UREMYYa (uraemia; Greek uron wetting - f haima blood; a synonym an uremia) — the syndrome of an endointoxication which is developing at the expressed renal failure as a result of a delay in an organism of nitrogenous metabolites and other toxicants, frustration of a water-salt, acid-base and osmotic homeostasis, followed by secondary exchange and hormonal disturbances, the general dystrophy of fabrics and dysfunction of all bodies and systems.
History of studying of the chemical nature of uraemia begins with Prevo and Dumas (J. L. Prevost, J. Century of A. Dumas, 1821), to-rye in an experiment with removal of kidneys at animals established the increased content of urea in blood. Similar changes were revealed then and at people with a serious illness of kidneys [R. Christison, 1829]. Since then a number of painful manifestations At. began to connect with accumulation in liquids of a body of toxic substances, to-rye in a normality are subject to allocation with urine. The concept «uraemia» is entered into a wedge, to the practician Pyorri and L'eritye (R. of Piorry, D. L’ Heritier) in 1840 when it was already known that in blood of patients with a serious illness of kidneys the content of urea and chlorides is increased. In Russia
A. I. Polunin gave to one of the first the detailed description of an urekhmiya (1853).
Uraemia is a kliniko-biochemical manifestation expressed acute or hron. a renal failure (see). Thus, the concept «uraemia» does not replace wider in patofiziol. sense of the concept «renal failure» together with tekhm the wedge, contents since a picture U also has more specific. it consists not only of direct symptoms of a renal failure, but also of diverse secondary disorders of activity of c. N of page, cardiovascular, respiratory and other systems. The adverse vital forecast, poly-systemacity and weight of manifestations At. defined the steady relation of clinical physicians to this state as having independent a wedge, value and demanding special studying revealed at At. disturbances of life activity in aspects of their pathogenetic diagnosis and creation of tactics of their prevention and treatment at patients with renal pathology. Depending on an origin, rate of development, reversibility uraemia, as well as a renal failure, divide on acute and chronic.
Etiology. Origin acute At. it is in most cases caused by disturbance of system and intra renal haemo circulation owing to the shock (see) burdened by pathological activation of a hemostasis and fibrinolysis, massive hemolysis, a myolysis, an immune cytolysis. Quite often shock happens result of an infection, poisoning or disturbance of water and electrolytic or acid-base balance. Action of this group of factors is implemented preferential at the irerenalny level. In case of the acute intersticial nephrite, pyelonephritis or a glomerulonephritis proceeding with an anury, poisonings with nefrotropny poison, obstruction of the main renal vessels uraemia of a renal origin develops. Sudden disturbance of passability of upper uric ways (on both sides or on side of the only functioning kidney) brings to prerenal U. Nakonets, uraemia can be caused by a renoprival state.
The most frequent reasons hron. uraemias are a glomerulonephritis, pyelonephritis, hereditary nephrite, iolikistoz nights, a diabetes mellitus, adenoma of a prostate, a nephrolithiasis.
Pathogeny. The leading role in a pathogeny of uraemia, both acute, and chronic, intoxication the products of exchange which normal are removed with urine plays. It is proved that in an organism of patients with At. the large number of organic matters, especially products of proteinaceous metabolism accumulates, many from to-rykh have toxicity. Except urea (see) ammonia (see), cyanate, creatinine (see Creatine), guanidines (see), uric acid (see), | 32 - m and to r og l about bu L of MONDAY, P2“ GLK) K0_
a protein, peptides of average molecular weight, amino acid, derivatives of pyridine (see), aliphatic and arylamines, polyamines (see Amines), an indole (see), phenols, mioinozitol, Mannitolum, acetone (see), lipochromes, cyclic AMF, glucuronic and oxalic to - you, a number of hormones (see), nek-ry enzymes collect, in particular, (see) etc.
Normal apprx. 85% of nitrogen it is excreted by kidneys in the form of the urea synthesized by a liver in a tricarbonic acid cycle — Genzeleyta from ammonia. In water solution urea partially dissociates to cyanate, about the Crimea as. assume, a considerable part of toxic effects of urea is connected. Symptoms of intoxication urea arise at its concentration in plasma of 200 — 300 mg! 100 ml are also characterized by preferential nervous breakdowns (fatigue, a headache, vomiting, a skin itch, a sleep disorder), a hypothermia, decrease in tolerance to glucose, bleeding. In an experiment urea in high concentration inhibits oxygen consumption by tissue of a brain, digestion of glucose muscles and erythrocytes, activity of renal monoamine oxidase, synthesis of protein in stimulated lymphocytes, aggregation of thrombocytes; in usual for patients with At. concentration it increases permeability of cellular membranes and sensitivity of a myocardium to potassium, and toxic action amplifies creatinine, guanidinsuktsinovy to - that, methyl guanidine. At hron. diseases of kidneys the content of urea increases in blood when glomerular filtering falls lower than 50 — 40 ml! mines, but if it remains
higher than 10 ml/min., then the level of urea can be skorrigirovan due to restriction of the consumed protein.
At the crushing accompanying or secondary damages of a liver, and also at a hypopotassemia (see) synthesis of urea and, therefore, inactivation of ammonia are broken. The last collects in cells and with the participation of a mitochondrial glu-tamatdegidrogenaza activates recovery amination and - keto-glutaric to - you, deleting it thereby from a cycle tricarboxylic to - t (see. Tricarboxylic acids a cycle) that conducts to respiratory depression and accumulation of ketone bodies (see). Ammoniac intoxication before everything is shown by symptoms of oppression of c. the N of page, in hard cases develops a coma (see).
A certain parallelism between expressiveness of symptoms is noted At. and the giperkreatininemiya (see the Creatinemia) arising at decrease in glomerular filtering to 50 ml/min. and less. Connect dizziness with a giperkreatininemiya, an adynamia, a depression and a row went. - kish. frustration. Actually toxicity of creatinine is proved only at its big concentration in blood, but under the influence of bacteria in intestines it is metabolized with education 1-me-tilgidantoina, methyl-aminoacetic acid, glioksi, and also the monomethylamine and methyl guanidine having toxicity.
The methyl guanidine formed of creatinine accumulates in cells (including adrenal glands, gangliyev), breaks formation of presynaptic depots of noradrenaline what presumably connect development with at At. sympathetic neuropathy. Besides, according to experimental data, it raises a catabolism, causes ulcerations of a mucous membrane went. - kish. a path, anorexia, transport of calcium and iron in intestines breaks. From other guanidines (see Guanidine) participating in a pathogeny of intoxication at At., are allocated gua-nidinsuktsinovy acid, edges it is found in cerebrospinal liquid and causes bradycardia, a giperlaktatemiya, slows down synthesis of hemoglobin, and also guanidinepro-pionovaya acid, edges inhibits glyukozo-6-phosphate — a dehydrogenase and strengthens spontaneous hemolysis.
At an acute renal failure elimination of uric acid is broken (see) with the bystry increase of its concentration in blood (to 12 — 15 mg / 100 ml) which is especially expressed at an intensive cytolysis. At hron. the renal failure which is not connected with gout, the hyperuricemia is usually less expressed (7 — 10 .ig/100 to ml) and in many respects connected with the raised catabolism since excretion uric to - you with urine long time remains increased (sometimes by one and a half times). Collecting in an organism, uric to - that forms salt deposits in fabrics that is followed by inflammatory and sclerous changes in them. At considerable disturbances of purine exchange (see). At. is followed by symptoms of secondary gout (see). Value of a hyperuricemia in an origin of an uraemic pericardis is discussed; it was shown, in particular, that the relation of concentration in blood uric to - you to an urea nitrogen at an uraemic pericardis are higher, than at patients without pericardis. Formation of salt deposits at At. it can be connected also with a delay in an organism shcha-conducted ev about y to and with l about you (see).
