Patient ___________________________ 72 years old

Diagnosis of the referring institution: ICD, chronicle pyelonephritis of the only left kidney.

Diagnosis on admission: chronic pyelonephritis latent course of "CHF III-IV"

Passport details

FULL NAME.: _________________________________

Age: 72 years

Location: ___________________________

Place of work: disabled person of group II

Date of admission to the hospital: 06/16/08 10-00

Supervision time: 27.06.08

Gr. blood: III, Rh “+“

Clinical diagnosis: hr. pyelonephritis of the only left kidney, latent course of chronic renal failure III-IV

Complaints

At the time of examination, complaints of weakness, dizziness, and minor periodic pain in the left lumbar region.

morbi

He considers himself sick since 1989, when his right kidney was removed due to m. After this, 18 years later, chronic pyelonephritis of the only left kidney was diagnosed. Every year he is treated in a hospital and takes ketoterrol. Suffering long time hypertension. She was referred for a course of steroid treatment. Hospitalized in the urology department as planned.

At the time of admission, she complained of weakness, dry mouth, nausea, dry skin, constipation, poor appetite, and periodic pain in the left lumbar region. A diagnosis was made: chronic pyelonephritis of the only left kidney, latent course, chronic renal failure 3-4.

vitae

Born January 9, 1936. She was the third child in the family. She grew and developed normally, and did not lag behind her peers in mental and physical development. Received incomplete secondary education. In 1952 she entered technical school. Then she worked as a radio operator all her life. Hereditary history is not burdened. In 1985, the uterus and appendages were removed, and in 1989, nephrectomy of the right kidney. Injuries - fracture of the left hand in 2007.

Epidemic history: tuberculosis, Botkin's disease, sexually transmitted diseases denies. Of the past diseases, he notes colds of the upper respiratory tract. Denies bad habits. Allergy history: No data on food and drug allergies were identified. No blood transfusions were performed.

praesens communis

General inspection: General state moderate severity, consciousness is clear, the patient’s position is active, the patient’s physique is proportional, the constitution is normosthenic, the gait is heavy, the posture is straight, height 165 cm, weight 83 kg, body temperature is normal (36.6 o C).

Examination of individual body parts:

Skin

· Pale color, without depigmentation;

· Skin elasticity is reduced;

· Thinning of the skin or induration is not detected, keratoderma is absent;

· Skin moisture is moderate;

· No rash detected.

Nails

· Round shape;

· No brittleness or cross-striations are observed.

Subcutaneous tissue

· Development of the subcutaneous fat layer is excessive (the thickness of the fold in the subclavian region is 3.5 cm);

· Place of greatest fat deposition on the abdomen;

· No swelling.

The lymph nodes

· Single palpated submandibular lymph nodes on the right and left, the size of a millet grain, round in shape, elastic consistency, painless, mobile, not fused to the skin and surrounding fiber; there are no ulcerations or fistulas;

The occipital, cervical, supra- and subclavian, ulnar, bicipital, axillary, popliteal, and inguinal lymph nodes are not palpable.

Saphenous veins

· Unnoticeable. No blood clots or thrombophlebitis were detected.

Head

· Oval shape. Head circumference 57 cm;

· Head position is straight;

· Trembling and swaying (Musset's symptom) negative.

Neck

· Curvature - not curved;

Palpation thyroid gland- not enlarged, uniform plastic consistency, painless.

Face

· Calm facial expression;

· The palpebral fissure is moderately widened;

· Eyelids are pale, not swollen; tremors, xanthelasmas, styes, dermatomyosin glasses are absent;

· Eyeball: no retraction or protrusion;

· The conjunctiva is pale pink, moist, without subconjunctival hemorrhages;

· Sclera pale with a bluish tint;

· The shape of the pupils is round, the reaction to light is friendly;

· Symptoms: Greffe, Stellwag, Moebius negative;

· Snub nose; there are no ulcerations of the tips of the nose, the wings of the nose do not participate in the act of breathing;

· Lips: the corners of the mouth are symmetrical, there are no cleft lips, the mouth is slightly open, the color of the lips is cyanotic; no rashes, no cracks, lips are moist;

· Oral cavity: no bad breath; the presence of aphthae, pigmentation, Belsky-Filatov-Koplik spots, hemorrhages, no telangiectasis on the oral mucosa, the color of the hard palate mucosa is pale pink;

· Gums: hyperemic, loose, bleed when touched, no border;

· False teeth, an abundance of hard dental deposits on the lower incisors from the oral surface

K - crown; L - cast tooth; P - seal; O - absent

· Tongue: the patient sticks out her tongue freely, there is no trembling of the tongue, the color of the tongue is pale pink, with typos of the teeth, partially covered with a white coating, there are no cracks or ulcers;

· Tonsils are regular in shape, do not protrude from the arches, pale pink in color; There is no plaque, purulent plugs, or ulcers.

Musculoskeletal examination:

Inspection

· There is no swelling, deformation or deformation of the joints;

· The color of the skin over the joints is not changed;

· Muscles are developed according to age; there is no atrophy or muscle hypertrophy;

· There is no deformation of joints or curvature of bones.

Superficial palpation

· Skin temperature over the surface of the joint is not changed;

· The volume of active and passive movements in all planes is preserved;

· There are no joint sounds.

Deep palpation

· The presence of effusion in the joint cavity and compaction of the synovial membrane were not detected during bimanual;

· No presence of “joint mice” was detected;

· Two-finger bimanual palpation is painless;

· Fluctuation symptom is negative; anterior and posterior “drawer” symptom, Kushelevsky’s symptom are negative;

· Muscle tone without pathological changes.

Percussion

· There is no pain when tapping the bones.

