy. Sometimes arises fluid lungs (see), against the background of to-rogo pneumonia quite often develops. The overhydratation, insufficiency of a left ventricle, decrease in oncotic pressure of blood, increase in capillary permeability are the main reasons for a fluid lungs.
Constantly at acute P. the N is observed anemia (see) — result of oppression of a hemopoiesis in marrow, blood loss and hemolysis. Defeat went. - kish. a path, except nausea and vomiting, it is shown by an abdominal pain, a diarrhea. Because of the raised bleeding in emetic masses and in Calais quite often find blood. Sometimes serous peritonitis develops.
The period of an oliguria or anury proceeds on average 2 weeks, however cases of longer oliguria are known (to 5 — 6 weeks).
Period of recovery diuresis (see) has two phases: an initial diuresis when per day it is allocated apprx. 500 ml of urine, and a polyuria — the diuresis exceeds 1800 ml. In a phase of an initial diuresis acute P.'s symptomatology of N significantly does not change or continues to accrue. This phase lasts only 2 — 3 days and is replaced by a polyuria. The phase of a polyuria sometimes develops violently, the amount of urine can reach several liters in this connection there is dehydration, patients lose flesh, skin becomes dry, shelled, language dry, thirst, weakness, pains in heart is noted. Premature ventricular contraction and heartaches — most often signs of a hypopotassemia, edge on an ECG is shown by decrease in a segment of ST, decrease and inversion of a tooth of T, emergence of a wave of U. The polyuria is followed by gradual decrease azotemias (see), contents of creatinine and urea in plasma, normalization of its electrolytic structure.
The period of recovery of a diuresis proceeds on average 20 days, but maybe longer.
The beginning of recovery it is considered to be normalization of content in blood of creatinine and urea. This period, during to-rogo the renal blood stream, glomerular filtering and concentration ability of kidneys are recovered, proceeds from 6 months to 2 years.
The most frequent complication of acute P. of N in the period of an anury is the fluid lungs (see), and also pyelonephritis (see) which can arise during any period of a disease.
Diagnosis the lab is based on a wedge, a picture, overseeing by a diuresis and on data. researches (acid-base composition and electrolytes of plasma, biochemical, changes of a nitrogen metabolism). For diagnosis of disturbances from heart and lungs carry out rentgenol, a research. At suspicion on obstruction of upper uric ways the retrograde ureteropiye-lografiya is shown (see. Piyelografiya ).
Character to lay down. actions is defined by the reason which caused acute P. of N. At disturbance of haemo circulation, shock (collapse) hold antishock events (see. Shock ), at acute poisonings — along with antishock therapy of an action for removal of poison from an organism: gastric lavage, infusional therapy (see), artificial diuresis, hemodialysis (see), hemosorption (see), haemo filtering (see), peritoneal dialysis (see), etc. At a massive intravascular hemolysis exchange is shown hemotransfusion (see), plasma exchange (see) with substitution by solution of albumine or plasma. If bacteriemic shock is acute P.'s reason of N, except antishock actions appoint antibiotics. At the beginning of the period of an oliguria or an anury the diuresis is stimulated with intravenous administration of furosemide on 160 mg by 4 times a day (to 1000 mg a day). If the diuresis at the same time increases, use of furosemide is continued. Further therapy is directed to regulation of a homeostasis. Appoint a caloric diet with the increased content of carbohydrates and fats (with restriction of protein and potassium). The volume of the entered liquid shall exceed a diuresis and an amount of water, lost by the patient with vomiting and excrements, no more than on 500 ml; at the same time surely enter 400 ml of 20% of solution of glucose from 20 PIECES of insulin. At hyperpotassemias (see), except glucose, appoint intravenously 10 — 20 ml of 10% of solution of a gluconate of calcium and 200 ml of 5% of solution of hydrosodium carbonate. Also anabolic steroids are applied. At the developed mental disorders tranquilizers, neuroleptics are shown. If the oliguria proceeds and symptoms of uraemia accrue, the patient should be transferred to department of a hemodialysis where it can be applied artificial kidney (see) or peritoneal dialysis. Indications to extrarenal clarification of blood are: increase in content of urea in blood of St. 200 mg / 100 ml (33,3 mmol/l), potassium of plasma of St. 6,5 mmol/l, an acidemia with deficit of the bases of 10 mmol/l, an overhydratation with clinical and rentgenol, manifestations of a fluid lungs, symptoms of acute uraemia.