Toxic effects are probable (hl. obr. inhibition of synthesis of protein) the nek-ry derivatives of pyridine found in a significant amount in plasma at At.
The general tendency of frustration of amino-acid composition of blood at At. it is characterized by increase in concentration of the conjugated and separate free not essential amino acids at simultaneous reduction essential and disturbance of transport of nek-ry amino acids, in particular tryptophane (see). Content in blood about ks and p a beater and on and metilirovanny derivatives of a histidine is increased. Amin derivatives are formed of amino acids as a result of bacterial decarboxylation, many from to-rykh are considered as potential toxins. In particular, mono - di - and trimetilalanin are capable to cause nevrol. and mental disorders. Communication between the increased content in free Holin's blood (see) and a peripheral neuropathy is supposed (see the Neuropathy in neurology). During the splitting of phenylalanine (see) and tyrosine (see) arylamines — a shooting gallery of mines, feniletilamin, 3-gidrok-cityramin are formed, to-rye are capable to inhibit oxidation suktsinovy and glutaminic to - t, to oppress activity of a karboangidraza and doia-kokarboksi-manholes. Among the polyamines found in a blood plasma at At., spermidine, spermiya, pentamethylenediamine (see), putrestsin are defined. Polyamines are capable to modify activity of many enzymes and to break transport of glucose. As a result of bacterial decarboxylation and deamination of tryptophane the indole, indoxyl, an in-dicap (see), indikanuksusny to - that, skatole are formed (see), skatoksit, triptamin, 5-gidroksitrintamin (serotonin), 5-gidroksindoluksusny to - that, N-atse-tiltriptofan, to-rye collect in an organism at At. They are capable to strengthen transamination of tryptophane, to inactivate an insulinase
of ii to slow down neoglucogenesis (see Glycolysis). In high concentration indoles inhibit oxidation in tissue of a brain.
Carry phenol to uraemic toxins (see Phenols), phenolic to - that and their derivatives, to-rye are formed in intestines of tyrosine and phenylalanine and partially inactivated in a liver by a konjyugirovaniye with glucuronic to - that. Contents them in an organism is influenced by consumption of food protein. Phenols possess a specific neurotoxicity and connect development in patients with their influence with At. depressions and nek-ry nevrol. symptoms. In high concentration (in an experiment) phenols suppress consumption by a brain of oxygen, glycolysis, aggregation of thrombocytes, and also activity of many enzymes, including electrolytes, responsible for transmembrane transport.
Possess a neurotoxicity also mioinozitol and sorbitol, found in the increased concentration in liquids of a body at At. along with other carbohydrate connections (Mannitolum, glucuronic to - that, 1,5-angidroglyutsitol). Mioinozitol carry to the neurotoxins involved in development at At. an iye-reef riches to oh not in r apathy.
In 1938 Mr. P. Cristol with sotr. reported that at At. in blood small peptides collect in high concentration. Later it was allocated characteristic for At. middlemolecular fraction of peptides. containing a number of the substances inhibiting a hemogenesis, synthesis of DNA, a gluconeogenesis, lymphoblastoid transformation, transport of amino acids, synthesis of hemoglobin, activity a lipoprotein-liiazy. phagocytosis. Assume that accumulation of these substances matters for development of such uraemic symptoms as exposure to infections, anemia, a neuropathy, decrease in tolerance to glucose, a dis-lipidemiya. Also the peptides having natriuretic activity and a neurotoxicity are emitted.
From the high-molecular substances collecting in an organism at At. (P2-mikroglobulin, R2'GLYUK0PR0" theine, a retinolsvyazyvayushchy protein, a lysozyme, etc.), the greatest significance in a pathogeny of intoxication is attached to ribonuclease (see Ribonucleases), toxic action a cut is most expressed in a growth ratio and maturing of erythrocytes, lymphocytes and a blastotransformation of lymphocytes (see).
Intoxication at At. it can be caused by accumulation or redistribution in an organism of inorganic matters in connection with a metabolic acidosis (see) and disturbances of a water salt metabolism. Quite often water-salt imbalance at At. is followed by a picture of intoxication potassium (see the Hyperpotassemia) or magnesium (see Gipermagniyemiya). The insufficient renal clearance of the toxics (see Clearance) getting sometimes in small amounts to drinking water, foodstuff (salts of heavy metals, pesticides, herbicides, phenols, etc.), and also nek-ry pharmaceuticals, microbic toxins can be one of the reasons of intoxication. The chemical substances used for improvement of quality of drinking water (aluminum, fluorine, chloroamine, hypocalcium chloride) at their usual content in water can collect in an organism of patients with At., aggravating intoxication. Existence in water of impurity is especially dangerous to the patients who are on dialysis (see).
Disturbances of water-salt and acid-base balance have not smaller value in a pathogeny At., than intoxication.
Rather stereotypic for At. the process designated as a transmineralization — redistribution of water and salts between extra-and intracellular sectors with reduction of distinctions in their electrolytic structure is: in cells the maintenance of extracellular cations (sodium, calcium), chlorine and water increases, and to the extracellular sector cells come out potassium, magnesium, inorganic phosphates, sulfates. The transmineralization is followed by threat of potassium intoxication, falling of effective osmotic pressure and volume of extracellular liquid.
Obkhmen of water is closely connected with exchange of sodium (see) since osmotic and volume relationship considerably depends on the maintenance of this cation. In most cases acute and chronic At. content of exchange and capable sodium in an organism is increased owing to disturbance of excretion. At hron. a renal failure at patients without anury ability in limited limits to raise excretion of sodium at its excess receipt in an organism by braking of a canalicular reabsorption is kept. It is supposed that functional and restructuring of nephrons happens under the influence of natriuretic hormone (see Kidneys). Due to excess products of this hormone permeability for sodium of cellular membranes increases.
A delay of water at At. practically it is always connected with existence of an oliguria (see) or anuries (see) and increase in content of exchange and capable sodium in an organism. Most often a giiyergidratation of a body at At. happens isotonic, i.e. contained many liquid matters close to normal effective osmotic and colloid pressure and it is distributed preferential extra-tsellyulyarno, creating hypostasis (see) surface and deep friable fabrics. The hypertensive overhydratation as a result of excess receipt in an organism of sodium is sometimes observed (from a diet, poor at non-compliance, or in the form of medical solutions) at its rather insufficient allocation by kidneys. In such cases dehydration of cells at considerable increase of volume of extracellular water is possible, especially at the uncontrolled use of water by the patients thirsting. Special danger is constituted by accumulation of osmotically free water and development of the hypotonic overhydratation designated as «water intoxication». It is observed at excess ingress of water in an organism in the form of drinks and medical solutions, easily metaboliziruyemy substances, endogenous formation of water in the course of oxidation of organic matters. Decrease in effective osmotic and colloid pressure of extracellular liquid (due to its cultivation) leads to movement it in cells that causes their swelling, damage of intracellular structures and considerable disorders of function of cells.
