Acute diffuse nephritis. Nephritis acute and chronic. Kidney disease nephritis - nephritis

(Nephritis, from Greek nephros - kidney), inflammation of the kidneys resulting from harmful effects on them various agents, especially. through blood. All types of animals get sick. The process is localized simultaneously in both nights, either in the glomeruli or in the interstitial tissue. In animals it will become inflamed. the phenomena begin in the interstitial tissue of the kidneys and proceed as a diffuse or focal process.

Etiology. N. develops with toxic infections, as well as with extensive burns, feeding coniferous branches and young birch leaves to animals [birch], alder, reed, as a result of improper use of certain medications (turpentine, tar [tar], creolin, phosphorus, arsenic). A predisposing factor is body cooling. N. is also possible as a secondary disease (with infectious anemia of horses, swine fever, paratyphoid fever, leptospirosis). N. begins with a change in the reactivity of the body and is manifested by a violation of the nervous and endocrine systems, damage to the vascular system, as well as metabolic disorders. Certain [Definite] Humoral factors of the affected kidney also play a role in P.’s development.

Course and symptoms. The course of the disease is acute and chronic. In acute N., depression of the animal, increased body temperature, pain in the kidney area, and edema are noted. [swelling] in the abdomen, dewlap, hips [hips]. Pigs are characterized by skin anemia and vomiting. Blood pressure increases. Hypertrophy of the heart muscle occurs, especially the left ventricle, which [how] evidence of solid [solid], tense [tense] pulse and accent of the second tone on the aorta. Characteristic signs are uremia and hematuria. The urine is cloudy, from light red to brown, contains a large number of red blood cells, casts, leukocytes, and renal epithelium. The number of red blood cells and hemoglobin in the blood decreases. The leukocyte formula with a normal total number of leukocytes deviates towards lymphocytosis. Acute N., depending on the degree of damage to the nights, can last 1-2 weeks and ends in recovery or death. Sometimes the acute course becomes chronic, with rapid fatigue of the animal, decreased fatness, and edema. [swelling], gastroenteritis, muffled heart sounds with an emphasis on the second heart sound. Body temperature is normal.

Pathological changes. Swelling is detected [swelling] subcutaneous tissue in the area of ​​the chest, head and limbs. The kidneys are slightly enlarged; The capsule is easily removed. Microscopically noted acute inflammation glomeruli, their enlargement, hyperemia, accumulation of neutrophilic leukocytes along the walls of the capillaries, sometimes proteinaceous, granular and insignificant. fatty degeneration of convoluted tubules.

Diagnosis is based on symptoms of the disease and laboratory tests of urine and blood.

Treatment. Improve maintenance and feeding, carefully care for the skin (cleaning and rubbing). In the case of N. infectious. origin, antibiotics are prescribed, intravenous solution of calcium chloride, intravenous or intramuscular magnesium sulfate (2% solution based on [calculation] 3 ml per 1 kg of animal weight). The administration of strophanthin, caffeine, and diuretin is indicated.

Lit.: Internal non-communicable diseases of agriculture. animals, ed. I. G. Sharabrina, 5th ed., M., 1976.

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Atlas of ultrasound diagnostics. Studies in dogs and cats

This publication is a very clear and well-illustrated guide to diagnostic sonography of all major organs and systems in small domestic animals. The material in the book is compiled in the form of convenient sections, each of which describes in detail and very clearly how a particular organ in a healthy animal will look during an ultrasound examination, and what changes may occur during various diseases.
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The reference book provides information on internal diseases of animals, taking into account the latest achievements of science and practice.
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The book is intended for veterinary workers at various levels.

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Atlas of Veterinary Hematology

The purpose of this book is to show in comparison the normal and abnormal morphological features of pet blood cells when magnifying blood smears under a microscope. Numerous color photographs clearly demonstrate both common abnormalities and rare disorders observed in the cages of domestic animals: dogs, cats, horses, ruminants and llamas.

This publication can be used by students of veterinary universities as a textbook, and by practicing veterinarians and hematologists as a reference guide.

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Kirk's modern course of veterinary medicine. In 2 parts (set of 2 books)

This course of veterinary therapy continues in the tradition of the original author, Dr. Robert W. Kirk, and has been preserved by the editor and compiler, John D. Bonagura, DVM. The consulting editors for sections of the book and the corresponding appendices are 20 of the most famous veterinarians in the world with extensive experience clinical practice. This publication contains more than 1,300 pages, which are divided into 14 sections covering a wide range of diseases of domestic animals. Specific questions modern practice treatments for pets are described in detail in 310 separate chapters written by almost 400 authors. Considered:
issues of special therapy;
emergency care;
toxicology;
immunology;
infectious diseases;
systemic disorders in domestic animals: diseases of the heart, kidneys, liver, lungs, reproductive organs and so on;
diseases of birds and exotic pets.

The authors have given the chapters of the book an easy-to-read structure, which includes a description of the characteristic clinical symptoms of diseases and functional disorders, the basics rational therapy, as well as clear practical advice and treatment recommendations. Most chapters deal with the treatment of a specific disease or disorder. Some chapters focus on important therapeutic principles or general approaches to treating diseases of small or exotic pets.

For ease of use, the book was published in two parts, which are a single whole publication.

diffuse nephritis calf treatment

Introduction

Chapter 1. Acute diffuse nephritis in calves

1 Definition of disease. Etiology. Clinical signs of acute diffuse nephritis in calves

2 Pathogenesis of acute diffuse nephritis in calves. Pathological changes in the kidneys

Chapter 2. Diagnostics. Treatment. Prevention of acute diffuse nephritis in calves

Chapter 3. Case history of a calf diagnosed with acute diffuse nephritis

Conclusion

References

Introduction

Relevance of the work. In farm animals, kidney pathology occurs within 5.3% in commercial farms and 8.2% in specialized complexes. The causes of nephritis may be poisoning with nephrotoxins or toxic substances, such as turpentine, tar, herbicides, feeding coniferous branches, birch leaves, alder, reeds, the use of certain medications (arsenic preparations, FOS, creolin), insect bites. According to I.M. Belyakov, the sensitizing role is usually played by hypothermia, poor-quality feed and unsatisfactory living conditions.

Acute diffusion nephritis can occur with leptospirosis, foot and mouth disease, babesiosis, theileriosis in cattle; parenchymal mastitis, endometritis, vaginitis, traumatic reticuloperitonitis and pericarditis, phlegmon, surgical sepsis, burns, intestinal blockages, and a direct dependence and consistency in the development of nephritis on the intensity of the infectious process is not typical.

The pathogenesis of the disease has not been sufficiently studied. Acute nephritis is characterized by metabolic disorders and disorders of the endocrine, nervous and vascular systems. As a rule, circulatory disorders occur first in the vascular apparatus of the kidneys. Morphological changes in the kidneys with nephritis are represented by proliferation of mesangial, endothelial and epithelioid cells of the glomerulus, thickening and splitting of the basement membrane of glomerular capillaries, sclerosis of vascular loops, dystrophy of the tubular epithelium. Clinical signs are very diverse, so they are usually combined into syndromes: acute glomerular inflammation syndrome, cardiovascular syndrome, edema syndrome, cerebral syndrome. Complications arising from nephritis include: acute cardiovascular failure (left ventricular, cardiac edema lungs); eclampsia (loss of consciousness, clonic and tonic convulsions); bleeding in the brain; acute disorders vision (sometimes blindness due to spasm and swelling of the retina).

Purpose of the work: to study the features of acute diffuse nephritis in calves, to compile a medical history of a calf diagnosed with acute diffuse nephritis.

Subject of work: acute diffuse nephritis.

Object of work: a calf diagnosed with acute diffuse nephritis.

Job objectives:

.Give the concept of acute diffuse nephritis.

.To study the etiology of acute diffuse nephritis in calves.

.Consider the pathogenesis and clinical signs of acute diffuse nephritis in calves.

.To study diagnostic methods, treatment and prevention of acute diffuse nephritis in calves.

.Compile a medical history of a supervised calf diagnosed with acute diffuse nephritis.

Research methods: analysis of literature on this topic, synthesis, abstraction, generalization, observation, medical research.

Scope and structure of work. Coursework presented on 33 pages of printed text. The coursework consists of an introduction, three chapters, including paragraphs, a conclusion and a list of references. The bibliography includes 40 sources.

Chapter 1. Acute diffuse nephritis in calves

1 Definition of disease. Etiology. Clinical signs of acute diffuse nephritis in calves

Acute diffuse nephritis (Nephritis acuta) is a kidney disease based on diffuse inflammatory processes affecting the vascular glomeruli. The main causes of nephritis are infectious diseases, poisoning, autointoxication, and the allergic state of the animal body. The disease is acute. Based on the nature of the exudate, serous, fibrinous, purulent, and hemorrhagic nephritis are distinguished. The disease occurs in all types of domestic animals. This is an acute immune-inflammatory disease with predominant damage to the glomerular apparatus of both kidneys.

Rice. 1. Kidneys of an animal with acute diffuse nephritis.