Forecast at acute P. the N substantially is defined by the reason and weight of structural changes in kidneys which caused it. Posttraumatic and postoperative acute P. N have heavier forecast (a lethality apprx. 50%), than acute P. of N owing to other reasons (a lethality apprx. 10%). After the postponed acute P. of N in most cases there comes the absolute recovery. Only at nek-ry patients the changed function of kidneys remains that leads in the subsequent to arterial hypertension, hron, pyelonephritis or a nephrocalcinosis sometimes develops. After an extensive ischemic heart attack, a symmetric cortical necrosis of kidneys the outcome in hron is possible. The item of N
the Chronic renal failure
the Chronic renal failure arises more often at persons of young and middle age.
Chronic P. of N is an outcome of many is long flowing (from 2 to 10 years) diseases of kidneys and uric ways with gradual decrease in functional capacity of kidneys. Treat their number hron, a glomerulonephritis, hron, the pyelonephritis, intersticial nephrite, general diseases which are followed by damage of kidneys, a diabetic glomerulosclerosis, a nephrolithiasis, tuberculosis of kidneys, a hydronephrosis, an atony and obstructions of uric ways cystous a dysplasia, the hypoplasia, inborn tubulopatiya, an amyloidosis, etc.
Chronic P. of N is characterized by the progressing defeat of the majority or all nephrons most of which often are replaced with connecting fabric. According to the theory of intact nephrons offered by Brikker (N. S. Bricker, 1969), at chronic P. of N a part of nephrons perishes, and a part remains intact, hypertrophies and is long supports homeostasis (see); the remained nephrons function like nephrons of a healthy kidney. However researches M. Ya. Ratner, V. V. Serova, N. A. Tomil of other (1977) revealed heterogeneity and variability of defeats of nephrons and the processes happening in them at development of a chronic renal failure.
Morfol, changes of kidneys depend on the nature of the disease which led to P.'s development by N. Generally this degrowth of the functioning nephrons owing to their atrophy and a sclerosis of a parenchyma of body. Pathological changes at uraemia are various. Uraemic encephalopathy is expressed by dystrophy of neurons, hemorrhages and hypostasis. At long and heavy uraemia demyelination of nerves owing to effect of toxins is observed. At an uraemic myocardiopathy find a hypertrophy and dystrophy of a myocardium, dilatation of cardial cavities, atherosclerosis of coronary vessels, subendocardial hemorrhages, a pericardis, signs hron, pneumonia and a fluid lungs. At chronic P. and. pharyngitis and an esophagitis with micro and macrohemorrhages is observed hron. In a stomach and intestines along with hypostasis of a mucous membrane and a submucosa find hemorrhages and erosion. Dystrophy, a plethora, hemorrhages develop also in a liver, edges quite often happens increased. For hron, uraemias the hyperplasia of epithelial bodies and an osteodystrophy is characteristic (see. Osteopathy nephrogenic ). In more detail data about morfol, changes at hron. The item of N — see. Glomerulonephritis , Glomerulosclerosis diabetic , Nephrosclerosis , Pyelonephritis , Uraemia .
A clinical picture
the Most widespread a wedge, chronic P.'s classifications N are constructed taking into account weight of its current and data a lab. researches. E. M. Tareev (1972) offered in a wedge, the chronic P.'s current of N caused by diseases of a nonsurgical profile to allocate two stages: conservative and terminal. At the Urals, the diseases differing in an intermittent current the most recognized is classification of H. A. Jlonam-kina (1972), according to a cut allocate 4 stages of P. of N: latent, compensated, intermittent, terminal.