Respiratory examination:

Inspection of the cage pile

The shape of the chest is not changed, without curvature, symmetrical, the excursion of both sides of the chest during breathing is uniform, the type of breathing is mixed, respiratory rate is 18, the breathing rhythm is correct, there is no difficulty in nasal breathing;

Chest excursion 5 cm

Palpation of the chest

· The chest is resistant, painless on palpation;

· There is no sensation of pleural friction during palpation.

Comparative percussion of the lungs

· With comparative percussion of the lungs, there is a clear percussion sound at 9 paired points.

Topographic percussion

Lower limits

Mobility of the lower pulmonary border

Auscultation of the lungs

Breathing on the right and left is vesicular,

· Adverse respiratory sounds: dry, moist, fine rales are not heard, crepitus and pleural friction noise are not heard.

· Bronchophony is carried out equally at all paired points.

Examination of the circulatory organs

Examination of the heart and blood vessels

· There is no deformation in the heart area; the apex and cardiac impulse are not visually determined; systolic retraction in

the area of the apex beat is not determined; there is no pulsation in the second and fourth intercostal spaces on the left;

· Pulsations in the extracardiac region: “carotid dance”, pulsation of the jugular veins in the jugular fossae, no epigastric pulsation was detected; Quincke's pulse is negative;

Palpation of the heart area

· The apical impulse is palpated in the fifth intercostal space along the midclavicular line, diffuse, resistant, high; systolic and diastolic tremors (symptom of “cat purring”) are absent; pulse 84 per minute, synchronous in both arms, pulse uniform, regular.

Percussion

Limits of relative and absolute dullness of the heart

· The length and diameter of the heart according to Kurlov are 13 and 11 cm, respectively.

· Percussion vascular bundle in II m/r 5 cm;

· Heart of mitral configuration;

Auscultation of the heart and blood vessels

· Heart sounds are muffled, weakening of the first sound at the apex of the heart; accent of the II tone over the aorta; slight tachycardia;

· Bifurcation, splitting, the appearance of additional noises (gallop rhythm, quail rhythm) are not heard;

Intracardiac murmurs

Decreasing systolic murmur at the apex

Extracardiac murmurs

· Pericardial and pleuropericardial friction rubs are not heard; Vascular murmurs are not heard

· Blood pressure on the right arm is 140/90; Blood pressure in the left arm is 140/90; Blood pressure in the right thigh is 140/90; Blood pressure on the left thigh is 145/95

Abdominal examinations:

Abdominal examination

· The abdomen is round, symmetrical, and is involved in the act of breathing; peristaltic and antiperistaltic movements are not visually determined; subcutaneous venous anastomoses on the anterior abdominal wall are not developed; abdominal circumference 96 cm.

Palpation of the abdomen

· On superficial palpation the abdomen is painless; There is no tension in the abdominal wall. No hernial openings were found in the area of the umbilical ring or along the white line of the abdomen. Shchetkin-Blumberg's symptom is negative; no tumor formations were detected;

· On deep palpation, the sigmoid colon in the left iliac region is in the form of a smooth dense cylinder, 2 cm in diameter, 4-5 cm long, painless, not rumbling, mobile. The caecum, the ascending parts of the colon and the vermiform appendix are not palpable. The lower border of the stomach is not determined by the “splash noise” method. By auscultofriction and auscultopercussion, the border of the stomach is determined 3.5 cm above the navel to the right and left of the midline;

· The transverse colon, stomach and pancreas are not palpable. When palpating the liver, the edge is rounded, the liver surface is smooth, soft, elastic consistency; gallbladder not palpable. Courvoisier's symptom, Frenicus phenomenon, Obraztsov-Murphy symptom are negative. The spleen is not palpable.

Percussion of the abdomen

· Percussion reveals a tympanic percussion sound. Mendel's sign is negative; free liquid not detected in the abdominal cavity.

· The borders of the liver according to Kurlov are 9*8*7 cm; Ortner's, Vasilenko's, Zakharyin's symptoms are negative;

· The dimensions of the spleen according to Kurlov are 5*7 cm.

Auscultation of the abdomen

· Intestinal peristalsis can be heard above the abdominal cavity. There is no peritoneal friction noise. Systolic murmur is not heard over the aorta or over the renal arteries.

Examination of the urinary organs

Inspection

· There is no redness, swelling, or swelling in the lumbar region, no protrusions above the pubis. There is a scar in the right lumbar region.

Palpation

· In horizontal and vertical positions, the kidneys are not palpable. Palpation in the suprapubic region revealed no foci of compaction; palpation is painless.

Percussion

· Pasternatsky's symptom is negative;

· The bladder cannot be determined by percussion.

Status localis

The lumbar region is symmetrical, without visible depressions or deformations. Palpation of the left kidney area is painless, left kidney not palpable. Palpation of the area of the right kidney is painless; there is a postoperative scar on the right. The effleurage symptom is negative on both sides. There is no pain along the ureters. The external genitalia are formed according to the female type and correspond to age.

Bladder: there are no protrusions above the pubic area, painless on palpation.

Federal Agency for Health and Social Development

GOU VPO

Altai State Medical University

Department of Pediatrics No. 1 with a course of childhood infections

Head kaPhaedra: Professor Vykhodtseva G.I.

Teacheravatar: assistant Lyubimov A.P.

Curator: student of group 561 Zhuravleva A.Yu.