Acute diffuse nephritis often occurs during infection of animals with pathogens of infectious diseases. These pathogens are leptospires, vibrios, streptococci, diplococci, pneumococci, staphylococci, Pseudomonas aeruginosa, listeria, adenoviruses, plague viruses, panleukopenia, parainfluenza, rhinotracheitis, hepatitis, enteroviruses, as well as their toxins. An allergic reaction (sensitization) as a result of the action of an infectious pathogen and its toxins on the animal’s body plays a decisive role in the etiopathogenesis of acute diffuse nephritis. Infectious agents can enter the glomerular apparatus of the kidneys in several ways - lymphogenous (through lymph), hematogenous (through blood), from neighboring tissues and from the genital organs. Infections of the genital tract are the most common and important cause of acute diffuse nephritis in animals.

A large group of nephrotoxins is known that easily penetrate and damage the glomeruli of the kidneys - heavy metals, zoocoumarins, ratindan, zinc phosphide, turpentine, mineral fertilizers and chemical active substances some poisonous plants. Sensitizing reasons can be the nature of feeding, living conditions (drafts, high humidity, cold floors), as well as operations, injuries, physical overload, swimming in cold water reservoirs, etc. The development of acute diffuse nephritis and improper administration of vaccines and serums to calves contributes , antibiotics, immunoglobulins, etc. Nephrotoxins also include metabolic products, birch and alder leaves, tar, spoiled feed, alcohol, insecticides, etc.

Acute diffuse nephritis is characterized by pain in the back and lower back on both sides of the animal’s abdomen; increased body temperature; oliguria (small amount of urine when urinating); reddish-colored urine or the color of “meat slop,” sometimes streaked with blood; proteinuria (protein in the urine), microhematuria (less often macrohematuria); the appearance of casts (hyaline, granular, erythrocyte) epithelial cells in the urine; decreased glomerular filtration; leukocytosis, increased ESR; increased levels of alpha and gamma globulins in the blood).

In acute diffuse nephritis, cardiovascular syndrome manifests itself in the form of shortness of breath; arterial hypertension(sometimes ephemeral), the development of acute left ventricular failure and the appearance of a picture of cardiac asthma and pulmonary edema are possible; signs of bradycardia; changes in the fundus - narrowing of arterioles, sometimes swelling of the nipple optic nerve, pinpoint hemorrhages. In acute diffuse nephritis, edematous syndrome may occur, characterized by edema, mainly in the area of ​​the muzzle, intermaxillary space; edema appears more often in the morning; in severe cases, hydrothorax, hydropericardium, and ascites are possible. In acute diffuse nephritis, cerebral syndrome also occurs. It is accompanied by soreness of the head, vomiting, weakness, decreased vision, increased muscle and nervous excitability of animals, and motor restlessness; sometimes decreased hearing, loss of sleep. The extreme manifestation of cerebral syndrome in acute diffuse nephritis is eclampsia, the main symptoms of which are: after a noisy deep sigh, first tonic, then clonic convulsions of the respiratory muscles and diaphragm appear; complete loss of consciousness, severe depression; cyanosis of visible mucous membranes; jugular vein overflow; dilated pupils; the flow of foamy saliva from the mouth, sometimes stained with blood; breathing is noisy, hard; pulse is rare and intense, blood pressure is high; increased muscle rigidity. Complications arising from acute diffuse nephritis in animals include: acute cardiovascular failure (left ventricular failure, cardiac pulmonary edema); eclampsia (loss of consciousness, clonic to tonic convulsions); bleeding in the brain; acute visual impairment (sometimes blindness due to spasm and swelling of the retina).

2 Pathogenesis of acute diffuse nephritis in calves. Pathological changes in the kidneys

The pathogenesis of acute diffuse nephritis is as follows. Toxins of microbes and viruses, especially streptococcus, damaging the structure of the basement membrane of the glomerular capillaries, cause the appearance of specific autoantigens in the animal’s body, in response to which antibodies of classes 10 and I M (anti-renal antibodies) are formed. Under the influence of a nonspecific resolving factor, most often cooling, a new exacerbation of the disease, a violent allergic reaction of the combination of antigen with antibody occurs, the formation of immune complexes with the subsequent addition of complement to them. Immune complexes are deposited on the basement membrane of the glomeruli of the kidney and damage them. There is a release of inflammatory mediators, damage to lysosomes and the release of lysosomal enzymes, activation of the coagulation system, disturbances in the microcirculation system, increased platelet aggregation, resulting in the development of immune inflammation of the glomeruli of the kidneys.

Pathoanatomical changes in the kidneys of animals with acute diffuse nephritis: on the dissection table, the initial stages of damage to the glomeruli are difficult to establish, since the size, pattern and color of the kidneys are normal.

Only a careful examination of the organ, especially with side lighting, makes it possible to establish changes in the glomeruli protruding on the cut surface of the organ in the form of gray grains of sand. The kidneys are enlarged in volume, flabby to the touch, the cortex is wide, moist, pale gray or gray-yellow in color, with a clearly defined border, with the medulla of the organ, which is darker colored (usually dark red).

The outcome of acute diffuse nephritis is twofold: either the organ is restored, or the process takes a chronic course and ends in sclerosis and shrinkage of the kidneys (wrinkled kidney). The capsule contains coagulated protein, red blood cells, fibrin fibers and proliferation of epithelial cells.

Rice. 2. Changes in the kidneys in acute diffuse nephrotoxic nephritis: A - discomplexation of epithelial cells of the animal’s kidney cortex; B - nuclear pyknosis; formation of cylinders due to cellular detritus in the kidney of a sick animal.

Macroscopically, a wrinkled bud has a smaller volume, light color, dense consistency and lumpy appearance. Its fibrous capsule is difficult to remove along with the parenchyma of the organ. The cortical layer is strongly narrowed and is sometimes represented only by a thin border. In the renal parenchyma itself (especially in the medulla) a large number of small cystic cavities can be observed.

Chapter 2. Diagnostics. Treatment. Prevention of acute diffuse nephritis in calves

Acute diffuse nephritis in calves is detected on the basis of such clinical data as the appearance of edema along the entire body of the animal, especially after a sore throat or acute respiratory disease, increased blood pressure. The diagnosis is helped by identifying protein, red blood cells and casts in the urine of a sick animal, increasing the titers of antistrentolysin-0 (ASL-0), antistreptohyaluronidase (ACT).

Most often, recovery occurs within a month to a year. A transition to the chronic form and back is possible, which depends on the individual characteristics of the animal, timeliness of diagnosis, therapy, exposure to infections, hypothermia and physical stress. Signs of transition to a chronic form: persistence of any extrarenal sign and protennuria throughout the year.

The causes of death of an animal from acute diffuse nephritis can be: circulatory failure, renal eclampsia, cerebral hemorrhage, acute renal failure.

To treat acute diffuse nephritis, first of all, it is necessary to normalize the maintenance and feeding of sick calves. They must be placed in a warm, dry, draft-free room; walking patients is often prohibited. Provide thorough skin care - cleansing with rubbing and massage.

During the first two days of the disease, fasting is recommended, then a limited amount of easily digestible, salt-poor food is prescribed - lactic acid, cereals from various cereals, boiled and raw vegetables and fruits. Feed should contain more carbohydrates and increased amount potassium and calcium ions, which have a diuretic, hypotensive effect, stimulating contractile function myocardium. The diet should include ascorbic acid, retinol, tocopherol and B vitamins.

If acute diffuse nephritis has developed against the background of a general infection or due to an exacerbation of a focal infection, it is necessary to use antibiotics - penicillins, cephalosporins, aminoglycosides, etc. Of penicillins, it is better to prescribe benzyl penicillin sodium or potassium, ampicillin, ampiix, isnpen or oxacillin. Tender therapeutic effect for this pathology they have: claforan, fortum, kefzol, cefamezine, etc. In parallel, nitrofurans, palin, 5-NOK or sulfonamides are prescribed.

In case of severe intoxication and the development of edema, bloodletting is indicated (up to 10-100 ml of blood), which not only reduces the amount of salt and water, but also leads to a significant restructuring of the reactivity of the animal’s body. After bloodletting, a 5-20% glucose solution is injected subcutaneously or intravenously. For cardiovascular failure, in addition to glucose solutions, agents containing cardiac glycosides are used: spring adonis herb, digalen-neo, digitoxin, digoxin, korglykon, cordigit, strophanthin in appropriate doses.

It is widely used to stimulate diuresis and relieve hypertension; Temisal 0.2-2 grams 3-4 times a day; veroshpiron 0.045-0.2 grams in 2-4 doses; furosemide intramuscularly or intravenously 20-80 mg once a day (preferably in the morning) for 7-10 days, and in case of severe renal failure the dose is increased to 200 mg 1-2 times a day for a week, as well as decoctions and infusions of bearberry , half a burnt tree, juniper fruits, blue cornflower flowers, lingonberry leaves, etc.

Care should be taken to use solutions of magnesium sulfate. It is a salt-removing, blood pressure-lowering, vasodilator and diuretic. It is administered intramuscularly in the form of 10-25% solutions with an equal amount of 0.5% novocaine solution 2-3 times a day for one or three weeks.

Treatment regimens for acute diffuse nephritis: as anti-inflammatory, desensitizing and antiallergic, it is necessary to include glucocorticoids - cortisone acetate intramuscularly 0.02-0.05 grams 1-2 times a day; hydrocortisone according to instructions; prednisolone orally 0.02-0.05 grams 1-2 times a day; hydrocortisone according to instructions; prednisolone orally 0.02-0.05 g/day (in 2-3 doses), then the dose is reduced to 0.001-0.025 grams; intravenously or intramuscularly, 2 ml 2-3 times a day, then the dose is gradually reduced. Less commonly prescribed are prednisone, salts and depomedrol, etc.