At patients with At. also negative balance of water up to development of dehydration (dehydration) with preferential reduction of volume of the extracellular or cellular sector is possible. Seldom restriction of drink — any or caused by shortcomings of care of helpless patients is the reason of dehydration (old men, children, patients with mental or nevrol. frustration, etc.). More often dehydration develops owing to not enough filled losses of water or bhoitochechnymi in the ways (excess perspiration at fever and carrying out artificial ventilation of the lungs, diarrhea, vomiting, etc.), or as a result of a floor at-rii (see). The last is often observed at hron. tubulointersti-tsialny damages of kidneys (pyelonephritis, a polycystosis, sponge kidneys, etc.), during recovery of a diuresis at an acute renal failure, after elimination of obstruction of uric ways, and also in the presence of nek-ry associated diseases (sugar or not diabetes mellitus, a tumor of a brain). Seldom uncontrolled use of diuretics happens the reason of dehydration.
Dehydration, at Krom an osmotic ratio between extracellular and cellular liquid significantly does not change, call the general or isotonic. At the same time along with losses of extracellular water also hydration of cells decreases that leads to their dystrophy and considerable dysfunctions. Expressed cellular, or hypertensive, dehydration is caused, as a rule, by deficit of water at relative excess of sodium, as determines the high effective osmotic pressure of plasma and intersticial liquid. It is followed by a hyper catabolism that promotes acidosis, a hyperpotassemia, an azotemia. Use of medical solutions with the high content of sodium can aggravate cellular dehydration.
Preferential loss of sodium, i.e. extracellular electrolytic basis, with secondary decrease in effective osmotic pressure causes extracellular dehydration with a partial overhydratation of the cellular sector. Restriction of water and salt at a polyuria at patients with tubulointerstitsialny damage of kidneys can cause extracellular dehydration and a hyponatremia with development of a hypovolemia, falling of an effective renal plazmotok and glomerular filtering that can lead to progressing of an azotemia (see) and intoxications, including potassium. At diseases of kidneys with preferential defeat of vessels and renal balls (glomeruloiyefrit, a nave-roangioskleroz) adaptation to a lack of water and salt is long kept, and only at reduction of glomerular filtering to 10 ml/min. when the oliguria usually is already noted, at the vast majority of patients irrespective of the nature of a renal disease the delay of water and salt begins to prevail.
At. it is always accompanied by changes of balance of the main cation of intracellular liquid — potassium. At patients with an anury ability to remove potassium is broken, and at them the hyperpotassemia quite often takes place (see), development a cut can be promoted increase in a catabolism (including in connection with therapy by glucocorticoids), accompanying an anoxemia (see the Hypoxia), by acidosis, gastrointestinal bleeding (see), hemolysis (see), use of kaliysberegayu-shchy diuretics (see), and also excess intake of potassium in an organism with poor or as a result of transfusions of stored blood.
At an acute renal failure concentration of intracellular potassium is reduced and its deficit can become even more considerable during recovery of a diuresis in connection with a gyuliuriya. Potassium exhaustion is aggravated went. - kish. frustration, overdose of diuretics, starvation, long introduction to an organism of unbalanced solutions, free of potassium.
Patients with hron. in general are capable to support by diseases of kidneys satisfactory potassium balance until glomerular filtering does not decrease to 10 ml/min. and there will not come the oliguria. For chronic At. without the expressed displays of the general dystrophy potassium exhaustion is not typical, it meets generally at a nephrosclerosis (see) a secondary aldosteronism (see Giperaljdosteronizm).
At. at an acute renal failure it is characterized by a metabolic acidosis (see). In process of development hron. a renal failure in intact nephrons the reabsorption of a hydrocarbonate and excretion of H+ increases, the capacity of buffer systems at the same time changes, promoting compensation of the shifts of metabolism directed to decrease in pH of blood.
Development of acidosis is promoted by the delay in an organism of phosphates which always is observed at an oliguria and an anury. The hyperphosphatemia (see Fosfa-temiya) develops at glomerular filtering lower than 30 ml/min. and, being combined with a hypocalcemia, participates in formation of a secondary giperpa-ratireoidizm (see the Osteopathy nephrogenic) that, in turn, promotes acidosis.
Along with phosphates sulfates participate in formation of a metabolic acidosis, to-rye are released in a large number at metabolism of the amino acids containing sulfur and collect in an organism from the moment of emergence of an azotemia. Their concentration in plasma at At. it is increased quite often by 10 times and more. It is considered that sulfates partially replace chlorine in intercellular liquid, supporting thus a hypochloraemia (see).
Existence At. does not exclude development of an alkalosis (see). Progressing hron. the renal failure is characterized by the slowed-down excretion of surplus of the bases and at patients the metabolic alkalosis as a result of excess introduction of a hydrocarbonate or misapplication of diuretic means can easily develop (see Diuretics). The heavy metabolic alkalosis and hypopotassemia are observed also as a result of persistent vomiting, at a constant suction from a stomach of acid contents, at injection of a large amount of glucose and other sugars for the purpose of food of the patient.
At. is followed by disorder of exchange of magnesium. In the period of an oliguria at acute and against the background of decrease in glomerular filtering to 30 ml/min. and less at hron. a renal failure usually develops hyper-magniyemiya (see) generally at the expense of an exit of magnesium from cells. In muscular tissue the content of magnesium at At. it is reduced. Development of a gipermagniyemiya is promoted excess intake of magnesium with medicines or the dialyzing solution, and also observed at chronic At. hyper parathyroidism. At concentration of magnesium in plasma higher than 4 mekv/l the expressed inhibiting effect on c is shown. N of page with development of drowsiness, muscular weakness, a sopor and coma. The moderate gipermagniyemiya accompanying chronic At., influences negatively a mineralization of a skeleton and contributes to an osteodystrophy.
Deficit of magnesium can arise in connection with a polyuria at hron. pyelonephritis (see), during recovery of a diuresis at an acute renal failure, as a result of an intensive care diuretics. Hypomagnesiemia (see. Mineral metabolism) is shown by neuromuscular frustration (a tremor, muscular twitchings, spasms, a positive symptom of Hvostek), anorexia, vomiting, confusion of consciousness.
General disorders of exchange and dysfunction of bodies and fiziol. systems of an organism at At. are directly connected with disturbance of a chemical homeostasis, dysfunction of cellular membranes and damage of cells and are caused by also secondary disorders of regulation of functions of an organism nervous and endocrine systems in connection with early disturbance of their activity.
For At. disturbances of oxidation-reduction processes, the anoxemia and a fabric hypoxia aggravated by acidosis and anemia are characteristic. Protein metabolism is early broken and the catabolism what is promoted acidosis, a hyperventilation, muscular twitchings amplifies. At the same time utilization of energy at At. it is reduced that is quite often expressed by a hypothermia, but at sharp increase of a catabolism patients with cellular dehydration have a hyperthermia. In general metabolism at patients with heavy At. it is characterized by dominance of processes of dissimilation with the general dystrophy of fabrics, reduction of Sukhoi of body weight. As a result the cachexia (see) which is quite often complicated by serosites of the toksiko-chemical nature with additional losses of protein at exudates in serous cavities develops.
Hormonal disturbances consider an important link of a pathogeny of uraemia. In blood somatotropic hormone (see), prolactin (see), insulin (see), a glucagon (see), metabolites of corticosteroids (see), a calcitonin collect (see), parathormone cosecretes much (see), but effect of hormones is changed in connection with patol. a condition of receptors in fabrics and damage of renal mechanisms of implementation of action of a number of hormones (antidiuretic hormone, Aldosteronum, parathormone, etc.). Renal products of a renin (see), erythropoetin (see Erythropoetins), prostaglandins (see), D3 vitamin are broken (see Calciferols)) that is expressed by arterial hypertension (see arterial hypertension), disturbance of a hemopoiesis (see), an osteodystrophy (see).