Clinical historyPainnOuch: ____________________________Clinical diagnosis: Chronic renal failureIIIArt. against the background of dysplasia.Complication: moderate anemiaBarnaul-2008 Passport details: FULL NAME.: Mother _________________ 38 years old, individual entrepreneur "Polovskikh" - confectioner Father ______________ 40 years old, OJSC "Altai-Koks", mechanic Age: 17 years Date of Birth: 03.05. 1998 Location: ___________________________Placestudy: PTU-41 Yesand admission to the hospital: 08/26/08. G. Supervision time: from September 5, 2008 to September 12, 2008 Clinical diagnosis: Chronic renal failure III stage. against the background of dysplasia. Complication: moderate anemia Complaints:on admission: for increased fatigue; at the time of supervision: makes no complaints. Anamnesis morbi: She has been ill for 16 years, when in the first 6 months she was diagnosed with bilateral renal hypoplasia. He was sent to the Regional Children's Hospital, where treatment was carried out. Until the age of three, he was examined regularly as planned. From 3-12 years old they did not go to the doctor. In 2003, he was sent for examination to the Regional Children's Hospital due to changes in the tests. And to this day it is examined regularly every year. During the course of the disease, health was satisfactory without complaints. P was normal, there was no edema. Now located in the Children's room Regional hospital on planned treatment, waiting in line for hemodialysis. Conclusion: Based on the fact that the disease has been going on for about 16 years, we can conclude that the nature of the disease is chronic. The nature of the symptoms indicates a progressive course of the disease. Anamnesis vitae Child from the 2nd pregnancy, which occurred against the background of anemia. Delivery on time, full-term fetus. Weight at birth 3300 grams, length 52 cm. He grew and developed according to his age. Vaccinated according to the calendar. Previous ARVI diseases are often chicken pox, rubella, enterobiasis, chronic tonsillitis, secondary hyperparathyroidism, chronic recurrent synovitis of the left knee joint, carriage of chlamydial infection. No blood transfusion was performed. No allergic reactions noted. There was no contact with infectious patients. Heredity is not burdened. Status praesents communis: The general condition of the patient is moderate. My health does not suffer. He reacts adequately to examination. The skin is pale pink, clean, dry, turgor is preserved. Pastiness of the eyelids. Subcutaneous fatty tissue is poorly developed and evenly distributed. Peripheral lymph nodes are not palpable. Visible mucous membranes are clean, moist, pink. In the oropharynx, the mucous membrane is pink, the tonsils are enlarged (grade I), there are no plaques. Breathing through the nose is free, above lungs breathing vesicular, no wheezing. Percussion clear pulmonary sound. Heart sounds are rhythmic and clear. The abdomen is soft and painless. The chair is decorated. The effleurage symptom is negative on both sides. Urination is painless. There are no varicose veins, seals along the veins or pain. Digestive organs: inspection: the tongue is moist, covered with a white coating at the root. The oral mucosa is pink, without changes, there are no ulcers, cracks or erosions. The pharynx is not hyperemic, the tonsils are not enlarged. The act of swallowing is not disturbed. The abdomen is rounded, not enlarged in volume, symmetrical, and participates in the act of breathing. There are no visible peristaltic movements. Subcutaneous venous anastomoses The “jellyfish head” type was not found. On superficial palpation the abdomen is soft, painless, the temperature in symmetrical areas is the same, dry, the abdominal muscles are relaxed. There are no pathological formations, muscle separation along the white line of the abdomen, or peritoneal irritation syndrome. Deepmethodicalpalpation according to Obraztsov - Strazhesko: sigmoid colon - in the left iliac region, elastic, painless, dense, mobile, 3 cm in diameter, does not rumble; descending colon - in the left part of the mesogastrium, elastic, painless, moderately dense consistency, mobile, 3 cm in diameter, does not rumble; blind intestine - in the right iliac region, elastic, painless, dense, 4 cm in diameter, rumbles upon palpation. The vermiform appendix is not palpable; the ascending colon is in the right part of the mesogastrium, elastic, painless, 3 cm in diameter, moderately dense consistency, mobile, does not rumble; the transverse colon is in the peri-umbilical region, elastic, painless, 3 cm in diameter, does not rumble, moderately dense consistency, mobile; lower edge of the stomach - on both sides of the midline of the body 3 cm above the navel, mobile, painless, smooth surface; liver- under the right costal arch along the midclavicular line, does not protrude beyond the edge of the costal arch. The edge of the liver is smooth, sharp, the surface is dense, smooth, painless on palpation; Liver dimensions according to Kurlov: along the midclavicular line - 9 cm; along the midline of the body - 8 cm; along the edge of the left costal arch - 7 cm. spleen- on palpation according to Sali, the size is 8x9 cm, the surface is smooth, painless, moderately dense consistency. The presence of free fluid in the abdominal cavity is not determined by palpation and percussion. Urinary organs: There is no swelling, edema or hyperemia in the renal area. Minor swelling in the periorbital area. The kidneys in 5 positions (standing, lying, on the right and left side, knee-elbow position) on the right and left sides are not determined. The effleurage symptom is negative on both sides. There is no pain along the ureters. The bladder is not palpable. No pathology was detected from the genital organs. Nervous and endocrine systems: Consciousness is clear, speech is intelligible, behavior is adequate, mood is good, he is well oriented in space and time, coordination is preserved, and communication is good. There is no tremor of the limbs. Tendon and skin reflexes are easily evoked, lively, without any peculiarities. Pain, tactile, and temperature sensitivity are not impaired. The pupils are round, medium in size. The reaction to light is direct, lively, friendly, Accamadation and convergence are not impaired. Movements eyeballs in full. The thyroid gland is not enlarged. On palpation it is painless, soft-elastic consistency. There are no symptoms of hyperthyroidism. Secondary sexual characteristics are developed according to the female type. Mammary glands of the same size, no lumps or tumor formations were detected. No increase in the size of the tongue, nose, jaws, ears, hands, or feet was detected. Physical development: The difference between actual growth and expected growth is 180-182 = -2, the growth rate is average. The difference between the actual weight and the expected weight is 55-65 = 10, degree I malnutrition. The difference in chest circumference is 81-84=- 3cm/3=-1, average. Head circumference difference 54-57.2 = -3.2 cm/0.6 cm = 5.3. Conclusion according to Vorontsov: grade I hypotrophy. Physical development is average, disharmonious, proportional. Plan for additional research methods: Laboratory research: 1. General blood test (leukocyte formula, Hb, ESR, Lei, E); 2. Biochemical blood test (bilirubin, ?- lipoproteins , sugar, diastase, thymol test, urea, K, Na, prothrombin activity, fibrinogen, total protein, force test, creatinine, transaminases: ALT, AST);3. General urine analysis (protein, Lei, epithelial cells);4. Biochemical analysis of urine (total protein, lipids, K, Na, Ca, P, urea, creatinine, bilirubin, titratable acids);5. Urine examination according to Zimnitsky, according to Nechiporenko; Functional studies: 1. Ultrasound of internal organs; 2. Duplex study of renal vessels3. ECG Results of additional research methods: Laboratory research:1. General blood test from27 .0 8 .0 8 Hemoglobin 85 g/l Red blood cells 2.8x10??/l ESR 24 mm/h Leukocytes 4.2x 109/l Conclusion: in general analysis blood there is a decrease in hemoglobin level, a decrease in the level of red blood cells, corresponding to moderate anemia. Increased ESR, eosinophilia. 2. Biochemicalanalysisblood from 27. 08 .0 8 : Serum sodium 142 mmol/l Serum potassium 3.9 mmol/l Fibrinogen 3250 Urea 19.03 mmol/l Creatinine 439.6 µmol/lAPTT 35 sec. K 5.3 Na 14 Conclusion: B biochemical analysis blood there is a slight increase in fibrinogen, increased levels of urea and creatinine. 3. General urine analysis05 .0 9.08 : Density: 1007Color: straw yellowTransparency: completeReaction: acidicProtein: 2.97 g/lSugar otLeukocytes: 2-3 in the field of viewRed blood cells: a large numberSalt oxalates + Single epitheliumConclusion: Hematuria, oxalaturia, no signs of inflammation.. 4. Biochemical urine analysis dated 09/04/08.: Day amount of urine 1800 ml C min. diuresis 1.25 ml Blood creatinine 476.7 µmol/l Urine creatinine 3.21 mmol/l Water resorption 85.6% Conclusion: creatininuria, creatininemia. 5. Urine examination according to 3AndMnitsky 04 . 09.08 .