To relieve attacks of renal colic and inflammatory process use cystone, indomethacin, baralgin, spazgan, no-shpu and other analgesics and antispasmodics according to the instructions. If blood or red blood cells appear in urine sediment, it is necessary to use specific hemostatic and blood-clotting medications: aminocaproic acid at the rate of 0.1 g/kg of animal weight every 4-6 hours intravenously (drip) up to 50-100 ml of 5% solution per injection; vikasol orally 0.01-0.3 g/day or intramuscularly (intravenously) 0.2-1 ml of 1% solution 2-3 times a day for 3-4 days in a row; dicinone intravenously or intramuscularly, 0.3-2 ml of a 12.5% ​​solution 1-3 times a day until recovery, as well as a 10% solution of gluconate and calcium chloride intravenously 1-2 times a day, 1-10 ml for one introduction. Symptomatic therapy sometimes includes narcotic, anabolic agents, adrenergic blockers, etc.

To prevent acute diffuse nephritis in animals, it is necessary to make a timely and correct diagnosis with a mandatory laboratory test of urine, identify and eliminate the cause of the disease. During treatment, hypothermia of animals and the entry of toxic and irritating substances into their bodies with food, water or medications are not allowed.

Chapter 3. Case history of a calf diagnosed with acute diffuse nephritis

Clinical status

Type: calf

Gender: male

Breed: Simmental

Date of birth of the animal: 06/15/12

1. Age: 3 months.

Nickname: Gosha

Color: fawn-variegated

Animal weight - 115 kg

Owner and address of the animal: -

Animal supervision start date: 09/03/12

End date of supervision: 09/18/12

Preliminary diagnosis: acute nephritis

Final diagnosis: acute diffuse nephritis

Anamnesis vitae. The calf was born in June 2012. It is kept in the yard in a barn, the floor is made of planed boards, the calf has a permanent and spacious individual place - a stall 2.5x2 m. The stall is located in the corner opposite from the door, with the feeder facing the window.

WITH early age the calf is accustomed to eating concentrated feed. They began to be fed from the third week of the calf's life - wheat bran, ground and sifted oats (oatmeal), flaxseed cake or meal. On average, a calf consumes about 0.8 kg of feed per day. The calf was accustomed to hay from the age of 15 days, using good cereal-forb, small-stemmed, green hay. In the summer, the calf was released into the pasture, where it became accustomed to eating green grass. Starting from 1.5 months of age, the calf was fed chopped root vegetables (carrots, rutabaga, beets), and from 2 months of age, potatoes were introduced into the diet. The calf was regularly brushed, and in warm sunny days Bathed once. All necessary vaccinations and deworming were carried out.

2. Amamnesis morbi. According to the owner, within a week the calf had poor appetite, over the last two days the calf has completely refused to feed, the calf is lethargic and depressed. Always hiding in dark places for a long time lies. Two days ago, the urine became reddish, urination was frequent, in small portions. Which was the reason why the owners sought veterinary help. No medications were used. There were also no infectious, invasive or non-infectious diseases observed.

Clinical examination

Examination of lymph nodes. Submandibular, slightly enlarged, mobile, dense consistency, painless. Inguinal - mobile, painless, oval-round in shape, not enlarged.

Examination of mucous membranes. The mucous membrane of the conjunctiva is pink and shiny. No damage. The oral mucosa is pale pink and pigmented. The animal’s body temperature in the rectum at the time of administration is high 39.5 º WITH.

Cardiovascular system. On palpation, the cardiac region is painless. The following borders of the heart were determined by percussion: anterior - along the anterior edge of the 3rd rib; upper - along the line of the scapulohumeral joint; posterior - up to the 7th rib. Absolute dullness of the heart in the 5th - 6th intercostal spaces. On auscultation, heart sounds are loud, crisp, and clear. The arterial pulse on the inner side of the thigh is rhythmic, rapid, frequency 140 beats/min. The arteries are well filled, the pulse wave gradually rises and falls the same, the artery wall is somewhat rigid. Blood pressure 110/70 mm. rt. Art. The heartbeat is moderately pronounced, limited, rhythmic, moderately strong, distributed locally. In the left half of the chest there is an apex impulse of moderate strength, slight vibrations of the chest wall are palpable. The lateral cardiac impulse is rhythmic and can be easily felt.

Respiratory system. Examination of the nasal cavity did not reveal serous discharge. Breathing is shallow, rhythmic, chest-abdominal, deep, symmetrical, rapid. There is no cough. The shape of the chest is symmetrical; when breathing, both sides of the chest rise and fall evenly. Respiratory rate: 27 breaths. dv./min. Palpation of the larynx and trachea is painless. Palpation of the pulmonary fields along the intercostal spaces from top to bottom is painless. Upon percussion, a clear pulmonary sound is heard. Auscultation revealed increased vesicular breathing.

Digestive system. There is no appetite, no thirst, food and water intake is free. The oral mucosa is pale pink, without damage. The tongue is moist, pink with a white coating. The arrangement of the teeth corresponds to the age of the animal. Palpation of the pharynx is painless. The salivary glands are not enlarged and painless. The shape of the abdomen is symmetrical. Abdominal wall painless, moderately tense. With deep palpation, the stomach is revealed. There is no pain on palpation of the intestinal area, but on percussion the sound is tympanic.

Intestinal motility is moderate, peristaltic sounds are heard. The intestines are painless, moderately full. Part of the liver is palpable with right side under the diaphragm is not enlarged, painless, the surface is smooth, the consistency is dense, elastic, with percussion the sound is dull. The spleen cannot be palpated. The anal hole is toned, pale color, clean. The act of defecation occurs once every day. The smell of feces is specific to this type of animal, brown in color.

Genitourinary system. External genitalia of a calf without pathological changes, correspond to the age and sex of the animal. There are no discharges from the genitals uncharacteristic of the animal. The posture when urinating is natural, the calf sits up, strains to release urine, urination is frequent 10-12 times, painful, in small portions or drops mixed with blood. Concentrated urine with a pungent odor. The walls of the bladder are enlarged and tense. Bladder filled, painful. The kidneys are enlarged, smooth, painful, and mobile.

Studies of the skull and spinal column. The skull is correctly shaped, symmetrical, consistent with the breed. The spinal column is without curvature. Palpation of the costal and vertebral processes revealed no signs of osteomalacia or displacement. The last ribs are whole, dense, without rickety beads; intercostal spaces are smooth.

10. Nervous system. The general condition of the animal is depressed. The coordination of movements is correct. Tactile and pain sensitivity are preserved. The animal is phlegmatic, inactive, head down. There was trembling of the pelvic limbs and decreased muscle tone. The position of the lips, ears, head, neck, limbs is without visible disturbances. The study also revealed good tactile and thermal integrity. Superficial reflexes are preserved, but the response to them is slow. The joints are dense, not thickened, painless.

11. Sense organs. Eye placement is correct, without deviations. The cornea of ​​the eyes is transparent, shiny, moist. The sclera is gray-pink in color, moderately filled with vessels, moist, shiny. The pupillary reflex is preserved, the eyeballs are correctly located in the eye orbits, the reaction to light is lively; vision preserved. The animal holds its head and neck naturally and correctly. Palpation of the base of the ears on the left and right is painless. The patency of the ear canals is not impaired. The reaction to surrounding stimuli is well expressed. Sense of smell: the mucous membrane of the nasal cavity is without pathologies, pale pink in color. The sense of smell is fully preserved, and there is a reaction to irritation. The hearing is not weakened, the outer ears are intact, of regular shape, without redness. There are no unnatural discharges from the auditory openings.

12. Study of the organs of movement. Coordination is not impaired. Paralysis and paresis were not observed. The bones are free of growths, painless, not bent, there are no growths or rosaries. The joints are painless, without deformation, without disruption of integrity, the range of motion in the joints is full.

Laboratory research

.General analysis blood, general urine analysis.

General urine test dated 09/03/12. The color of urine is meat slop. The transparency is cloudy, the smell is specific. The consistency of urine is liquid. Relative density 1.034 g/l. The reaction is alkaline. Protein 1, 885 g/l Glucose negative. Billirubin is negative. Urobillin is negative. Red blood cells 4-5 per cell. Leukocytes 15-20 per cell. The reaction is sour.

General blood test dated 09/03/12.

Red blood cells 5.5*1012 /l

Leukocytes 17.0*109

Neutrophils 7

Band 0

Segmented 61

Lymphocytes 29

Monocytes 3

ESR 5 mm/h

Conclusion: the number of leukocytes is increased.

Biochemical blood test.

Biochemical blood test dated 07/08/12.

General Protein 56 g/l

Bilirubin total 4.4 µmol/l

Creatinine 0.08 µmol

Thymol test 2.0 units.

AST 14.8 units/l

ALT 21.6 units/l

Conclusion: within normal limits.

Analysis for pathogens of invasive diseases. a) The study on larvae using the Berman method was not found. b) Testing for helminth eggs using the Fulleborn method was not detected. c) Examination for helminths; their fragments were not detected by helminthoscopy. d) Testing for pathogens of protozoal diseases using the Darling method was not found.