Exchange of carbohydrates suffers at most of patients with At., and more than at a half of patients tolerance to glucose is reduced that allows to speak about an uraemic diabetes mellitus. Sensitivity of R-cells of a pancreas to glucose is considerably reduced; the increased content in blood of insulin and its more long circulation (to 5 hours instead of 2 hours at healthy) and increase by 2 — 6 times of maintenance of a glucagon are caused by reduction of their renal clearance. The ratio pro-insulin/insulin is changed in favor of the first. Sensitivity of fabrics to insulin, including and to exogenous, is weakened. The proteinaceous catabolism and development of dystrophy of a myocardium can be connected with high content in blood of a glucagon. Except decrease in renal clearance of insulin in an origin of disorders of carbohydrate metabolism at At. can matter disorder of exchange of calcium, potassium exhaustion, acidosis, excess of pro-insulin, the increased content in plasma of kontrinsulyarny hormones, accumulation in an organism of the toxicants inhibiting fermental systems and competing for fabric receptors and substrates. Digestion of glucose muscles at At. it is broken at a stage of transport in a cell, the reutilization of a lactate and synthesis of acetyl coenzyme A is lowered; at the same time the content in blood of pyruvate increases, and - ketoglutarate, malate. In nervous tissue inclusion of pyruvate in a cycle lemon to - you is broken, in erythrocytes it is inhibited fruktokina-for and cumulation of makroer-gichesky connections is reduced that creates metabolic premises for frustration of transport of electrolytes and hemolysis. In kidneys, in comparison with other bodies, utilization of glucose is increased though there are defects in metabolism of pyruvate, and - ketoglutarate and transport of acids. It is known that dialysis leads to temporary improvement of metabolism of glucose.
At At. it is expressed lipidic exchange (see the Lipometabolism) is broken that connect with the accelerated synthesis and the slowed-down metabolism of triglycerides (see). The last can be a consequence of deficit of cholesterol and nek-ry lipoproteids of high density, from to-rykh activation a lipoproteid lipase (see) and fabric metabolism of lipoproteids of very low density depends (see Lipoproteids). Besides, in blood of patients with At. the peptides of average molecular weight inhibiting a lipoproteid lipase, and contain in muscles at chronic At. deficit of a carnitine is noted, from to-rogo transport fat to - t in a mitochondrion where they are exposed to oxidation depends. The type of a dislipopro-teinemiya does not depend on the nature of a renal disease. More than in half of cases reveal plasma cholesterol, hyper-triglitseridemiyu with normal or moderately reduced contents, that classify as the IV type of a giiyerli-poproteinemiya by Fredrikson (see Lipoproteids). With a smaller frequency reveal a giperlipoproteinemiya of Pa of type, at Krom the content of triglycerides normal, and cholesterol raised, or the 116th the type which is characterized by the increased content of triglycerides and cholesterol. Most often it appears very low density increased concentration of lipoproteids at the subnormal maintenance of fraction of lipoproteids of high density and cholesterol.
Exposure of patients with At. a hyperpegmentation are explained with accumulation of melanin (see) and lipochromes from group of carotinoids (see).
Hormonal regulation of sexual functions at At. it is broken. Inefficiency of a feedback mechanism in regulation of products of a number of hypophyseal hormones leads to hypersecretion folliculin - the stimulating hormone, and also luteinizing hormone (see) and prolactin, the renal clearance to-rykh is reduced. At the same time the content in blood of testosterone (see) at men and estrogen (see) at it female is reduced.
Content of tpreotropny and thyroid hormones at At. remains close to normal therefore an observed xeroderma, reasonably connects decrease in standard metabolism, a hypothermia with ekstrati-reoidny factors of a pathogeny At., but not with hypofunction of a thyroid gland. Since products of parathormone (see) as it was stated above, at At. it is increased as a measure of protection against its surplus regard the increased content in blood of patients with At. thyrocalcitonin and its derivatives. At the same time sensitivity of fabrics to effect of thyrocalcitonin at At. it is reduced.
Nevrol. frustration at At. — encephalopathy (see) and a polyneuropathy (see the Neuropathy in neurology) hl are caused. obr. toksiko-me-tabolicheskimi factors and hypersensitivity of a nervous system to a hypoxia, disturbance: chemical homeostasis and hydration of cells. At a hypotonic cellular overhydratation of function of c. N of page are broken earlier and is more expressed, than functions of other systems. Along with possible wet brain and action on c. N of page of neurotoxic products of metabolism in a pathogeny of uraemic encephalopathy attach significance also to accumulation in a cerebral cortex of salts of calcium under the influence of parathormone that finds confirmation in changes of electric activity of a brain. Especially high the content of calcium happens at acute U. Otmecheno also accumulation in nervous tissue of magnesium, potassium, aluminum at simultaneous decrease in content of sodium. Elimination of an acute renal failure, dialysis reduce the content of calcium in nervous tissue and displays of encephalopathy.
The uraemic polyneuropathy develops at decrease in glomerular filtering approximately to 12 ml/min. Major importance in its origin is attached to influence of a mioino-zitol, middlemolecular peptides and other toxins, to-rye inhibited to a transketomanhole of nervous tissue and break metabolism of a myelin. Changes of nervous tissue are characterized by an axonal degeneration, segmented demyelination, a chromatolysis in neurons of front horns, dystrophy of neurons in a medial part of back columns of a spinal cord, less in chest departments is preferential in lumbar.
Importance in a pathogeny of manifestations At. have hematologic and hemocoagulative frustration. Chronic At. is followed by the acquired qualitative and quantitative defects of a platelet hemostasis and development of anemia (see). Thrombocytes differ in the lowered ability to aggregation, activation of thromboplastin, adhesion that connect with toxic effect of urea, guanidine - acetum to - you, compounds of phenol. Approximately at V5 of patients with At. reveal the average degree of a thrombocyte not of Pia (see) depending on a gshgerparatireoidny myelofibrosis or on a hypersplenism (see the Spleen). As a result of these changes a bleeding time at patients with At. it is increased, and hemorrhagic diathesis develops (see. Hemorrhagic teza of a bottom).
The pathogeny of anemia is connected as with oppression of a hemopoiesis by toxins and insufficient eritroioetichesky function of kidneys, and with an increased hemolysis under the influence of toxicants and as a result of disturbance of hydration of erythrocytes. The big group of the substances accumulated in blood at At possesses the action inhibiting a hemogenesis and hemolyzing., including middlemolecular peptides. Additional value the hidden and explicit blood losses (including in connection with a gepa-rinization and dialysis), a low-proteinaceous diet, deficit of iron, folic to - you have, loss of anabolic function of steroids. In general degree of anemia is proportional to an azotemia.
In the conditions of uraemic intoxication life expectancy of the lymphocytes circulating in blood is considerably shortened. For T-limfotsi-tov (see. Immunocompetent cells) insufficiency of reaction of hypersensitivity z and honey of lenny type, blastogenic response is proved and products of interferon. Immune disturbances are shown by also defective phagocytosis (see) owing to what stability to inf. to diseases at At. it is reduced. Also atrepsy is significantly weakened (see Immunity of pro--t of willows about about down about l evy).
Respiratory organs is involved in patol. process at At. in connection with influence of toxic products of metabolism, a delay of edematous liquid in lungs and its transudation in a pleural cavity with dysfunction of external respiration lowered by tolerance to an infection, immune and dystrophic frustration. More than 2/3 patients with At. have different expressiveness a fluid lungs (see), in a pathogeny to-rogo along with the general delay of water an important role is played also by a circulatory unefficiency.