Quantity	Density	Total
		daily diuresis 325.0



		night diuresis 465.0

Conclusion: hyposthenuria, nocturia. 6. Urine examination according to NechiporenkoL 750E - Conclusion: normal Functional research methods: 1. Ultrasound examinationtioninternalorgansfrom27 . 0 8.08 : Conclusion: slight increase in the size of the liver, tail of the pancreas, hypoplasia with dysplasia of the kidney parenchyma in the form pronounced changes echogenic structure. There is a dynamic decrease in liver size. Duplex study of renal vessels from 27.08.08 With CDI and EDC, the vascularization of the renal parenchyma is sharply reduced, and the vascular pattern is deformed, with fragments of laced intrarenal vessels. The spectra of blood flow through the renal arteries are deformed. The spectrum of blood flow through the renal veins is phasic. 3. ECG from 08/27/08. Ectopic atrial rhythm, heart rate 65-68 b?. Increased bioelectrical activity of the left ventricular myocardium. In orthostasis: short-term recovery sinus rhythm with a heart rate of 83 b?. Clinical diagnosisand its rationale: Based on the patient's complaints of increased fatigue. From the medical history: sick for 16 years ( chronic course) when renal hypoplasia was first discovered. From laboratory studies it is clear that creatinine and urea are increased in the biochemical analysis of blood and urine; from an ultrasound scan dated 08/27/08 it is clear that hypoplasia with dysplasia of the renal parenchyma in the form of pronounced changes in the echogenic structure. Based on this, we can conclude that the urinary tract is involved in the pathological process system, the disease is chronic. Based on the level of creatinine in a biochemical blood test (439.6 µmol/l), the third stage of chronic renal failure can be diagnosed. Based on the level of hemoglobin in a general blood test (decrease in the level of red blood cells, 85 g/l), moderate anemia can be diagnosed. Based on complaints patient, medical history and additional research methods, a diagnosis can be made: Chronic renal failure stage III. against the background of dysplasia. Complication: moderate anemia Treatment for this patient: 1) Diet: reducing the amount of B (limit meat consumption), fish, vegetable fiber, fruits and vegetables are recommended. 2) Ketosteril 11 tablets per day 3) Fenuls 25 ml once a day (for the treatment of anemia) 4) Renogrigon 5 thousand units 3 times a week (to improve renal blood flow) During treatment we evaluate the level: 1. Blood pressure 2 times a day; 2. Diuresis (we count the amount of fluid consumed and excreted); 3. Examination by an ophthalmologist once a month.4. Biochemical analysis of blood and urine Bibliography: Sh Children's Diseases, ed. Baranova A.A. 2007, 1006s.Sh Basic physical and paraclinical constants of childhood, Yu.F. Lobanov, A.M. Malchenko, E.V. Skudarnov 2006.Sh Clinical classifications diseases of childhood and examples of diagnosis formulation, Department of Pediatrics No. 2, 2007. Sh Malchenko A.M., Lobanov Yu.F., Fugol D.S. Lecture material for 3rd-4th year students of the pediatric faculty on propaedeutics of childhood diseases. 2005-

This is a sudden and rapidly progressing disorder of renal function, manifested by oligoanuria, azotemia, and disturbances in water and electrolyte balance.

Occurrence of the disease Acute renal failure

The causes of acute renal failure are varied. E. M. Tareev highlights the following groups reasons: 1) shock kidney, 2) toxic kidney, 3) acute infectious kidney, 4) vascular obstruction, 5) urinary tract obstruction.