Diagnosis and its rationale

Based on the history and clinical examination of the animal, a diagnosis was made: acute diffuse nephritis. Identified on the basis of such clinical data as the color of urine - meat slop, pain in the kidney area on both sides, oliguria. The diagnosis is helped by identifying protein, red blood cells and casts in the urine.

Treatment plan

First of all, it is necessary to normalize the maintenance and feeding of the sick calf.

It must be placed in a warm, dry, draft-free room; walking is prohibited. Provide thorough skin care - cleansing with rubbing and massage.

During the first two days of illness, there is hunger, then a limited amount of easily digestible, salt-poor food.

For treatment we used: antibiotic - Enroflox 5% subcutaneously once a day, 5.5 ml for 7 days; hemostatic drug - vikasol 1% intramuscularly 2 times a day for 6 days; restoring blood and immunity - gamavit subcutaneously once a day for 15 days, 6 ml; desensitizing, anti-inflammatory and antiallergic drug - prednisolone intramuscularly once a day in the morning, 2 ml for 3 days; a drug that stimulates diuresis - furosemide intramuscularly 2 times a day, 2 ml for 3 days; a drug that relieves attacks of renal colic - no-shpa intramuscularly 2 times a day, 2 ml for 5 days; For prevention, Phytoelite-healthy kidneys were prescribed for one month, 1 tablet 2 times a day.

Rp.: Sol. Enrofloxi 5% - 100.0 ml.t.d. 1 in flaconi. Subcutaneously 1 time per day, 5.5 ml for 7 days: Sol. Gamaviti 10 ml.S. Subcutaneously 1 time per day for 15 days, 6.0 ml.,: Sol. Prednizoloni 1.0 ml.t.d. 1 in ampul.. according to the diagram. Intramuscularly 1 time per day in the morning, 2.0 ml for 3 days: Sol. Vicasoli 1%-1.0 ml.S. intramuscularly 2 times a day. According to indications..: Sol. No-shpa 2.0 ml.t.d. 1 in ampul.. Intramuscularly 2 times a day, 2.0 ml for 3-5 days: Sol. Furosemidi 2.0 ml.t.d. 1 in ampul.. Intramuscularly 2 times a day, 2.0 ml for 3 days.

Course of the disease

Date °CPulse RR Symptoms Treatment 09/3/1239, 514027 Poor appetite, for the last two days there has been no food at all, the calf is lethargic and depressed. He hides in dark places all the time and lies for a long time. Urine is the color of meat slop, frequent urination is 9-11 times a day, sometimes more, up to 15 times, in small portions. Breathing and pulse are increased, body temperature is elevated 39 .5º C. The kidney area is painful upon palpation. Place the calf in a warm, dry, draft-free room, provide thorough skin care - cleaning with rubbing and massage. During the first 2 days of illness, fasting is recommended, then a limited amount of easily digestible, salt-poor food. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 2 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 4.09.1239,013527The general condition of the calf is unchanged, there is no appetite, depression, lethargy. He drinks water willingly. When palpating the kidney area, pain is noted. Starvation diet. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 2 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 5.09.1239, 213729 The general condition of the calf is unchanged, there is no appetite, depression, lethargy. When palpating the kidney area, pain is noted. Starvation diet. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 2 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 09/06/1238,912829 The calf is depressed and refuses to feed. The kidneys are enlarged and painful. Urination - large portions, frequency decreased to 6 times a day. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1.5 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 7.09.1239, 113031 The animal is depressed, refusing to feed. The kidneys are enlarged and painful. Urination portions are large, the frequency has decreased to 5 times a day. Enroflox 5% subcutaneously 1 time a day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1.5 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 8.09.1238,512728 The animal is depressed, refusing to feed. The kidneys are enlarged and painful. Urination portions are large, the frequency has decreased to 5 times a day. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1.5 ml; Vikasol 1% intramuscularly 2 times a day; no-spa intramuscularly 2 times a day, 2 ml; furosemide intramuscularly 2 times a day, 2 ml. 09/09/1238, 712527 The calf’s condition is satisfactory, appetite has appeared, the urine is light yellow, without blood, urination is rare up to 5 times a day, painless. The kidney area is less sensitive to palpation. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1.5 ml; no-spa intramuscularly 2 times a day, 2 ml. 09/10/1238, 612728 The calf’s condition is satisfactory, appetite has appeared, the urine is light yellow, without blood, urination is rare up to 5 times a day, painless. The kidney area is less sensitive to palpation. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1 ml; no-spa intramuscularly 2 times a day, 2 ml. 09/11/1238, 712827 The calf’s condition is satisfactory, appetite has appeared, the urine is light yellow, without blood, urination is rare up to 5 times a day, painless. The kidney area is less sensitive to palpation. Enroflox 5% subcutaneously 1 time per day, 5.5 ml; Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 1 ml; no-spa intramuscularly 2 times a day, 2 ml. 09/12/1238, 712025 The condition of the calf is satisfactory, appetite is present, urination 4 times a day, urine is straw-yellow in color. The kidney area is painless. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 0.5 ml. 09/13/1238, 612126 The calf’s condition is satisfactory, appetite is present, urination 4 times a day, urine is straw-yellow in color. The kidney area is painless. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 0.5 ml. 09/14/1238, 412025 The calf’s condition is satisfactory, appetite is present, urination 4 times a day, urine is straw-yellow in color. The kidney area is painless. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 0.5 ml. 09.15.1238,512126 The condition of the calf is satisfactory, appetite is present, urination 4 times a day, urine is straw-yellow in color. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 0.2 ml. 09/16/1238,612027 The calf’s condition is satisfactory, appetite is present, and the kidney area is painless on palpation. Urinating 4 times a day, urine is light yellow. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly once a day in the morning, 0.2 ml. 09.17.1238.512224 The animal is actively moving, the appetite has improved. Signs of stress have disappeared. Urination has stabilized 3 times a day. The color of urine is straw yellow. Transparency is transparent. The kidneys are painless. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly once a day in the morning, 0.2 ml. 09/18/1238, 212024 The animal is actively moving, the appetite has improved. Signs of stress have disappeared. Urination has stabilized 3 times a day. The color of urine is straw yellow. Transparency is transparent. The kidneys are painless. Gamavit subcutaneously 1 time per day, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 0.2 ml. For prevention during the 1st month, Phytoelita-healthy kidneys, 1 tablet 2 times a day.

Rice. 3. Graph of temperature, pulse and respiratory rate of a calf with acute diffuse nephritis during the days of the disease.

Acute diffuse nephritis (Nephritis acuta) is a kidney disease based on diffuse inflammatory processes affecting the vascular glomeruli. The main causes of nephritis are infectious diseases, poisoning, autointoxication, and the allergic state of the animal body. The disease is acute. Based on the nature of the exudate, serous, fibrinous, purulent, and hemorrhagic nephritis are distinguished. The disease occurs in all types of domestic animals. This is an acute immune-inflammatory disease with predominant damage to the glomerular apparatus of both kidneys. Acute diffuse nephritis often occurs during infection of animals with pathogens of infectious diseases. These pathogens are leptospires, vibrios, streptococci, diplococci, pneumococci, staphylococci, Pseudomonas aeruginosa, listeria, adenoviruses, plague viruses, panleukopenia, parainfluenza, rhinotracheitis, hepatitis, enteroviruses, as well as their toxins.

The pathogenesis of acute diffuse nephritis is as follows. Toxins of microbes and viruses, especially streptococcus, damaging the structure of the basement membrane of the glomerular capillaries, cause the appearance of specific autoantigens in the animal’s body, in response to which antibodies of classes 10 and I M (anti-renal antibodies) are formed. Under the influence of a nonspecific resolving factor, most often cooling, a new exacerbation of the disease, a violent allergic reaction of the combination of antigen with antibody occurs, the formation of immune complexes with the subsequent addition of complement to them. Immune complexes are deposited on the basement membrane of the glomeruli of the kidney and damage them. There is a release of inflammatory mediators, damage to lysosomes and the release of lysosomal enzymes, activation of the coagulation system, disturbances in the microcirculation system, increased platelet aggregation, resulting in the development of immune inflammation of the glomeruli of the kidneys. An allergic reaction (sensitization) as a result of the action of an infectious pathogen and its toxins on the animal’s body plays a decisive role in the etiopathogenesis of acute diffuse nephritis. Infectious agents can enter the glomerular apparatus of the kidneys in several ways - lymphogenous (through lymph), hematogenous (through blood), from neighboring tissues and from the genital organs. Infections of the genital tract are the most common and important cause of acute diffuse nephritis in animals.

Sick calf, Simmental breed, male, born June 15, 2012. was under supervision from 03.09. to 18.09. 2012 with a diagnosis of acute diffuse nephritis. The owner of the calf complained that the calf had had a poor appetite for a week, that over the last two days the calf had refused to feed at all, the calf was lethargic and depressed. He hides in dark places all the time and lies for a long time. Two days ago, the urine became reddish, urination was frequent, in small portions. Which was the reason why the owners sought veterinary help. No medications were used. There were also no infectious, invasive or non-infectious diseases observed.

An examination was carried out: physical, analysis for causative agents of invasive diseases, CBC, TAM, blood HD.