A considerable azotemia, acidosis are followed by dryness of a mucous membrane of respiratory tracts, disturbance of its barrier and drainage functions that promotes development of the inflammation extending to bronchial tubes and intersticial tissue of lungs. Against the background of hron. stagnation in lungs there are secondary infiltrative and proliferative changes which are followed by a thickening of alveolar partitions, a hyalinosis of transudate and walls of vessels, the fibrosklerotichesky transformation of lungs breaking diffusion of gases in alveoluses. The so-called uraemic pneumonitis, signs develops to-rogo reveal almost at all patients with chronic At.; it promotes emergence of respiratory insufficiency with development of an anoxemia, sometimes and hypercapnias (see).
The most characteristic displays of pathology of cardiovascular system at At. are presented by dystrophy of a myocardium with development of its insufficiency, a pericardis, arterial hypertension and the progressing development of atherosclerosis of arteries with secondary regional circulatory disturbances. The pathogeny of arterial hypertension (see arterial hypertension) in the leading links is not connected directly with At. also depends on the nature of damage of kidneys, but at At. maintenance of hypertensia is promoted by a hypervolemia and decrease in clearance of hypertensive substances.
The pathogeny of dystrophy of a myocardium includes as factors of an overload of heart (in connection with a hypervolemia and arterial hypertension), and deficit of power ensuring work at insufficiency of oxidizing phosphorylation in connection with anemia, an anoxemia, disturbances of carbohydrate and lipidic metabolism, and also a lack of amino acids in connection with disturbances of protein metabolism. Multiple melkoochagovy necroses, proteinaceous dystrophy, the expressed intersticial hypostasis of a myocardium, formation of a cardiosclerosis are characteristic (see). Hyperfunction of a myocardium because of dystrophy is not followed by that degree of its hypertrophy, edges is necessary for adaptation of heart to arterial hypertension; the sizes of heart increase generally at the expense of dilatation of cavities that accelerates development of heart failure (see).
Uraemic pericardis (see) treats private manifestations of defeat of serous covers at uraemia, a cut can be widespread (polyserositis) and has generally toxic genesis. Major importance in its origin is attached by retention of metabolites, in particular uric to - you and middlemolecular components. Dialysis eliminates manifestations of a pericardis, but use at the same time of anticoagulants can bring in the subsequent to a hemopericardium.
The strengthened atherogenesis at At. it is caused by the expressed dislipi-demiya, disturbances of exchange of carbohydrates and damage of cellular membranes. Also arterial hypertension, a low-proteinaceous diet, disturbance of elimination of phosphate and a secondary hyper parathyroidism (see and a per paratireoz) have pathogenetic value in this connection there is an intensive infiltration of walls of arteries salts of calcium. Sometimes the myocardium and the carrying-out system of heart are exposed to calcification that can be the cause of life-threatening frustration of a rhythm and conductivity.
Defeats went. - kish. a path at At. are shown by a picture of a toxic inflammation of a mucous membrane went. - kish. path (gastritis, duodenitis, etc.). However diverse disiyeptichesky manifestations At. significantly weaken or disappear after dialysis that indicates their communication also with a retention of the toxicants which are directly breaking function of digestive glands, motility of a stomach and intestines. Such disiyeptichesky frustration as anorexia, nausea, vomiting, can be in some cases display of intoxication of c. N of page. Ulcerations of a mucous membrane of a stomach and a duodenum, often observable at At. and quite often complicated by bleeding, explain with high content in blood of gastrin and parathormone, damage of a protective mucous barrier; other frustration attribute to disturbances calcium - phosphorus exchange and ectopic calcification.
Clinical picture. Manifestations At. consist of a set of the symptoms reflecting polysystemacity of defeats at this state. Their formation depends both on character of a basic disease, and on rates of increase of a renal failure that causes nek-ry features of manifestation acute and chronic At. Many symptoms At. are not strictly specific, but a combination of symptoms of defeat of this or that system, especially at hron. At., quite often designate as syndromes. Allocate, e.g., asthenic, dispeptic, dystrophic, serous and joint, anemic, hemorrhagic and other syndromes, emphasizing typicalness for At. combinations of several of them.
Outward of patients with is rather characteristic At. They are sluggish, apathetic, sleepy. The person is bloated, pale with yellowness, and at ill a long time with brownish «suntan». Skin is thin, dry, flabby: the scabby hyperkeratosis, an atrophy of indumentum and nails is noted. At nek-ry patients it is possible to observe on skin salting-out of crystals of urea in the form of «uraemic powder». Due to the deposits of salts in skin patients have a painful itch that conducts to raschesa of skin and a pyoderma (see). Quite often a furunculosis (see the Furuncle), fungus diseases of skin come to light (the SI.), very often petechias (see) and the ecchymomas (see Hemorrhage) arising in various parts of a body without visible occasion. Due to hron. strips of stretching, sites of an induration and trophic frustration up to necroses of skin can be hypostases. Sometimes in occipital area, on extensor surfaces of large joints, the outer surface of hips can observe nodulyarny calcificats, fistulas and hems after their healing. A recurrent bursitis and synovites occur at certain patients.
Rather early at At. there is a muscular weakness expressed preferential in muscles of a shoulder and pelvic girdle, a back — manifestation of a proximal miopa-gpiya (see) that complicates a rising from a bed, the movement on a ladder. In process of increase of the general dystrophy symptoms of a distal myopathy — paresis and an atrophy of separate groups of muscles of extremities appear. Come to light characteristic for At. changes of bones and joints (see the Osteopathy nephrogenic).
Displays of encephalopathy at chronic At. correlate with degree of a renal failure. The general weakness, disturbance of attention, storing, a dream belong to the first symptoms. Appear apathy later (see. An apathetic syndrome), a lethargy (see), sometimes hallucinations (see), nonsense (see), convulsive attacks; development of the coma (see) differing in gradual change of consciousness against the background of symptoms of the accruing acidosis, a gipermagniye-miya is possible; emergence of an ammoniac smell in expired air is characteristic. At acute At. symptoms of encephalopathy differ in exclusive weight and dynamism. Quickly the adynamy, a disorientation, euphoria which is replaced by a depression, drowsiness accrue. At nek-ry patients are observed a delirium (see. Delirious syndrome), system hallucinations, a mutism (see the Speech, frustration), a catatonia (see. Catatonic syndrome). In hard cases the oglushennost (see Devocalization), the stupor (see Cmi/porous of a state) passing into a coma accrues.
The uraemic ggolinevropatiya is shown by symmetric, preferential distal sensory-motor frustration. Hyper - and paresthesias in the form of burning, feelings of crawling of goosebumps, prickings, an itch, swelling or numbness (a syndrome of uneasy legs) are characteristic. Paresthesias (see) are more expressed at rest, in the evening, weaken at the movement. Suffer superficial, deep, painful and vibration sensitivity (see), deep reflexes are lost. Depending on extent of damages the speed of carrying out electric impulses on nerves decreases that is used for objective diagnosis of a neuropathy and control of efficiency of its treatment. At an acute renal failure uraemic defeats peripheral and cranial nerves differ in inconstancy and variability, there can sometimes be passing paresis and paralyzes (see Paralyses, paresis).
Disturbances of taste and sense of smell are always present at an overall picture chronic At.; acoustical and vestibular frustration are less natural and are observed preferential as complications of medicinal therapy. To deterioration in sight, and a hole and the retinopathy (see) at patients with arterial hypertension, and also a hyper parathyroidism, the shown iritativny conjunctivitis (a symptom of red eyes), a keratitis (see), a cataract leads to a total blindness (see) (see). Occasionally also toxic optic neuritis (see), medicinal deposits in transparent environments of an eye, an embolic hemianopsia (cm) meet.