Can lead to the development of shock kidney traumatic shock, electrical injuries, burns, massive blood loss, crush syndrome with muscle crushing, surgical shock, transfusion incompatible blood, toxicosis of pregnancy, myocardial infarction, exhausting vomiting. Toxic kidney occurs when poisoning with salts of heavy metals, primarily mercury salts, organic poisons (carbon tetrachloride, dichloroethane, acetic acid, methyl alcohol, etc.), some medications (barbiturates, quinine, pachycarpine), poisons of plant and animal origin (snake, mushroom and insect venom).

Acute infectious kidney disease occurs with sepsis of various origins, primarily anaerobic, and in patients with septic abortions. Acute renal failure can also occur with thrombosis and embolism of the renal arteries, with periarteritis nodosa, acute diffuse glomerulonephritis and acute pyelonephritis. Finally, this syndrome may be caused by mechanical obstacles to the outflow of urine due to kidney stones or compression of the ureters.

Course of the disease Acute renal failure

Considering the variety of causes leading to the development of acute renal failure, it is hardly possible to reduce its development to any one mechanism. The most important factor is the ischemic factor.

With a significant decrease in heart function, a decrease in stroke volume due to blood loss, loss of a significant amount of fluid, or pathological redistribution of blood during shock and collapse, renal blood flow drops sharply. Impaired renal circulation inevitably leads to decreased filtration and disruption of other kidney functions. In some cases, a decrease in circulating blood volume occurs due to a decrease in plasma volume.

An important mechanism of renal circulatory impairment in various types shock is a spasm of the renal vessels due to the neurohumoral effects on the renal vessels of histamine and serotonin, released during shock or destruction of blood cells and tissues in pathological conditions.

The final mechanism of renal ischemia is anoxia of the renal tissue, to which the latter is very sensitive. However, decreased renal blood flow is not the direct cause of oligoanuria. In chronic kidney disease, a sharp decrease in renal blood flow and filtration does not result in a decrease in diuresis. Therefore, it is difficult to explain oligoanuria by a drop in renal blood flow and a sharp decrease in filtration. Apparently, the filtrate is almost completely reabsorbed in the damaged tubules. Due to damage to the tubular basement membrane, the glomerular filtrate can come into direct contact with the renal interstitium and be easily absorbed back into the blood and lymph.

Another important factor is nephro-toxins. Various nephrotropic poisons disrupt enzymatic processes in the kidney tissue, and by damaging the lysosomal cell membranes, they can lead to necrosis. According to modern concepts, tubular blockage should not be considered as a cause of impaired renal function, but rather as a consequence of oligoanuria, although this blockage may be an additional factor that worsens the course of acute renal failure.

Pathological anatomy

Macroscopically, in acute renal failure, the kidneys are enlarged, flabby, the cortex is swollen, the pattern of the cortex loses its clarity. The basis of pathomorphological changes in acute renal failure is tubular damage, primarily tubulonecrosis and tubulorhexis, as well as edema of the interstitial tissue of the kidneys. For a toxic kidney, tubulonecrosis is more typical, for a shock kidney - damage to the basement membrane of the tubules with fragmentation of the main membrane, referred to as tubulorexis. In the epithelium of the tubules there is swelling of the cytoplasm, granular, vacuolar, less often fatty degeneration. Electron microscopic examination reveals swelling, swelling and breakdown of mitochondria. Morphological changes in acute renal failure undergo rapid dynamics. The necrotic epithelium sloughs off and is rejected, the swelling of the interstitial tissue decreases and regeneration of the epithelium begins along the preserved main membrane. However, where the basement membrane has ruptured, complete restoration of the nephron does not occur. The consequence of the transferred process is focal fibrosis of the nephron.

Symptoms of the disease Acute renal failure

During acute renal failure, four periods or stages are distinguished: 1) shock, 2) oligoanuria, 3) restoration of diuresis with an initial diuresis phase and a polyuria phase, and, finally, 4) recovery period. In the first period, the symptoms of the underlying disease, leading to acute renal failure and shock, are most pronounced. There is tachycardia and a decrease in blood pressure, which, however, may be transient. During the period of oligoanuria, urine formation decreases or completely stops. This is accompanied by a gradual increase in all components of residual blood nitrogen, phenol and other excreted metabolic products.

Sometimes at the beginning of this period, patients feel better for a while, despite the absence of urine. Gradually they begin to complain of weakness, loss of appetite, headache. Nausea and vomiting appear. As the disease progresses, the smell of ammonia is detected when breathing.

Disorders of the central nervous system diverse. Most often, apathy is observed, but sometimes the patient may be agitated, have poor orientation in the environment, and confusion. Hyperreflexivity and convulsive seizures are often observed.

In cases where acute renal failure was a consequence of sepsis, herpetic rashes around the mouth and nose can be noted. The nature of skin changes in acute renal failure developed as a result of allergic reactions, can be varied: fixed erythema, urticarial rash, toxicoderma. Pulse exceeds 100 beats per minute. The boundaries of the heart are expanding. The expansion of the heart is especially demonstratively determined on radiographs. A systolic murmur is heard above the apex of the heart, an accent of the second tone and a gallop rhythm are detected. Systolic blood pressure is elevated in some patients. Sometimes there is a decrease in diastolic pressure, in some patients - to zero. Rhythm and conduction disturbances are noted: extrasystole, atrioventricular and intraventricular block, mainly associated with disturbances

electrolyte metabolism and acidosis. Fibrinous pericarditis with pericardial friction rub, pain in the heart area, and changes in the electrocardiogram may be observed. Interestingly, the symptoms of pericarditis increase after hemodialysis.

Nausea and vomiting, loss of appetite are observed in almost all patients. Less common are diarrhea and melena. Especially often phenomena from the digestive organs are observed when hemorrhagic fever with renal syndrome. The occurrence of gastrointestinal lesions is primarily associated with the development of excretory gastritis and enterocolitis, which are erosive in nature. However, some of the symptoms are due to profound electrolyte imbalances. Interstitial edema develops in the lungs, which is based on increased permeability of the alveolar capillaries. Pulmonary edema is poorly recognized clinically and is diagnosed primarily by chest x-ray. In this case, a bilateral, symmetrical, with unclear contours, darkening in the root zone is detected.