Treatment was carried out: enroflox 5% subcutaneously once a day, 5.5 ml for 7 days; Gamavit subcutaneously 1 time per day for 15 days, 6 ml; prednisolone intramuscularly 1 time per day in the morning, 2 ml for 3 days; Vikasol 1% intramuscularly 2 times a day for 6 days; no-spa intramuscularly 2 times a day, 2 ml for 5 days; furosemide intramuscularly 2 times a day, 2 ml for 3 days. For preventive purposes, we prescribe the drug phytoelite healthy kidneys for a month, 1 tablet 2 times a day.

The disease in the calf presented with typical clinical signs. The prescribed treatment had the desired effect, because... the animal's condition improved significantly, urination and urine color returned to normal, and kidney pain disappeared.

Conclusion

A sick calf named Gosha was diagnosed with acute diffuse nephritis of the kidneys.

When making a diagnosis, the results of a clinical examination of the animal, anamnesis data and laboratory urine tests were taken into account.

When collecting anamnesis, the initial clinical symptoms of the disease observed by the owner were taken into account.

We determined its duration, the nature of the urinary disorder, clarified the conditions of detention, the structure of the diet and the frequency of feeding the animal, and found out whether urinary disorders had previously been observed.

The final diagnosis of acute diffuse nephritis of the kidneys was made based on the combined results of a clinical examination of the animal, anamnesis data, clinical, morphological and biochemical studies of urine.

Based on the diagnosis, appropriate treatment was prescribed: antibiotic - Enroflox 5% subcutaneously once a day, 5.5 ml for 7 days; hemostatic drug - vikasol 1% intramuscularly 2 times a day for 6 days; restoring blood and immunity - gamavit subcutaneously once a day for 15 days, 6 ml; desensitizing, anti-inflammatory and antiallergic drug - prednisolone intramuscularly once a day in the morning, 2 ml for 3 days; a drug that stimulates diuresis - furosemide intramuscularly 2 times a day, 2 ml for 3 days; a drug that relieves attacks of renal colic - no-shpa intramuscularly 2 times a day, 2 ml for 5 days; Phytoelite was prescribed for prophylaxis for one month - healthy kidneys, 1 tablet 2 times a day.

During the treatment, the calf's general condition improved. By repeated analyzes urine protein decreased to a minimum, there were 1-2 red blood cells in the field of view, the density decreased to 1.03.

For prevention, it is prescribed to take a course of the drug phytoelite - healthy kidneys. And also take urine tests once a month for 3 months.


Defeat in to the same degree glomeruli, tubules and kidneys. Divided into glomerulonephritis, interstitial nephritis and nephrito-nephrosis. The disease is recorded in all animal species. Interstitial nephritis is more common. Nephritis and pyelonephritis are observed in all animals, but more often in dogs.
In ordinary farms, kidney disease accounts for approximately 5%, in specialized complexes - 8% of cases from internal non-contagious diseases. Nephrites are divided into primary and secondary by origin.
Secondary nephritis often accompanies illness gastrointestinal tract, liver, lungs.
Glomerulonephritis is an inflammatory process of the kidneys of infectious-allergic etiology with a predominant lesion of the glomerular apparatus of the nephron (Fig. 119).
Etiology. The disease occurs as a result of infections, allergic sensitization, hypothermia, and poisoning. The main etiological factor glomerulonephritis is an infection, predominantly
streptococcal, especially hemolytic streptococcus, to a lesser extent staphylococci and pneumococci. Diffuse glomerulonephritis occurs with anaerobic enterotoxemia.

Nephritis is also considered as an allergic post-infectious disease. Specific renal allergies, which are based on autosensitization processes, are also important.
An important reason for the development of the disease is hypothermia and dampness in the premises. They can play the role of a decisive factor in a sensitized organism; it is possible that it converts inactive antibodies into active ones, that is, it activates them. There is a possibility of serum and vaccine nephritis.
Sensitizing reasons may also be the quality of feed, living conditions, etc.
Inadequate feeding of animals leads to a decrease in nonspecific resistance body, to loss of nutrition. Emaciated animals are predisposed to developing nephritis. There have been cases of animals contracting nephritis when they escape coniferous trees, birch, alder leaves and spoiled feed. Mycotoxicosis and candidomycosis play a role in the occurrence of nephritis in animals. There may be cases of nephritis developing when animals are poisoned with various types of chemicals.
The pathogenesis of glomerulonephritis is complex. It is believed that a foreign substance entering the blood (bacterial toxin, chemical agent, drug or its metabolite, pathological proteins formed as a result of fever, administration of serums, vaccines, etc.), eliminated by the kidneys, enters the primary urine, then reabsorbed by the tubules, damages the tubercular basement membrane and combines with its proteins, thus turning into a renal antigen and causing an immunological reaction.
In the initial period of glomerulonephritis, there is a decrease in the concentration function of the kidneys, and subsequently in the filtering function, which primarily affects the excretion of nitrogenous products and other factors of interstitial metabolism.
With the development of nephritis in animals, azotemic uremia occurs. The mechanism of its development is not entirely clear; there is no doubt that uremia itself is a manifestation of severe renal failure. With it, diuresis is reduced. All this leads to a delay in the animal’s body of nitrogenous metabolic products.
The content of residual nitrogen and especially urea in the blood serum increases 5-10 times. Along with this, hypochloremic
uremia. Loss of chlorine and sodium from the body is accompanied by tissue dehydration (exicosis). Under these conditions, the processes of protein breakdown sharply intensify. This is accompanied by an increase in the blood not only in the content of amino acids and ammonia, but also in the products of incomplete hydrolysis in the form of polypeptides, which are very toxic. They have a toxic effect on the vascular system, causing an increase in capillary permeability, a reflex drop in blood pressure and vasotropic radicardia. A rapid decrease in the concentration of chlorine in the blood and extracellular exicosis lead to hypovolemia, a further reduction in the volume of glomerular filtration, an increase in the level of residual nitrogen, and the development of acidosis.
There is a disturbance in the acid-base balance towards a sharp acidotic shift, caused by the retention of predominantly volatile acids and ketone bodies in the body.
It should also be noted that the stomach and intestines are involved in compensating for impaired renal function in nephritis. Long-term intoxication contributes to protein-granular degeneration of liver cells and the occurrence of liver failure. This leads to changes in protein metabolism. In particular, the cause of hypoalbuminemia in glomerulonephritis is the accelerated breakdown of albumin, disruption of its synthesis by the liver and increased permeability of the renal capillaries due to congestion. There is a release of protein from the vascular bed, it is excreted in the urine, and proteinuria develops.
When a partial compensatory function of the gastrointestinal tract occurs during azotonemia, uremic gastroenteritis develops, the release of nitrogenous substances from the skin and oral mucosa.
Long-term uremic intoxication of the bone marrow leads to suppression of hematopoiesis and the development of hypochromic anemia.
Damage to the cardiovascular system is manifested by hypertension, accompanied by an increase in diastolic pressure. Poor circulation and cardiac hypertrophy are directly related to hypertension.
The most severe change in blood circulation develops when hypervolemia (increased blood mass) is combined with arteriolar spasm. Due to the development of hypervolemia, hypertension and spasms of cerebral vessels, animals often develop eclampsia.
Numerous and prolonged exposures that cause renal dysfunction cause the development of uremic polyneuropathy. In this case, animals experience adynamia, apathy, drowsiness, inactivity, impaired coordination of movements, decreased reflexes, severe sweating, and subsequently a comatose state develops. The duration of coma with nephritis in animals can be from several minutes to 2-3 days.
Jade is one of the most severe forms renal pathology in animals, in which a number of organs and systems are involved in the process and, first of all, the humoral, cardiovascular, gastrointestinal tract,
liver, blood systems, nervous system and almost all types of metabolism (Fig. 120).
a a

Rice. 120
Atrophy of the glomeruli due to stagnation of urine in chronic interstitial nephritis a- atrophied glomeruli; 6- proliferation of interstitial tissue.


Symptoms According to clinical signs, three forms of glomerulonephritis are distinguished: hematuric, nephrotic and mixed.
The hematuric form of the disease is characterized by hypertension, hematuria and edema syndrome.
The nephrotic form is accompanied by edema, proteinuria and cylindruria.
The mixed form (protein-hematuric) is characterized by persistent hypertension, edematous syndrome, gross hematuria, and proteinuria.
There are mild and severe forms of the disease.
Light form nephritis is almost asymptomatic and is recognized only by urine tests. Usually the disease begins with depression of the animal, weakness, decreased or lack of appetite, and increased thirst.
Body temperature is in the upper limits of normal or slightly elevated, pulse is rapid, blood pressure is high (17.0/6.0 hPa).
Vibrating percussion causes pain in the kidney area.
The subcutaneous tissue in the lower wall of the abdomen is loose. Urination is rare, there is slight albuminuria in the urine, qualitative tests for sugar, blood and bile pigments and urobilin are positive.
In urinary sediments, erythrocytes, leukocytes, renal epithelium and hyaline casts are found. The number of red blood cells and the amount of hemoglobin in the blood is reduced, while the number of leukocytes is increased.
In severe cases of the disease, animals are exhausted and lie down more. Body temperature is low, pulse is slow, breathing movements reduced. There is slight swelling in the area of ​​the lower abdominal wall, heart sounds are difficult to hear, and there is an emphasis on the second sound on the aorta. Oliguria occurs, turning into anuria. The urine is cloudy, with the presence of protein, sugar, bile pigments, urobilin, erythrocytes, leukocytes and renal epithelium, hypochromic anemia.
In the stage of renal failure, signs of brain damage dominate. There is marked adynamia, apathy, drowsiness, and inactivity. Hearing and vision are reduced. Sensitivity disorder is accompanied by attenuation of reflexes (ear, corolla and eye). In this case, hypoproteinemia, dysproteinemia, hyperazotemia, hypochloremia and anemia are noted.
Flow. Acute glomerulonephritis in a few (8~10) days or after
With timely treatment, 1-2 weeks ends in recovery; more often it becomes chronic, lasting for months. Mortality is low.