Frequency and depth of breath at patients with At. depend on development of respiratory or heart failure and on existence of an acid-base imbalance. Breath like Kussmaul (see Kus-smaul breath) is typical for a metabolic acidosis, and at heavy acidosis — like Cheyn — Stokes (see Cheyn — Stokes breath) that is followed usually by a myoclonus (see the Myoclonia), a mioplegiya, confusion of consciousness. Rare shallow breathing in combination with tetanic spasms and disorders of consciousness (a sopor, a coma) is characteristic of a metabolic alkalosis.
Recognition of disturbances of water-salt balance, life-threatening the patient, - — hyperpotassemias, gipermagniye-miya, hypopotassemias, different types of an overhydratation and dehydration is very important for therapeutic tactics.
The hypertensive overhydratation, edges develops in connection with excess receipt in an organism of sodium, is shown by thirst (see), dryness of mucous membranes, increase of arterial hypertension and other symptoms of an overload liquid.
At a hypotonic overhydratation the picture of «water poisoning» develops: disgust for water, vomiting, headache, concern, frustration of mentality, focal nevrol. disturbances up to a hemiplegia, attacks of a renal eclampsia, disorder of breath, a lump.
Dehydration of isotonic type is shown by reduction of the weight (weight) of a body, a Crocq's disease, loss of elasticity of soft tissues, weakness of muscles, decrease in the ABP, patol. bleeding, osiplost of a voice, disturbance of passability of respiratory tracts and gullet. At extracellular dehydration body weight is reduced slightly; skin and mucous membranes dry, but thirst insignificant or at all is absent; are expressed muscular weakness, the headache, the ABP decreases, vomiting, attacks of spasms, a lump are possible. At cellular dehydration one of the first symptoms — considerable reduction of body weight. Skin remains wet, but features are pointed, eyes deeply sink down, release of the lacrimal liquid stops. Thirst is constant, unsatiable and it is transferred painfully because of the termination of department of saliva. Characteristic symptoms of dehydration of a brain are apathy, muscular twitchings, hallucinations, nonsense, a hyperthermia, disturbances of breath. In hard cases the coma develops.
At a research of a respiratory organs at patients with chronic At. most often the overhydratation of lungs is found, edges at an early stage comes to light only radiological (strengthening of the pulmonary drawing, oblakovidny infiltration of roots of lungs), then is shown by wet rattles (see), and in hard cases the developed picture of a fluid lungs (see). Symptoms of bronchitis (see), the pneumonia (see) which is often observed at patients with At can be defined. At development of an uraemic pneumonitis symptoms of respiratory insufficiency (see) mixed ooze (restrictive and diffusion disturbances) dominate. In rare instances (at the expressed giperparatireoi-dizm, the strengthened glucocorticoid therapy, misapplication of vitamin D) there is a massive infiltration of tissue of lungs salts of calcium to development of an irreversible pulmonary heart (see. Pulmonary heart). Radiological at the same time reveal bilateral melkoochagovy infiltration of lungs, to-ruyu differentiate with tuberculosis (see Tuberculosis of a respiratory organs) and other diseases with similar rentge-nol. manifestations.
The plastic pleuritis (see) is noted approximately at 20% of patients, quite often it is combined with a pericardis (sagas.) and other manifestations of an uraemic polyserositis. At an exacerbation of uraemic gout parietal pleurisy arises as consensual reaction in relation to a costal iyerikhondrit and a periostitis. At patients with the expressed hypostases the hydrothorax comes to light, as a rule, (see).
To the main manifestations of cardiovascular frustration at At. belong arterial hypertension, edges it is observed approximately at 80 — 90% of patients, symptoms of dystrophy of a myocardium (see the Myocardial dystrophy), heart failure (see), a pericardis. Arterial hypertension in most cases gives in to partial or full correction by pharmaceuticals or dialysis, but at 10 — 15% of patients it has malignant character. Dystrophy of a myocardium is clinically shown by an asthma, increase in the sizes of heart, deaf tones, a cantering rhythm (see Gallop a rhythm), sometimes ekstr an asystolia (see) and other arrhythmias of heart (see). Stenocardia (see) as display of coronary atherosclerosis is quite often observed. The developing circulatory unefficiency concerning a rezistentn to therapy by cardiac glycosides and to dialysis.
Emergence of signs of a pericardis (see) confirms transition of a renal failure to an end-stage. The pericardis develops approximately at 50% of the patients receiving conservative therapy and only at 10% of patients, to-rye are treated by regular dialysis. Various options of a pericardis — fibrinous, serous or serous and hemorrhagic (to-ry can be followed by a cardiac tamponade), and also subacute, representing a transitional phase from vypotny to the chronic cardial compression which is characterized hron are observed. current.
The most important symptoms of the beginning uraemic pericardis are stethalgias (in 60 — 70% of cases), fever (in 75 — 95% of cases), a pericardial rub (in 90 — 95% of cases), a leukocytosis (in 60 — 70% of cases), atrial arrhythmia (in 20 — 30% of cases) and changes of an ECG. For a vypotny pericardis and development of a cardiac tamponade (see) considerable expansion of borders of heart, tachycardia, short wind, sometimes paradoxical pulse, swelling of cervical veins, painfully increased liver, emergence or increase of ascites, weight in breasts, the progressing decrease in the ABP and increase in the central venous pressure and filling pressure of a right ventricle, considerable reduction of cordial emission are characteristic. For diagnosis of a pericardis and a cardiac tamponade use a X-ray analysis, radio isotope and ultrasonic investigation. For the purpose of differential diagnosis of heavy heart failure in some cases sounding of a right ventricle of heart is shown. Vypotna the pericardis and a cardiac tamponade are differentiated with heart failure and with chronic cardial compression.
Zhel. - kish. frustration arise already at a moderate azotemia and typical manifestations — anorexia, nausea, vomiting, a hiccups, an ammoniac smell from a mouth, stomatitis, heartburn accrue to an end-stage U. Naiboley. In an end-stage of uraemia often observe parotitis (see), round gastroduodenal ulcers, pancreatitis (see), locks, uraemic colitis. The ulcers of a large intestine inclined to bleeding and perforation can be formed. As the component of an uraemic polyserositis sometimes arises aseptic peritonitis (see). At nek-ry patients the sprue is observed (see Mal-absorbtsii a syndrome). Sexual frustration at At. at children are shown by infantilism, at men — progressiruyushchy weakening of a libido, oppression of a spermatogenesis (oligoazoospermiya). At women disturbances of a menstrual cycle (see), infertility are usually observed (see).
Anemia develops, as a rule, in that case when glomerular filtering is less than 25 ml! mines, but at nek-ry renal diseases it can arise and earlier. Uraemic anemia is characterized as normotsitarny, normokhrom-ny with normotsellyulyarny marrow, normoblastic maturing of erythrocytes. Along with anemia thrombocytopenia, often a lymphocytopenia comes to light.
From a lab. researches for diagnosis At. the greatest value has definition in blood of nitrogen-containing substances (see the Azotemia), creatinine (see Creatine), urea (see), an uric kislotna (see), the main electrolytes — sodium (see), potassium (see), magnesium (see), calcium (see), and also phosphates, pH. For assessment of extent of disorders of exchange of organic matters investigate the maintenance of jb of blood of protein and its fractions, lipids, sugar, including in test with loading glucose. The changes revealed at At. in urine, depend on the nature of renal pathology and degree of a renal failure.