Chronic P. of N develops gradually that is connected with slow increase of content in blood of creatinine, urea, derivatives of guanidine, sulfates, phosphates and other metabolites. In a conservative stage when the diuresis is kept (the polyuria is often observed), the level of sodium, chlorine, magnesium and potassium in plasma does not increase. The constant iya is connected by hypocalcium with disturbance of exchange of D3 vitamin and absorption of calcium in intestines. The polyuria can lead to a hypopotassemia. The metabolic acidosis is often observed. Set of humoral disturbances causes symptoms hron, uraemias. Patients complain of bystry fatigue, decrease in working capacity, a headache, a loss of appetite, sometimes note off-flavor in a mouth. There are nausea, vomiting. Pallor, skin dry, flabby is noted. Muscles lose a tone, their small twitchings, a tremor of fingers and brushes appear. Sometimes arise an ostealgia and joints. Anemia develops, the leukocytosis accrues. Bleeding is raised. Often observed arterial hypertension leads to cordial frustration. Borders of heart are expanded, its tones are muffled, changes on an ECG are noted (they are sometimes connected with a diskaliyemiya). The adynamy with dominance of irritability, vegetative frustration develops in early terms of chronic P. of N and hypochiondrial reaped-bakhmi.
The conservative stage can last several years. The state allows the patient to work, but increase in an exercise stress, mental tension, errors in a diet, restriction of drink, inf. diseases, operations can lead to deterioration in function of kidneys and aggravation of uraemic symptoms.
At decrease in glomerular filtering lower than 10 ml/min. conservative correction of a homeostasis is impossible. There comes the end-stage: gradually the oliguria develops, the azotemia, acidosis, an overhydratation accrues; there is a Hyponatremia, a hypochloraemia, a gipermagniyemiya, the hyperpotassemia is possible. Emotional lability, block and inadequacy of behavior, mental disorders, character are characteristic of an end-stage to-rykh depends on degree of uraemia. In early terms there is an adynamy. Its feature is dominance of sharp fatigue, a hyperesthesia, disturbance of a rhythm of a dream (sleeplessness at night and drowsiness in the afternoon). In process of increase of weight of a state there is an adynamia, the adynamy in one cases is replaced by devocalization of various degree, up to coma (see), psychoses can develop in others. There is a gipnagogichesky delirium more often. Its feature is the ordinary of maintenance of hallucinations, contemplation, lack of motive excitement. Less often the amentia and twilight stupefaction develops. Development of psychoses in an end-stage of chronic P. of N always testifies to the adverse forecast of a basic disease. Somatic changes are various. The person is bloated, serozhelty color. There is a skin itch. On skin of a raschesa. Hair are dim, fragile. Dystrophy accrues, the hypothermia is characteristic. Voice hoarse. The ammoniac smell from a mouth is felt. There is aphthous stomatitis, sometimes parotitis. Language is laid over. The stomach is blown up. Often vomiting, vomiting, quite often a diarrhea repeat; kcal fetid, dark color. Anemia and hemorrhages accrue. Muscular twitchings become frequent and painful. At long development of uraemia appear an ostealgia and joints, fragility of bones is noted. Noisy breath is often caused by acidosis, a fluid lungs or pneumonia. Uraemia is complicated by a pericardis, pleurisy (see), ascites (see), a pseudoperitonitis, encephalopathy and an uremic coma develop (see. Uraemia ).
The end-stage lasts from several weeks to several months.
Diagnosis is established on the basis of data of the anamnesis about hron, a disease of kidneys, characteristic symptoms — uraemias, azotemias and others typical biochemical, disturbances.
In a conservative stage to lay down. actions are directed generally to recovery of a homeostasis, decrease in an azotemia and fight against displays of uraemia. During the falling of glomerular filtering it is lower than 50 ml/min. and increase in creatinine / 100 ml (177 µmol/l) the amount of the protein coming to an organism to 30 — 40 g a day is reasonable to reduce higher than 2 mg, and at glomerular filtering lower than 20 ml/min. appoint a low-proteinaceous diet (protein content of 20 — 24 g a day). The diet shall be high-calorific (apprx. 3000 kcal) and to contain irreplaceable amino acids (a meatless potato and egg diet and fishes). Food is cooked with limited amount of salt (to 2 — 3 g), and for patients with high hypertensia — without salt. At disturbance of calcic exchange and development of an osteodystrophy appoint a gluconate of calcium and D3 vitamin to 100 000 ME a day to a long time. It is necessary to remember, however, that use of D3 vitamin in high doses at a hyperphosphatemia can lead to calcification of internals therefore for decrease in level of phosphorus appoint Almagelum on 1 — 2 chayn. l. 4 times a day. Control of level of calcium and phosphorus in blood is regularly exercised.