Pathological changes. Animal corpses are often emaciated. The subcutaneous tissue is edematous, and there is often transudate in the serous cavities.
The kidneys are usually enlarged and full of blood (Fig. 121). The cortex is expanded and contains many scattered red dots and dark red spots.
Histologically, dilation and filling of large and small vessels with blood, swelling and partial desquamation of the vascular endothelium, an increase in the size of most glomeruli, and degeneration of the tubular epithelium are established. In the Shumlyansky-Bowman capsule there are epithelial cells, subjected to granular degeneration.
Superficial lymph nodes(submandibular, knee folds) slightly enlarged, flabby, gray-yellow in color, the pattern is smoothed, the surrounding tissue is swollen. The mucous membranes are swollen. The heart is slightly enlarged due to the left half. The epicardium is flabby, edematous, and there are pinpoint hemorrhages. There are pinpoint hemorrhages on the endocardium and valves. The liver is slightly enlarged and flabby. It has a dark brown color, is dryish, and the pattern is weakly expressed. The spleen is wrinkled, the capsule is collected in folds, there are multiple pinpoint hemorrhages under it, and is somewhat dry on section. The stomach (abomasum) contains liquid chyme mixed with mucus; the mucous membrane is gray-red, slightly swollen, and eroded in places. The intestinal mucosa is hyperemic.
The diagnosis of acute nephritis does not present difficulties. Anamnesis data, the results of a clinical examination and laboratory tests of urine and blood are taken into account. The diagnosis is established based on identifying the nature of the symptoms: hematuria, hypertension and edema. Azotemia, hypochloremia and anemia are established in the blood. Acute nephritis is characterized by oliguria and following changes urine: the presence of protein up to 1%, erythrocytes, leukocytes, renal epithelium. Urine the color of meat slop.


Glomerulonephritis is differentiated from nephrosis according to the following data. Nephrosis usually occurs without hematuria, increased arterial blood pressure, or cardiac hypotrophy. In urine with nephrosis, the protein content is up to 2 percent or more, there are no red blood cells, leukocytes, renal epithelium and casts are present.
The prognosis is favorable to cautious. An unfavorable prognosis should be expected when oliguria is observed from the very beginning of the disease, turning into anuria with symptoms of renal failure.
Treatment. Complex. It should be aimed at eliminating the causes of the disease, combating inflammatory processes and intoxication, restoring diuresis, correcting the water-electrolyte balance and acid-base balance of the body.
During treatment, special attention is paid to the proper maintenance and feeding of sick animals. They are placed in a dry, warm and well-ventilated room, and the skin is kept clean. Feed is prescribed with the lowest possible sodium chloride content, and watering is limited.
It is better to give carnivores milk, bread, oatmeal and pearl barley, boiled vegetables.
At drug treatment sick animals are primarily prescribed penicillin antibiotics (penicillin, bicillin-3, bicillin-5, ampicillin, oxacillin, ampiox) in therapeutic doses. In this case, the degree of impairment of the functional activity of the kidneys should be taken into account. Penicillin antibiotics are prescribed to eliminate or reduce the microbial inflammatory process in the kidney tissue. Clinical observations of the results of treatment of animals with glomerulonephritis show that the use of antibiotics alone does not completely solve this problem.
One of the ways to increase the effectiveness of antibiotic therapy for nephritis is their combined use, as well as pathogenetic therapy. In the background antimicrobial therapy It is recommended to carry out novocaine blockade of the border sympathetic trunks and splanchnic nerves according to V.V. Mosin or perinephric blockade. These blockades, applied against the background of developing inflammation in the kidneys, stop it, correct the functional disorders that have arisen in the body, increase the defenses and cause the animals to recover in a shorter time.
In case of severe disease, along with the blockade, it is necessary to use replacement and symptomatic therapy. Specific place in complex treatment Acute nephritis in herbivores is treated with vitamin therapy and, first of all, the administration of vitamins A, B, E, and better combined - trivitamin, trivit or tetravit; in carnivores - B vitamins.
To neutralize and remove toxins from the body of patients, hemodez should be administered intravenously at a dose of 0.3 ml/kg of animal body weight. Positive results were obtained in the treatment of nephritis in calves with intravenous administration of a medicinal mixture consisting of a 6% solution of polyvinylpyrrolidone - 100 ml, a 20% solution of glucose - 50 ml and a 40% solution of hexamethylenetetramine - 10 ml.
Symptomatic treatment for nephritis depends on the severity of the disease and the severity of a particular syndrome. Particular attention should be paid cardiovascular system. To maintain cardiac activity, solutions of caffeine, camphor oil and cordiamine should be used.
A relatively new method of treating nephritis in animals is the use of corticosteroid hormones (prednisolone, prednisone and hydrocortisone) at a dose of 1 mg/kg of animal body weight twice a day, for | 8 days. The proposed hormonal drugs have anti-inflammatory and desensitizing effects.
In order to improve diuresis, reduce the effect and relieve tonic contraction of blood vessels in the kidneys, use a 20-25% solution of magnesium sulfate in a dose of 100-200 ml or a 10% solution of calcium gluconate 30-50 ml.
To improve diuresis, decoctions and tinctures of bearberry leaves, calendula, juniper fruits, and rose hips are used.
The use of etiotropic, pathogenetic, replacement and symptomatic therapy in the complex treatment of animals with nephritis helps to create favorable conditions for the restoration of vitamin, nitrogen and water-electrolyte metabolism, as well as the acid-base balance of the body and the functions of organs involved in metabolic processes.
Prevention. Eliminate the impact of the pathogenic factor, which is infection. *
Particular attention should be paid to the prevention of primary gastrointestinal and respiratory diseases of infectious and non-infectious origin. *
IN general prevention pay attention to the procurement, preparation and storage of feed, as well as checking its quality. Poor quality feed (affected by fungi, rotten, sour) should not be included in the diet.
In addition, the conditions that cause sub-cooling are eliminated, and temperature, humidity and gas conditions in the premises are stabilized. Regular walks, brushing of animals and cleaning of premises are recommended.
An important point is to conduct a routine medical examination. Based on the results of random laboratory tests, kidney disease is detected. Drugs are used whose action is aimed at increasing protective forces animal body (heterogeneous blood, trivitamin or tetravit, a mixture of citrated horse blood, tetravit and sodium norsulfazole, etc.). ’
The effectiveness of specific measures in the prevention of renal complications largely depends on the timely implementation of general nonspecific measures for infectious and non-infectious animal diseases.
Interstitial nephritis (Nephritis interstitialis acuta) is an inflammation of the interstitial tissue of the kidneys.
Interstitial nephritis is an independent disease that has its own nature, most often immune, a clinical picture, and patterns of development. In clinical practice, it is diagnosed relatively rarely.

Due to these circumstances, there is no accurate data on the frequency and prevalence of this disease. Therefore, in most cases, this form of nephritis is diagnosed during forced slaughter or during the slaughter of animals in meat processing plants.
The process can be focal or diffuse in nature. In the diffuse form, both kidneys are involved in the process with the development of necrosis of the tubular epithelium and acute renal failure.
Etiology. Slowly developing nephritis is often interstitial. This is due to long-term use of medications (antibiotics, sulfonamides, etc.). Acute course The disease occurs with an overdose of broad-spectrum antibiotics (gentamicin, kanamycin, polymyxin, neomycin, neovitin, streptomycin, etc.). ^
It may occur due to previous infection, as well as a reaction to the administration of vaccines and serums.
It can also occur in animals suffering from chronic glomerulo- and
pyelonephritis.
Pathogenesis. Most researchers believe that the disease is of immune origin and that kidney damage is a manifestation of a general reaction. A foreign substance entering the blood (drug, chemical agent, bacterial toxin, etc.), being eliminated by the kidneys, enters the primary urine, combines with its protein, turns into an antigen and causes an immunological reaction with the fixation of immune complexes in the membrane.


A reflex spasm of tubular vessels, an increase in intratubular pressure, and a decrease in renal blood flow develop. Compression of the tubules gradually leads to their atrophy and death. There is a decrease in glomerular filtration and increasing edema, which leads to a decrease in water reabsorption and the development of polyuria.
The concentration function of the kidneys is also impaired due to cellular infiltration and inflammatory changes the main substance of the medulla. As the foci of infiltration increase, gradual development is possible connective tissue. Subsequently, the acute process often becomes chronic (Fig. 122, 123).
Symptoms Acute interstitial nephritis is accompanied by symptoms of the underlying disease that caused it. Occurs more often against the background of acute infectious gastroenteritis, acute nonspecific bronchopneumonia, colibacillosis, leptospirosis, salmonellosis, candidiasis, etc., when using broad-spectrum antibiotics on the 3-5th day after their administration in loading doses.
In sick animals, there is a decrease in appetite, body temperature varies in the first days
from the underlying disease, at first it is slightly increased, and then returns to the physiological norm. Blood tests reveal slight leukocytosis, a decrease in the number of red blood cells and the amount of hemoglobin.