Treatment. In a complex of actions for treatment of patients with At. enters: the medical and guarding mode, a diet, conservative therapy, dialysis and other methods of extrarenal clarification of blood, renal transplantation (see), an all-surgical grant, rehabilitation and social adaptation. The choice to lay down. tactics depends on the nature of pathology of nights, a condition of the patient, and also opportunities of establishment, in Krom he is given help.
At an acute renal failure at a stage of the first medical assistance hold the events directed to stopping of action of a disturbing factor (shock, dehydration, an infection, poisoning, hemolysis, obstruction of uric ways) and apply an artificial diuresis (see Poisoning). Then the patient is evacuated in the specialized institution (see. Renal center) having conditions for complex laboratory diagnostiche-skogo monitor observation (see) and uses of dialysis. Evacuations are not subject patients with not resolved surgical problems (internal bleeding, perforation of hollow body, a nedrenirovan-ny abscess, pheumothorax), with incurable hron. diseases, in a condition of extreme exhaustion and an agony. In the period of an anury the diet shall provide receipt not less than 30 kcal (126 kJ) on 1 kg of the weight (weight) of a body a day preferential at the expense of carbohydrates and fats at restriction of protein, sodium, potassium, organic to - t and waters. Appoint generally sweet and fat porridges, mashed potatoes, cream, sour cream, honey, puddings, in limited quantity fruit and vegetables.
In need of parenteral food (see) appoint 20 — 40% solutions of glucose, 20% solution of sorbite of 200 — 300 ml, 20% solution of lipofundinum of 500 ml a day, solution of amino acids or plasma (250 — 500 ml a day), polyionic solution. During recovery of a diuresis (especially in a phase of a polyuria) to cover water-salt losses, increase consumption of liquid, sodium, potassium and other salts, and then and protein that is reached by introduction to a diet of compote from fruit (2 — 3 l a day and more), milk, fruit juice, vegetable soups and a podsalivaniye of food to taste.
Conservative treatment chronic At. it is directed to elimination of disturbances of nitrogenous balance and consists in adaptation of metabolism to the reduced function of kidneys and features of tubulointerstitsi-alny dysfunction. Partially it is reached by limited consumption of protein with food, formation of renal and extrarenal removal of nitrogen. At glomerular filtering more than 25 ml! min. food protein content is limited to 0,5 g! kg, at glomerular filtering less than 25 ml! mines — to 0,3 g/kg of the weight (weight) of a body a day. Preference is given to proteinaceous products, in to-rykh all essential amino acids are presented in a proper correlation. Limit at the same time phytalbumin, and also the products rich oxalic and uric to - that, phosphates. In rise periods of an azotemia appoint a protein-free diet to 4 — 6 weeks, supplementing it 5 — 6 g in days of irreplaceable amino acids.
In an end-stage At. treatment by a diet with the minimum protein content and with additive of amino acids is continued when it is impossible to apply dialysis. From the beginning of regular dialysis treatment after symptoms of uraemic intoxication are eliminated, food protein content is increased to 1 — 1,2 g/kg a day. Strict restrictions remain for the products rich with potassium and acids. The general caloric content of food is supported at the level of 40 kcal (167 kJ) on 1 kg of body weight a day that has anticatabolic effect and prevents neoglucogenesis with excessive release of nitrogen. This effect can be potentiated by injections of 20 — 40% of solution of glucose with insulin, use of androgens and anabolic steroids. To men Testosteroni propionas on 100 mg intramusculary every other day or me-tiltestosteron in (25 mg 4 times a day), to women — methandrostenolone (Nerobolum) on 10 — 15 mg a day or nerobolil on 25 mg or Phenobolinum (retabolil) on 50 mg of 1 times in 7 — 10 days can be appointed.
For the purpose of desintoxication cause artificial diarrhea intake of osmotic laxatives (sorbite, a mannitol, glycerin) and 4 — 6 l of polyionic salt isotonic solution within 3 — 4 hour. Apply antibiotics of a broad spectrum of activity to suppression of a bacterial flora of intestines. At patients with the kept diuresis release of nitrogen with urine can be increased by purpose of high doses of furosemide (200 — 1000 mg) and additional loading chloride or hydrosodium carbonate (to 6 g).
Much attention is paid to correction of water-salt disturbances. In case of the expressed polyuria and symptoms of dehydration recommend to increase water consumption with addition of salt. Salt and water are limited (irrespective of weight At.) at the expressed arterial hypertension, a nephrotic syndrome (see) and hypostasis of a cordial origin, and also at an oliguria. If necessary apply diuretics, osmotic laxatives, the managed vazoplegiya, ultrafiltration, a gemofiljtration (see t. 15, milk. materials), exchange plazmozameshcheniye.
Treatment of water intoxication includes correction of effective osmotic pressure infusion of the concentrated solution of glucose, a mannitol, chloride or hydrosodium carbonate, a gluconate of calcium, administration of albumine, Prednisolonum and the subsequent ultrafiltration. The isotonic dehydration caused by excess ultrafiltration 5% of solution of glucose treat replaceable infusion of isotonic solution of sodium chloride.
The patient predisposed to continuous or incidental loss of potassium with urine, to a hypopotassemia and an aggravation At., carry out replaceable treatment by drugs of potassium (4 — 12 g a day) and veroshpirony. When the renal disease is combined with a hypoaldosteronism (see) and a hyperpotassemia, appoint a diet poor in potassium, diuretics and cortexone. Consumption of potassium by the patient with an oliguria is limited to 40 — 50 mekv (1,6 — 1,9 g) in days to support the normal or slightly increased level of potassium in plasma. Potassium intoxication is reduced infusion of 200 — 300 ml of 40% of solution of glucose with addition of insulin (40 — 60 PIECES), by 20 ml of 10% of solution of a gluconate of calcium and 200 — 250 ml
of 4 — 5% of solution of hydrosodium carbonate, use in 30 — 50 g of cation-exchange resin rezonium And yes 200 — 300 ml of 20% of solution of sorbite; in hard cases carry out hemoperfusion through a column with cation-exchange resin or the emergency dialysis.
At development of a metabolic acidosis in patients with a polyuria appoint inside alkalizing solutions (1% solutions of citrate or hydrosodium carbonate, potassium citrate in sugar syrup), selecting the general dose for pH and a hydrocarbonate of blood. At an oliguria development of acidosis is prevented a diet with low protein content, the use in calcium carbonate, hydrosodium carbonate on 3 — 4 g, gel of aluminum hydroxide. In case of a decompensated acidosis pour in 4 — 5% solution of hydrosodium carbonate, calculating a dose (K) on deficit of the bases (— BE) in blood:
Body weight x (— BE)
1 l —---,
or apply dialysis.
Treatment of anemia is directed at the same time to stimulation of erptro-poetin by anabolic steroids and to substitution of deficit of iron, folic to - you and cyanocobalamine. Systematic treatment by dialysis considerably improves an erythrogenesis and reduces patol. bleeding. The prevention of a loss of blood in connection with dialysis, a geparinization and a lab is important.
research. Use of androgenic hormones increases products of erythropoetins and can increase sensitivity of marrow to them, but it is admissible only at patients with gematokritny number less than 25%. At all stages At. carry out treatment folic to - that on
1 — 2 mg a day and appoint cyanocobalamine on 500 mkg once a week. If iron preparations are shown, appoint them under control of content in blood of ferritin and serumal iron.