Depending on degree of acidosis intravenously enter 100 — 200 ml of 5% of solution of hydrosodium carbonate. At decrease in a diuresis furosemide (lasixum) in the doses causing a polyuria is shown. For the purpose of decrease in the ABP use usual antihypertensives (see. Idiopathic hypertensia ) in combination with furosemide.
Treatment of anemia complex: appoint 5% oil solution of Testosteroni propionas on 1 ml intramusculary daily or other anabolic steroids, iron preparations, hemotransfusion, B12 vitamin, folic acid. Antibiotics and chemotherapeutic drugs use carefully. Only erythromycin is appointed in usual doses; doses of penicillin, ampicillin, Methicillinum, a tsepo-rin (Cefaloridinum) and streptocides reduce by 2 — 3 times. Use of streptomycin, Monomycinum, Neomycinum, polymyxin even in the reduced doses at chronic P. the N can cause neuritis of an acoustical nerve and other complications. Derivatives of nitrofurans are contraindicated. At edematization of lungs owing to an overhydratation it is possible to appoint sorbite (50 g in solution inside); it causes diarrhea and allocation of a significant amount of liquid. N apply glycosides concerning heart failure at chronic P. in the reduced doses, especially at a hypopotassemia. At a pericardis appoint small doses of Prednisolonum or make a hemodialysis which is more effective; in hard cases operational treatment is necessary. As symptomatic means tranquilizers can be used, at psychoses — neuroleptics. Nootropic drugs are effective. The hemodialysis is shown at chronic P.'s aggravation of N. After improvement of a condition of the patient it is possible to renew and for a long time to carry out usual conservative therapy.
In an end-stage when conservative treatment and an operative measure on kidneys and uric ways are inefficient, the patient is transferred to regular treatment (2 — 3 times a week) a hemodialysis, peritoneal dialysis. Indications to extrarenal clarification of blood at chronic P. of N arise usually when the clearance of creatinine falls lower than 10 ml! min., and its level in plasma exceeds 10 mg! 100 ml (884 µmol! л).
Use of a hemodialysis and renal transplantation (see) improved results of treatment of patients of chronic P. of N, allowed to prolong their life and to reach rehabilitation for many years. Thanks to a hemodialysis by 1981 in the world life more than 150 thousand patients of chronic P. of N is kept.
At timely use in late stages of chronic P. of N of new operational methods (a hemodialysis and transplantation of a kidney) there is a reduction of mental disorders, however the asthenic symptomatology and the phenomena of a psychoorganic syndrome remain. In adverse cases at long use of a hemodialysis so-called dialysis and uraemic dementia with slackness and apathy can develop. Long stay of the patient in a condition of uraemia, the expressed dystrophy, encephalopathy worsen results of treatment by a hemodialysis and do not allow to make renal transplantation.
The renal failure at children
the Renal failure at children proceeds, as well as at adults, in acute and hron, a form.
The main etiol, acute P.'s factors of N at children are: shock after operative measures and injuries, the toxi-infectious diseases which are especially followed by vomiting, a diarrhea, dehydration, acute infections, sepsis, a gemolitiko-uraemic syndrome, an acute intravascular hemolysis and a lipolysis, anaphylactic reactions, poisoning with nephrotoxic poisons, inborn damages of kidneys and renal vessels, fibrinferments of renal veins. Insufficient or excess administration of water and electrolytes at various serious illness and development on this basis in a short space of time of heavy dehydration or an overhydratation and a diselektrolitemiya can lead to acute P.'s development by N also.