Prevailing clinical sign at this stage - oligoanuria. The amount of daily urine ranges from 20 to 300 ml with a density of 1003-1008. The urine is cloudy, dark brown or bloody. The sediment is large, contains many erythrocytes, leukocytes, and clumps of hemin-impregnated cylinders. There is a lot of protein in the urine. The excretion of urea and creatinine in the urine is reduced. High leukocytosis, a pronounced shift in the leukocyte formula, anemia, and an increase in ESR are observed in the blood.

Anemia in acute renal failure develops constantly. Anemia is most pronounced in cases where acute renal failure is preceded by intravascular hemolysis. Anemia, increasing during the period of oliguria, reaches a maximum in the initial phase of diuresis restoration and persistently continues during the recovery period.

Severe homeostasis disturbances develop. The content of residual nitrogen increases from 14-26 to 140-260 mmol/l (from 20-40 to 200-400 mg%). Urea nitrogen increases to a greater extent than residual nitrogen in general. Creatinine levels increase at a faster rate than urea, especially in patients with massive muscle lesions. The ammonia content in the blood also increases sharply, especially with combined renal and hepatic failure. Concentrations of uric acid and indoxine increase less significantly. Metabolic acidosis develops, usually uncompensated. For acute renal failure

sufficiency is characterized by hyperkalemia and hypermagnesemia, manifested electrocardiographically by a high T wave, a decrease or disappearance of the U wave, and impaired atrioventricular and intraventricular conduction. High potassium levels are explained by the appearance of pathological neuromuscular symptoms such as increased muscle excitability, hyperreflexia and even paralysis.

However, in some cases of acute renal failure, with repeated vomiting, profuse diarrhea, on the contrary, there is excessive excretion of potassium and the development of hypokalemia with weakness, decreased reflexes, and bloating due to intestinal paresis. In this case, the electrocardiogram shows a decrease in the ST segment, a decrease in the voltage of the T wave, and a high Q wave. The S-T interval is significantly lengthened.

During the period of oligoanuria, as a rule, there is overhydration with a decrease in hematocrit. *

Liver damage in acute renal failure is almost constant. Clinically, liver damage is manifested by icteric sclera and jaundice of the skin.

Anuria or oliguria usually lasts 5-10 days, but in some cases - 30 or more days. It is clear that in the latter case, to maintain the patient’s life, methods of active therapy for renal failure are required.

An increase in diuresis can begin several days after oliguria and occurs gradually. At first, the amount of urine exceeds 500 ml, and then, gradually increasing, amounts to more than 2000 ml/day. From this time on, the third period of acute renal failure begins.

During this period, clinical improvement does not develop immediately, and sometimes the patient’s condition may worsen. At the beginning of the diuretic period, the level of azotemia may increase and hyperkalemia may increase. The concentrating ability of the kidneys remains low. The patient loses weight during polyuria. The period of polyuria usually lasts 4-6 days. Patients' appetite improves, pathological changes in the nervous system and circulatory system disappear.

It is conventionally accepted that the recovery period begins from the day of illness when the level of residual nitrogen or urea becomes normal. It lasts 3-6-22 months, during which not only homeostasis is completely restored, but also filtration, the concentrating ability of the kidneys, and tubular secretion gradually increase.

However, for 1-2 years, signs of functional failure of individual organs and systems (heart, liver, etc.) may persist.

Acute renal failure, if not leading to fatal outcome, ends with gradual recovery without a tendency to develop chronic disease kidney

After 6 months, more than half of the patients fully regain their ability to work, although in some patients by this time their ability to work remains limited, and they are recognized as group III disabled. In many ways, the ability to work of patients depends on the underlying disease that caused acute renal failure

Treatment of the disease Acute renal failure

Measures aimed at reducing the effect of nephrotoxins and preventing circulatory disorders reduce tubular damage. Early removal of poison from the body, the prescription of specific antidotes and the use of drugs that prevent and eliminate circulatory disorders are also measures to prevent acute renal failure.

In cases where there is a risk of developing acute renal failure, in order to prevent it, mannitol in a 10% solution can be administered intravenously at the rate of 1 g per 1 kg of patient weight. It improves renal blood flow, increases glomerular filtration and acts as an osmotic diuretic. At the stage of oliguria, the use of mannitol is ineffective and inappropriate.

It should be noted that etiological treatment of acute renal failure in most cases is effective only in the early stages of the disease. Patients with acute renal failure must be hospitalized. Careful care of the oral cavity, skin and mucous membranes is necessary. In normal cases, the amount of fluid administered should not exceed 600-700 ml/day. With polyuria, it is necessary to completely replace the loss of fluid and electrolytes.

Prescribing large amounts of fluid to a patient during periods of oliguria and anuria in the hope of stimulating diuresis and reducing the concentration of nitrogenous waste does not produce results. It increases hyperhydration, reduces the effective osmotic pressure of plasma and increases water “intoxication”.

In the initial stage of the disease, the most effective treatment is exchange blood transfusion. With its help, part of the non-dialyzed plasma hemoglobin is extracted, bloodstream is replenished with red blood cells, anemia is eliminated. If it is not possible to perform an exchange transfusion, a blood transfusion should be performed, the purpose of which is to eliminate anemia and restore the volume of circulating blood.

Measures are being taken to combat shock and blood loss. In cases where there is a picture of shock and replacement of blood loss does not eliminate hypotension, the use of corticosteroids (intravenously 30-60 mg of prednisolone or 100 mg of hydrocortisone) is indicated. However, the feasibility of such therapy is limited by initial period diseases.