In a complex of therapy of heart failure at At. include treatment of anemia, arterial hypertension, a hyper parathyroidism, restriction of salt and water, use of means of desintoxication. Treatment by cardiac glycosides is carried out only at lack to them of tolerance, choosing drugs taking into account features of their removal from an organism. It is preferable to apply glycosides with preferential extrarenal elimination (digitoxin). Approximately average doses for the drugs which are removed kidneys (digoxin) define proceeding from the level of a kreatininemiya. E.g., at concentration of creatinine in plasma about 2 mg / 100 ml reduce an average therapeutic dose of digoxin twice. In case of an acute heart failure and a fluid lungs nitrodrugs of bystry action (nitroglycerine) under language or kapelno intravenously, if necessary antihypertensives, and also ultrafiltration or haemo filtering are shown; ventricular premature ventricular contraction and tachycardia are stopped injection of lidocaine; supraventricular arrhythmia and tachycardia — infusion of Isoptinum.
For treatment of arterial hypertension rau-volfiya use drugs, dopegit, various | 3-adre-noblokatory, minoksidit, saluretics, captopril. In case of malignant hypertensia apply haemo filtering, and in the absence of effect consider shown embolization of renal vessels (see Rent-genoendovaskulyarnaya surgery) or a bilateral nefrektolyiya (see) with the subsequent renal transplantation (see).
Fibrinous and vypotny a pericardis without signs of a cardiac tamponade treat intensive dialysis or haemo filtering, avoiding the general ge-parinization. Appoint also Monday to - meta shchgp 75 — 100 mg a day, Prednisolonum of 20 — 30 mg a day. Treatment is continued by from 10 to 60 days, controlling quantity of an exudate in a pericardium by means of ultrasonic or rentgenol. researches. Remission is reached in 70% of cases. At the phenomena of a cardiac tamponade drain a cavity of a pericardium for 72 hours r e and t ge N about to about N a trust of N y m and about l and e ti - to a flax family a catheter; in case of a recurrence of a tamponade and at development of chronic cardial compression n e r and r de to t of ohms and I is shown (see).
Recovery of sexual activity at men happens under the influence of therapy by Bromocriptinum (iar-lodet), Testosteroni propionas, and also after successful renal transplantation. The hemodialysis recovers a menstrual cycle (sometimes there is a hypermenorrhea), and in some cases cures also infertility. The complete recovery of reproductive function at women after transplantation of a kidney does possible conception, and in some cases — incubation of pregnancy and the birth of the child.
At encephalopathy (see) at patients with acute At. dialysis gives bystry, but often short improvement therefore daily procedures are recommended. At patients with chronic At. emergence of symptoms of a nolinevropatiya is a reason for an intensification of dialysis treatment or transplantation of a kidney. The cataract as one of serious consequences of uraemia is subject to surgical treatment.
Forecast. Uraemia at an acute renal failure is characterized by rapid development and almost full reversibility at adequate treatment, except for the most hard cases. Without treatment by dialysis it in most cases comes to an end with a lethal outcome. If the period of an anury drags on up to 5 — 7 days and more, there can come death from a hyperpotassemia, acidosis, an overhydratation. During the use of methods of extrarenal clarification, first of all dialysis, it is possible to keep life of 65 — 95% of patients, from to-rykh the majority it is restored to full-fledged life.
During chronic At. allocate conservatively kurabelny and terminal stages. Decrease in glomerular filtering to 10 mlimin below with exhaustion of opportunities of adaptation to disturbances of functions of kidneys is characteristic of the last. Various life expectancy of persons with uncured chronic At. it is noted preferential in a conservative stage or at an intermittent current At., observed at the patients suffering from loss of water and salt, tubular acidosis, the infection broken urodynamic. Considerably make heavier a current and high arterial hypertension, a circulatory unefficiency, a pericardis worsen the forecast.
An end-stage At. demonstrates proximity of a lethal outcome. It is possible to prolong life of the patient in this stage only regular dialysis. Among causes of death of patients with At. the most frequent are cardiovascular frustration (including a pericardis with a cardiac tamponade), a hyperpotassemia, joined inf. diseases (pneumonia, etc.), sepsis, hemorrhagic complications, uremic coma. At regular treatment by a hemodialysis (see) life expectancy of patients with chronic At. it can be considerably prolonged. The known maximum life expectancy on the supporting treatment by a hemodialysis makes 22 years, peritoneal dialysis — 12 years.
Bibliography: Of l about r and about z about in and T. G.,
Hondkarian O. A. and Shultsev of G. P. Sostoyaniye of a nervous system at chronic diseases of kidneys, M., 1980; Hormones and kidneys, under the editorship of B. M. Brenner and Dsh. G. Steyna, the lane with English, M., 1983; Dzhavad-Za-
d e M, - M. D. and P. S Whitebaits. Chronic renal failure, M., 1978; Ermolenko V. M. Chronic hemodialysis, M., 1982; Kiselyova A. F. and 3 about z at l I to V. I. Nefroskleroz, Kiev, 1984; To l e y-z and V. Yu. and D and y N and with B. E. Angiokhirurgicheskiye aspects of training of the patient for a hemodialysis, Vilnius, 1980; Clinical nephrology, under the editorship of E. M. Tareeva, t. 1 — 2, M., 1983; Lopatkin N. A. and Kuchinsky I. H. Treatment of an acute and chronic renal failure, M., 1972; Fundamentals of nephrology, under the editorship of E. M. Tareeva, t. 1 — 2, M., 1972;
Residents of Perm N. K. and Zimin of JI. H. Acute renal failure, M., 1982; Kidneys, under the editorship of F. K. Mostofi and D.E. Smith, the lane with English, M., 1972; P y-tel A. Ya. and Goligorsky S. D. Acute renal failure, Chisinau, 1963; Rosenthal P. JI. and Ilyinsky I. M. Organ pathology at treatment by a program hemodialysis, Riga, 1981; The Chronic renal failure, under the editorship of S. I. Ryabov, D., 1976; Acute renal failure, ed.
by A. Chapman, Edinburgh, 1980; B a b b A. I. a. o. The genesis of the square meterhour hypotesis, Trans. Amer. Soc. artif. intern. Org., v. 17, p. 81, 1971; In a 1 i n t P. Normale und pathologische Physiologie der Nieren, B., 1969; Blutreinigungsverfahren, Technik und Klinik, hrsg. v. H. E. Franz, Stuttgart — N.Y., 1981; Dutz H. u. M e b e 1 M. Die chronische Niereninsuffi-zienz, Lpz., 1973; D z u r i k R. Uremia,
Bratislava, 1973, bibliogr.; The kidney,
ed. by B. M. Brenner a. F. C. Rector, v.
1 — 2, Philadelphia, 1981; Manual of clinical nephrology, ed. by J. S. Cheigh a. o.,
Hague, 1981; Pericardial disease, ed. by P. S. Reddy and. lake, N. Y., 1982; Peritoneal dialysis, ed. by R. C. Atkins a. o., Edinburgh — N. Y., 1981; Peritoneal dialysis, ed. by K. D. Nolph, Hague, 1981; Replacement of renal function by dialysis, ed. by W. Drukker a. o., Hague a. o., 1979;
Schreiner G. E. a. Maher J. F. Uremia, biochemistry, pathogenesis and treatment, Springfield, 1961; Strauss and Welt’s diseases of the kidney, ed. by L. E. Earley a. C. W. Gottschalk, v. 1 — 2, Boston, 1979; Uremia, ed. by R. Kluthe a. o. Stuttgart a. C. Burton, N. Y., 1972.
G. P. Kulakov, V. S. Timokhov.