Violation of the nitrogen excretory function of the kidneys is accompanied by an increase in the content of residual nitrogen and urea in the blood serum by 1.5-
2 times. Disorders of water-electrolyte metabolism are manifested by hypochloremia, hypocalcemia and hyperphosphatemia. In most cases there is no swelling. Polyuria is noted. A characteristic sign is a decrease in the relative density of urine to 1.010, which remains at a low level for several months. Changes in urinary sediment are uncharacteristic; sometimes leukocytes are found, rarely erythrocytes, casts and renal epithelium.
Pathological changes. The kidneys are enlarged. Their capsule is difficult to remove. The surface of the cortical layer is lumpy. When cut, there may be gray-white dots of varying sizes. Histological examination reveals significant cellular infiltration of connective tissue, accumulation of plasma cells, lymphoblasts and fibroblasts, dystrophic and atrophic changes in the parenchyma.
In the interstitial tissue of the kidney there is plethora, stromal edema, serous exudate with single neutrophilic leukocytes, pronounced dystrophic and necrotic changes in the tubular epithelium. In the medulla, their infiltrates are usually more pronounced than in the cortex.
Diagnosis. Diagnosis of acute interstitial nephritis is difficult. When making a diagnosis, it is taken into account that acute renal failure develops after taking medications during the treatment of the underlying disease. There is prolonged polyuria, urine with low relative
density.
It should be differentiated from glomerulonephritis, in which a triad of symptoms is pronounced: hypertension, hematuria, edema. Frequent urge to urinate due to oliguria and even anuria. Urine has the color of meat wash, contains red blood cells, white blood cells, and the epithelium of the renal tubules. During the period of anuria, acute renal failure develops, leading to uremic coma and even death of animals.
The course of the disease is long. Full recovery Functional activity of the kidneys occurs 2-3 months after treatment. If treatment is not completed, the process becomes chronic.
The prognosis with timely treatment is favorable. If acute interstitial nephritis develops against the background of another disease, it is questionable. Treatment. In the initial period of the disease, penicillin antibiotics (penicillin, bicillin, ampiox, etc.) are prescribed.
During treatment with antibiotics, to reduce their sensitizing effect, the use of antihistamines and desensitizing drugs - diphenhydramine, suprastin, tavegil, etc. is indicated. These drugs must be prescribed in combination with ascorbic acid and calcium preparations.
This combination medicinal products, in addition to the desensitizing effect, has the ability to reduce the permeability of capillary walls and, therefore, prevents the development of tissue edema and sharply reduces their toxicity. Histamine has not only a desensitizing, but also an anti-inflammatory effect.
Symptomatic treatment includes the use of diuretics. Purine derivatives (aminophylline, diuretin, caffeine, etc.) have a diuretic effect, improving renal hemodynamics and enhancing glomerular filtration.
It is advisable to use herbal medicine - decoctions of black elderberry, bearberry leaves, corn silk, St. John's wort, juniper berries, etc.
In order to normalize metabolic processes, vitamins A, D, E, ascorbic acid are prescribed; for carnivores - vitamins Bj, B12.
In case of severe nephritis with symptoms of acute renal failure, a 5% glucose solution and a 0.9% sodium chloride solution are administered intravenously.
Prevention. Complex. To increase the body's defenses, create good sanitary and hygienic conditions in the premises, as well as regular exercise.
The prevention of respiratory and gastrointestinal diseases, especially those of viral origin, deserves attention.
It is important to select the correct dosage of drugs, adherence to the timing of use, frequency of administration, taking into account synergies and side effects.

Nephritis(nephritis) – the disease is characterized by inflammation of the kidneys (often on an immune basis) with subsequent impairment of their function. All parts of the nephron, interstitial tissue of the kidney, blood vessels and nerve endings can be involved in the inflammatory process. Depending on the degree of damage to the main structures of the kidneys, glomerulonephritis and interstitial nephritis are distinguished. According to the size of the lesion, nephritis can be focal and diffuse, according to its course - acute and chronic.

Etiology. The main causes of nephritis are various infections, an allergenic factor, penetrating radiation or exposure to radioactive substances into the body. Of all the parenchymal organs, the kidneys are the most sensitive to radiation, especially in young animals. Nephritis can develop when feeding spoiled hay, pine branches, young leaves of birch, alder, as a result of improper use of certain medicinal substances (turpentine, tar, phosphorus, arsenic, antibiotics, etc.), as well as as a complication of various gastrointestinal and respiratory diseases .

Symptoms . In acute nephritis, general depression, loss of appetite, increased body temperature, pain in the kidneys, and frequent urination in small portions are noted. In severe cases, swelling of the subcutaneous tissue appears in the eyelids, chest, abdomen, and limbs, and blood pressure increases with an increase in the second sound in the aorta. With the development of uremia, thirst increases, dry mouth, and vomiting appears. At chronic course observed fatigue, fatness decreases, signs of heart failure and uremia increase, edema progresses and anemia develops.

Urine increased density, cloudy and often with flakes. It reveals shaped elements blood, casts, deflated epithelium, protein, sugar and often microorganisms. In the blood - leukocytosis.

Diagnosis and differential diagnosis. Characteristic features is an increase in body temperature, pain during urination and palpation in the kidney area, a sharp decrease in urine output. Laboratory testing of urine is crucial.

It is necessary to differentiate nephritis from pyelonephritis and nephrosis. Pyelonephritis is characterized by persistent fever, frequent urination and excessive pain. In the urine, along with blood cells, a large number of cells renal pelvis and microbes. With nephrosis, there is no pain, the temperature is not elevated, increased urination, in the urine high content protein and deflated convoluted tubule epithelium.

Treatment. Improve the maintenance and feeding of sick animals. Feeds rich in vitamins are prescribed. Limit the intake of proteins and table salt. To improve diuresis and metabolic processes, a 40% glucose solution, hemodez, polyglucin is administered intravenously at a dose of 0.5-1.0 ml/kg of animal weight. Diuretics are also prescribed disinfectants: potassium acetate orally at 0.04-0.1 g/kg, Temisal, respectively at 0.01-0.02 g/kg, intravenously 20-25% solution of magnesium sulfate at a dose of 0.2-0.4 ml/kg, hexamethylenetetramine - orally and intravenously at 0.01-0.04 g/kg.

Be sure to use anti-allergic and anti-inflammatory drugs medicines: novocaine in the form of perinephric blockade and intravenous calcium chloride or gluconate, as well as hormonal drugs (ACTH and corticotropin intramuscularly for large animals 3-10 IU/kg, cortisone orally 0.002-0.003 g/kg, prednisolone orally 1 mg/kg).

To suppress microflora, sulfonamides (urosulfan, etazol), antibiotics of the penicillin, tetracycline, gentamicin group, as well as drugs of the nitrofuran series are used.

Prevention is to prevent complications of infectious and other diseases, rational use of substances that have an irritating effect. Animals should also be protected from hypothermia and their natural resistance should be increased.

Acute nephritis (Nephritis acuta)- rapid inflammation of the kidneys with predominant damage to the vessels of the glomeruli and with the transition of inflammation to the interstitial tissue; degenerative changes in the epithelium of the tubules they do not appear clearly or are attached only later.
The disease occurs in all types of animals, but most often occurs in pigs and dogs, less often in cattle and horses.

Etiology. Acute nephritis in animals can occur after they have been ill with infectious diseases (, , etc.), as a result of endo- and exogenous toxicoses due to non-communicable diseases, colds, burns, feeding of poisonous plants, as well as coniferous branches, leaves of birch, alder, reeds, the use of certain medications (arsenic preparations, organophosphorus compounds, creolin, etc.), insect bites (bees, midges, ticks).

Pathogenesis. Focal nephritis occurs when microorganisms enter individual renal glomeruli (with septicemia, pyemia, wound sepsis). Diffuse nephritis is considered as secondary hyperergic inflammatory reaction as a complication after infections.

The occurrence and development of nephritis involves a complex of reactive phenomena from the whole organism and its individual systems (especially nervous, humoral and endocrine), as well as metabolic and vascular disorders. Irritation of the interoreceptors of both kidneys, which occurs reflexively from the nerve endings of the skin (during sudden cooling), can lead to prolonged spasm of the vessels of the glomerular apparatus of the kidneys and the development of the inflammatory process.

The central vasomotor effect is common mechanism, which at kidney diseases combines renal and extrarenal changes in the capillary bed with increased permeability of the walls of blood vessels and glomeruli. Toxins of microorganisms entering the bloodstream contribute to overirritation of the pituitary gland and stimulate the production of the hormone of its posterior lobe, leading to the development of hematuria and anuria. If not all glomeruli affected by microorganisms function simultaneously in the kidney, focal damage occurs.