If there is an infection, treatment with antibiotics is necessary, to which the isolated flora is sensitive, but antibiotics are often used for prophylactic purposes. However, we must not forget that most antibiotics are excreted by the kidneys, which forces us to reduce the dosage and frequency of antibiotic administration. It is better not to use antibiotics such as streptomycin, monomycin, neomycin in acute renal failure due to their nephrotoxicity.

In connection with the danger of urinary tract infection, it is necessary to pay attention to the fact that the introduction of a permanent catheter, especially in men, in order to accurately control diuresis is dangerous due to the development of urethritis, prostatitis and cystitis with subsequent pyelonephritis.

During the first three periods of the disease, protein is completely excluded from the patient's diet. You can give patients cream, sour cream, syrups. In case of dyspeptic disorders, the patient is fed parenterally.

To combat acidosis, use a 5% solution of sodium bicarbonate at an initial rate of 0.5-1 ml per 1 kg of weight under the control of determining acid-base balance.

To correct protein catabolism, anabolic steroid hormones are administered: methyl androstenediol, nerobol, retabolil.

Intravenous infusion of hypertonic solutions of 40% glucose (up to 100 ml/day) is effective. At the same time, insulin is used at the rate of 1 unit per 3-4 g of glucose.

Long-term gastric lavages are indicated to wash out nitrogenous waste; this relieves patients from uncontrollable nausea and vomiting. Parenteral administration of calcium salts is necessary, especially with the development of convulsive attacks.

Acute renal failure, which cannot be treated conservatively, is an indication for hemodialysis using an artificial kidney or peritoneal dialysis. In the first days of the development of oligoanuria, the use of hemodialysis is inappropriate, since in a significant proportion of cases conservative treatment allows you to restore kidney function. Hemodialysis is indicated when the blood creatinine level is above 114 mmol/l (15 mg%"), urea is above 49 mmol/l (300 mg%), residual nitrogen is above 113-140 mmol/l (160-200 mg%), potassium 6, 5 mmol/l Indications for hemodialysis should be assessed only in conjunction with clinical picture. Contraindications to hemodialysis are septic process, acute thromboembolism, myocardial infarction, gastrointestinal bleeding, severe heart and liver failure.

Question about spa treatment is decided in each case individually and no earlier than 6 months after discharge from the hospital.

The resorts of Bayram-Ali, Bukhara, and the southern coast of Crimea are shown.

2015-04-19 08:22

On March 23, 2015, Alfiya and her husband Sergei came to our clinic for treatment with Chinese medicine. Alfiya came from Novosibirsk, Russia. She recalled her medical history and medications and told us that 5 years ago she was diagnosed with chronic glomerulonephritis. Since diagnosis, she has been on aggressive treatment and multiple medications. I have always been treated as prescribed by the doctor, but the condition is gradually worsening and uremia is still present. The doctors hurt her...

Her attending physician, Li Zheng, was asked in more detail about the patient’s medical history and learned the following:

First hospitalization:

In 2010, one day Alfiya had swelling in his legs and at the same time headache, dizziness, chest tightness, shortness of breath and other symptoms. Analyzes showed that the pressure was 200/120 mm Hg, proteinuria +++, and hidden hematuria ++, creatinine in the blood was 180 mmol/l. Local doctors diagnosed him with CKD (chronic kidney disease) and prescribed Moxonidine, Methyldopa and Hydrochlorothiazide. These 3 medications lower blood pressure, meaning local doctors have tried to treat CKD by controlling blood pressure. In this case, chronic renal failure is at a decompensated stage.

Second hospitalization:

After being discharged from the hospital, Alfiya always took medications regularly, but there was swelling in the lower extremities, and creatinine increased to 250 mmol/l. In 2012, the condition of the cutting worsened and Alfiya was hospitalized for the second time. Then the pressure was 220/120 mmHg, hemoglobin up to 98 g/l, proteinuria +++, hidden hematuria ++, creatinine 400 mmol/l. Then there was hypertension and anemia. Amlodipine and injection of erythropoietins were also supplemented.

Third hospitalization:

After the second discharge, Alfiya was still taking medication, her blood pressure was 140-180/90-100 mmHg, the effects of the treatment were not so ideal, creatinine was more than 600 mmol/l. One day in 2014, severe shortness of breath arose and the third hospitalization began. The pressure was 230/110, creatinine was up to 800, and there was still Ischemic disease heart disease, myocardial ischemia and other diseases. And then dialysis began, 3 times a week.

Alfiya did not understand why for 5 years she never stopped treatment, but her condition gradually worsened?

Alfiya received program treatment with us:

Kidney disease is caused by the accumulation of multiple harmful substances in the blood. With blood circulation, various wastes and toxins increase the load on the kidneys and accumulate in the kidneys, causing kidney damage. And therefore it is necessary to cleanse the blood of waste and toxins from the blood and kidneys.

Blood pollution therapy, enema, Micro-Chinese medicine Osmotherapy, medicinal foot baths and others were carried out.

After 21 days, Alfiya returned home with satisfaction.

History of the development of the present disease. Diseases suffered during the patient's life. General condition of the patient. Results of laboratory and instrumental studies. Clinical diagnosis and its rationale. Criteria for chronic kidney disease. Treatment plan.

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Ministry of Health and social development Russian Federation

GOU VPO "Kazan State Medical University"

Department of Hospital Therapy with a Course in Endocrinology

Disease history

End-stage renal failure. Chronic kidney disease stage 5 - outcome of nephropathy mixed origin(ischemic + hypertensive nephroangiosclerosis)

Kazan - 2015

I. General information

FULL NAME. A.R.M.