At morfol, a research it is revealed that acute P.'s development by N in the post-natal period is quite often connected with a cortical necrosis of kidneys, prevalence to-rogo causes the forecast of a disease.
Acute P. of N at children quite often has resistant character, the symptomatology accrues against the background of the general serious condition, especially newborns and children of the first year have lives. At the advanced children's age during acute P. the N can allocate the same four periods, as at adults (initial action etiol, a factor, an oliguria or an anury, recovery of a diuresis and recovery), with identical clinical and biochemical changes.
Acute P. of N at a diffusion glomerulonephritis develops at children gradually. In the beginning P. of N especially expressed comes to light than more actively nephrite proceeds. In blood the content of urea, uric to - you, the general lipids, cholesterol, fibrinogen increases; level of creatinine slightly increases in blood serum (2 — 4 mg! 100 ml, or 177 — 354 µmol! k) and potassium (to 5,6 mmol). The diuresis decreases to 200 ml at normal or slightly reduced glomerular filtering. At inadequate treatment the acute renal failure with an azotemia, a hyperpotassemia and acidosis develops.
N at children plan acute P.'s treatment depending on its weight, duration of the period of an oliguria or an anury, degree of an azotemia and a diselek-trolitemiya. Conservative therapy is carried out taking into account age and the weight (weight) of the child. It is directed to normalization of a water salt metabolism and correction acid shche - l of internal balance, braking patol, a catabolism, recovery of volume and rheological properties of blood. Infusional therapy consists in administration of heparin, an Euphyllinum, glucocorticoids, glucose with insulin, isotonic solution of sodium chloride, cocarboxylase, strophanthin. At a hyperpotassemia appoint a gluconate of calcium, anabolic hormones; at acidosis — hydrosodium carbonate; at an alkalosis — glucocorticoids, veroshpiron and heparin, the blocking action and synthesis of Aldosteronum. Hemotransfusion, plasmas, albumine make according to the general indications. In the absence of symptoms of dehydration infusional therapy is supplemented with introduction of lasixum in a dose to 20 mg/kg. At level in blood of urea of 200 mg / 100 ml (33,3 mmol/l), residual nitrogen of 150 mg / 100 the ml (107,1 mmol/l), hyperpotassemias of 6,5 mmol/l is shown a hemodialysis or peritoneal dialysis. Dialysis according to indications is carried out to children from the first days of life.
Acute P.'s forecast of N at children is very serious, especially in the first two days of life. It is caused by rather low tolerance to acute P. in N and imperfection of adaptable mechanisms at newborns and babies. The N at children is important for acute P.'s prevention early recognition of different types of displaziya of kidneys (a polycystosis of the III type, a segmented beskistozny dysplasia, a hypoplasia with a dysplasia, an oligonefro-niya), and also inborn and hereditary damages of kidneys (hereditary nephrite, oxarods, oxalic nephrite, a cystinosis, a juvenile не-фронофтиз of Fankoni). Such children should be preserved against various stressful states, inoculations are contraindicated to them; active treatment inf is necessary. complications.
Chronic P. of N at early children's age extremely seldom proceeds typically. At chronic diseases of kidneys chronic P. of N at children passes in the development usually the same 4 stages, as at adults: latent, compensated, intermittent and terminal. Under favorable conditions, hl. obr. at diseases with defeat in the basic of the canalicular device (intersticial nephrite, pyelonephritis), the long time is observed the compensated chronic P.'s stage of N. Complex treatment of an aggravation of chronic P. of the N proceeding rather violently is carried out using high doses of diuretics or temporary use of a hemodialysis that quite often allows to recover function of kidneys and to transfer process to the compensated stage.
Intercurrent diseases, especially infectious, promote early approach of an end-stage, at a cut the hemodialysis or peritoneal dialysis is shown. According to special indications make renal transplantation (see).
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H. A. Lopatkin, A. P. Danilkov, G. P. Kulakov; L. H. Zymin (stalemate. An.), V. P. Lebedev (ped.), M. A. Tsivilno (psikhiat.).