Diffuse inflammation of the kidneys develops when long-term action irritants in the blood. Affected glomerular capillaries are separated rich in proteins urine, causing disruption of water-salt metabolism; The reabsorption of water and salt by the tubules increases (the specific gravity of urine increases). Significant defeat vascular wall glomeruli leads to a decrease in their total filtering surface. Severe damage to blood vessels causes protein and even red blood cells to escape through their walls. In this case, azotemia is mild, but the proportion of urea in the total residual nitrogen (due to excessive reabsorption of urea) is usually high.

The accumulation of large amounts of protein in the lumen of the tubules, especially globulins and fibrinogen, and an increase in urine acidity lead to the occurrence of cylindrouria. The resulting swelling should be considered as a kind of unloading of blood circulation. The retention of water and salt in the body is caused by increased secretion of antidiuretic hormone.

In focal forms of nephritis, the functional ability of the kidneys is slightly impaired; in diffuse nephritis, it sharply decreases.

When endotoxins and plant poisons enter hematogenously, both kidneys are affected, first in unevenly located foci, and then diffusely. Serous-cellular exudate penetrates into the capsule cavity. Due to ischemia, the glomeruli and tubules atrophy.

Clinical picture. At the onset of the disease, the sick animal's appetite decreases, depression and an increase in body temperature are observed. In horses, due to pain in the kidney area, there is severe anxiety. Sick animals stand with their limbs spread wide apart or tucked under their stomach. Sometimes they arch their back and tend not to move; when moving, they show clumsiness. Pressure on the kidney area and palpation through the rectum causes anxiety in animals. There is swelling in the eyelids, larynx, chest, abdomen, thighs and even the sacrum. Visible mucous membranes are pale and swollen. Dyspeptic symptoms and vomiting are observed (especially in dogs and pigs). Thirst often increases. Blood pressure increases (in cattle up to 210 mmHg), hypertrophy and expansion of the left ventricle of the heart occurs, which is diagnosed by a hard, tense or weakened pulse and an accent of the second tone on the aorta; increased diastolic sound, systolic murmur and dull tones often appear during auscultation of the heart area. In seriously ill patients, a gallop rhythm can sometimes be heard. Due to cardiac weakness, blood stagnation develops in the pulmonary circulation, venous pressure increases (sometimes up to 300 mm of water column and above). Cyanosis appears.

On the part of the respiratory system, due to circulatory failure and accumulation of acidic products in the blood - shortness of breath, upon auscultation - moist congestive rales, in some animals slight cough. In sick animals, especially in the presence of fever and blood overflow of the pulmonary circulation, bronchitis and bronchopneumonia are diagnosed. There is a noticeable weakening of gastrointestinal peristalsis.

Nephritis in an animal begins with a frequent urge to urinate. The animal develops oliguria, and in some cases anuria. The urine becomes cloudy, light red to brown in color, usually has a high specific gravity, and contains a lot of red blood cells, casts and salts. The urine reaction is often acidic.

Acute nephritis is characterized by short-term (7-10 days) release of large amounts of protein in the urine; later, during the entire period of the disease, protein is released in the urine insignificantly. The excretion of sodium chloride in the urine is significantly reduced or completely stops.

The blood, as a result of containing a large amount of water in it, is diluted, the specific gravity of whole blood and especially serum is reduced. The serum albumin-globulin ratio is usually reduced due to high content globulins; the amount of residual blood nitrogen in severe cases increases to 500 and even 1000 mg%. Simultaneously with the increase in indican in the blood, the sick animal develops symptoms of azotemic uremia (drowsiness, constriction of the pupil, complete refusal to feed, vomiting, itching, shortness of breath, hyperhidrosis, convulsive twitching). The number of red blood cells and hemoglobin drops. In dogs leukocyte formula with a normal total number of leukocytes, it may deviate towards lymphocytosis or monocytosis. IN acute period nephritis in the blood there is thrombocytopenia, which is replaced by hyperthrombocytosis during recovery.

Pathological changes. The subcutaneous tissue of the abdomen, the area of ​​the chest, head and limbs are swollen. In acute focal and diffuse nephritis, the kidneys are sometimes enlarged in size, and altered glomeruli in the form of gray grains of sand or small red dots are visible on the cut surface. The capsule is easily removed, the surface of the kidneys looks slightly spotty. Histologically, acute inflammation of the glomeruli, their enlargement, hyperemia, and accumulation of neutrophilic leukocytes along the walls of the capillaries are detected in the kidneys. With severe inflammation, coagulated protein, red blood cells, fibrin fibers and proliferation of epithelial cells are found in the capsule.

Sometimes, when autopsying dead animals, we find granular protein and slight fatty degeneration of convoluted tubules and loops of genl. The tubules are narrowed, they contain loose protein exudate, leukocytes, erythrocytes, as well as single cylinders. In acute nephritis, fibrinoid swelling and necrosis of blood vessels in the brain, liver, spleen, adrenal glands and other organs are observed. Sometimes it develops around swollen small vessels serous inflammation. Similar changes occur in the heart muscle.

Flow. Acute nephritis, depending on the degree of kidney damage, can last 1-2 weeks and end in recovery or death of the animal with symptoms of uremia and acute heart failure. Sometimes the disease drags on for quite a long time and turns into a chronic form of diffuse nephritis, which lasts for months or even years.

Diagnosis Nephrosis is diagnosed based on medical history (infection, toxicosis, cold) data clinical picture(swelling, frequent painful urination, increased body temperature) and results laboratory analysis urine and its sediments - cloudy urine, often with flakes, reddish or brown in color, increased density (on average above 1.025 -1.035), with an average protein content of up to 3%. When carrying out microscopy of sediment in the urine, large quantities of red blood cells, leukocytes, erythrocyte and leukocyte casts are found, and in severe cases of the disease - microbial flora. When examining the blood we find neutrophilic leukocytosis and increased ESR. Blood pressure is increased.

With nephrosis there is no inflammation, hematuria or high blood pressure. With pyelonephritis, protein, pus are found in the urine, and red blood cells, leukocytes, renal epithelial cells, casts and bacteria are found in the sediment. With pyelitis, the urine remains cloudy for a long time. Prolonged and persistent hypertension with hematuria and delayed recovery of renal function serves as an indicator of the transition of an acute process to a chronic one. Glomerulonephritis with nested localization of focal nephritis should be distinguished from diffuse nephritis.

Forecast nephritis depends on the degree of kidney damage, the course of the disease and the resistance of the body of the sick animal. With rapidly developing uremia, the prognosis for a sick animal is unfavorable.

Treatment. Management of sick animals with symptoms of nephritis should assume that the animals may be sick infectious diseases. Therefore, animals with nephritis are isolated and complex treatment is prescribed.

The causes of nephritis are eliminated (primarily colds), the sick animal must be placed in a warm, dry, well-ventilated room. Careful skin care is required - cleaning and rubbing the skin.

In the first 1-2 days of illness, fasting is recommended for sick animals, then a limited amount of easily digestible food, poor in protein and table salt, is prescribed: for herbivores - good meadow hay, grass flour, root vegetables and mash made from flour and bran; omnivores and carnivores - milk, bread, cereals from various cereals and boiled vegetables. The feed supplied to animals should contain more carbohydrates, a small amount of sodium and a sufficient amount of potassium and calcium ions (sodium antagonists), which have a diuretic, hypotensive effect on the sick animal and stimulate the contractile function of the myocardium. In addition, the feed ration should be enriched with ascorbic acid, vitamin A and B vitamins.

From common funds, affecting nervous system, the use of perirenal novocaine blockade is indicated for sick animals, and as desensitizing agents - intravenous administration 10% solution calcium chloride or 0.5-1% solution of novocaine in an amount of 100-200 ml along with ascorbic acid. If acute nephritis develops against the background general infection or due to an exacerbation of a focal infection, a course of treatment is carried out with antibiotics, including modern cephalosporins.

In case of severe toxicosis and the development of edema, sick animals are shown copious bloodletting (in large animals up to 2-3 liters). Bloodletting not only reduces the amount of salt and water in the body, but also leads to a significant restructuring of the body's reactivity. After bloodletting, sick animals must be administered intravenously a 20-40% glucose solution in normal doses.

If an animal develops heart failure and in order to increase diuresis, it is necessary to use digitalis, adonis, strophanthus, digitalis preparations and oxygen.

To enhance diuresis, Temisal is used (5-10g for large animals, 0.5-2g for pigs and small cattle), which can be given 3-4 times a day. As diuretics, you can use decoctions and infusions of bearberry leaves, dill fruits, infusion of Astragalus fluffy flower, diacarb and others.

To improve diuresis and metabolic processes, sick animals are administered intravenously a 40% glucose solution, hemodes, polyglucin at a dose of 0.5-1.0 ml/kg of animal weight.

For nephritis, it is recommended to use a 25% solution of magnesium sulfate intramuscularly at the rate of 0.2-0.4 ml per 1 kg of animal weight to relax vascular spasms, lower blood pressure and improve diuresis. To reduce pressure, reserpine is administered intravenously (horses 0.005-0.008g, dogs 0.0005-0.001g).

The use of chloral hydrate, novocaine, suprastin, pipolfen, etc. is recommended as antiallergic drugs and pain relievers.

Prevention. Animal owners must promptly eliminate the causes of acute nephritis ( timely treatment infectious, gynecological and surgical sick animals with purulent and purulent-septic foci). Do not allow the animal to become hypothermic or allow irritating substances to enter the animal’s body with food or medications. Avoid feeding toxic feed to animals and overdosing on table salt.