Age: 69 years old

Date of admission to the clinic: 02.12.16

II. Complaints

Complaints upon admission:

Main: general weakness, increased fatigue, swelling in the legs, shortness of breath. chronic kidney diagnosis research

III. Anamnesis morbi

In 2014, the patient was in surgical department RCH with diagnosis: left-sided inguinal hernia. The examination revealed moderate anemia. A routine renal ultrasound revealed signs of renal failure. A biochemical blood test revealed an increase in creatinine and urea. He was sent to the nephrology department of the Republican Clinical Hospital, where he was diagnosed with ESRD, stage 5 CKD. The patient was transferred to hemodialysis.

IV. Anamnesis vitae

Previous illnesses: at the age of 12 he suffered from bilateral kidney inflammation; At the age of 20, he suffered from pneumonia, complicated by dry pleurisy.

There is no allergic history.

Family history: the patient’s mother diabetes, at my father's peptic ulcer stomach.

Denies blood transfusions.

Denies sexually transmitted diseases.

He abused alcohol and smoked for 20 years. On this moment does not drink alcohol and does not smoke.

V. Status primary objectives

The general condition is serious due to the underlying disease. I feel satisfactory. Active position, clear consciousness, calm facial expression, normal behavior, asthenic constitution.

Skin and mucous membranes. The skin is pale and dry. Visible mucous membranes ( oral cavity, nasal cavity, conjunctiva) pale pink in color, without enanthems, ulcerations, or bleeding.

Respiratory system. The voice is not changed, breathing through the nose is free. Breathing is rhythmic, 23 respiratory movements per minute. The shape of the chest is correct, the course of the ribs is oblique, there is no retraction or bulging of the intercostal spaces, the participation of both halves of the chest in the act of breathing is symmetrical. There is no shortness of breath at the time of examination. The posterior wall of the pharynx and tonsils are pink, without rashes or ulcerations.

On palpation: rib cage elastic, painless. During percussion: in symmetrical areas over the entire projection area of the lungs, a clear pulmonary sound is heard.

Auscultation of the lungs: vesicular breathing, no wheezing.

Cordially- vascular system. Visually, the development of the upper and lower halves of the body is proportional. When examining the heart area, the chest is not deformed. There are no visible vascular pulsations. Heart beat and epigastric pulsation are not visually detected. The shape of the fingers is normal, there is no capillary pulse. The venous network is not expressed.

Palpation: When palpating the cardiac region, an apical impulse in the V intercostal space 1 cm outward from l. Mediaclavicularis sinistra, localized, moderate strength, height, area 1*1 cm2. When changing body position, the nature of the apical impulse does not change. The symptom of "cat purring" is negative. The arterial pulse on both aa.radialis is the same, symmetrical, rhythmic, 100 beats. per minute, moderate filling, tension, normal value.

urinary system. The skin is pale, no pastiness or swelling was detected. Edema of the lumbar region, sacrum, and legs is not detected by palpation. The kidney area is visually unchanged and painless on palpation.

Examination plan:

General blood analysis.

General urine analysis.

Blood chemistry:

Albumen

Bilirubin

Cholesterol

Creatinine

Urea

Total protein

Electrolytes.

Electrocardiography.

Echocardiography.

Ultrasound examination of the abdominal organs and kidneys.

Consultation with an ophthalmologist.

Results of laboratory and instrumental studies:

General blood analysis from 03/03/16

WBC - 7.7 * 10 9 /l (N=6.0-9.8*10 9 /l)

RBC - 2.46 * 10 12 / l (N = 3.5-4.4 * 10 12 / l)

PLT - 198 * 10 9 /l (N=180-400*10 9 /l)

HGB - 83g/l (N=114-134g/l).

Leukocyte formula: e - 3, b - 1, p/i - 1, s/i - 40, lymph - 28, mon-7, ESR-53 mm/h.

Conclusion: anemia. Acceleration of ESR, which may indicate the presence of some kind of inflammatory process.

General urine analysis from 03/03/16

Color: straw yellow

Transparency - transparent.

Specific gravity - 1003

Reaction - alkaline

Protein - no

Epithelium class - ----

Leukocytes - single in p.z.

Red blood cells - -----

Salts - ur. to-you are insignificant. quantity

Conclusion: hyposthenuria may be the result of a violation of the concentration function of the kidneys, or as a result of heavy drinking. The presence of uric acid indicates a metabolic disorder.

Blood chemistry from 03.03.16

Albumin 35.4 g/L 35.0-60.0 g/L

ALT 11 U/L 0-42 U/L

AST 19 U/L 5-37 U/L

Bilirubin 4.3 umol/L 3.4-20.5 umol/L

Cholesterol 6.48 mmol/L 3.11-5.20 mmol/L

Creatinine 487 mkmol/L 28.0-60.0 mkmol/L

Glucose 4.7 mmol/L 3.5-6.0 mmol/L

Total protein 61.9 g/L 60.0-80.0 g/L

Urea 8.8 mmol/L 1.70-7.50 mmol/L

Potassium 5.5 mmol/L 3.50-5.0 mmol/L

Sodium 137 mmol/L 135-145 mmol/L

Calcium 1.19 mmol/L 1.15-1.27mmol/L

Chlorine 100 mmol/L 97-115 mmol/L

Conclusion: Hypercholesterolemia. Elevated levels of creatinine and urea, which indicates a pronounced impairment of the filtration and reabsorption function of the kidneys. Hyperkalemia.

Calculation of GFR according to MDRD(Creatinine 487, age 69, weight 65): 11 ml/min/1.73 sq. m.

Test according to Nechiporenko from15.02.16

Protein ------

Red blood cells 500 (2000-4000)

Leukocytes 500 (4000-6000)

Conclusion: no pathology.

Ultrasound br.cavities and kidneys from 09/26/13.

LIVER: reduced, the hepatic edge is blunt, the boundaries are clear. A significant amount of fluid (100 mm) is visualized under the liver.

CONCLUSION: signs of liver cirrhosis. Fluid in the abdominal cavity.

KIDNEYS: located in a typical place, the shape is not changed, the contours are smooth, size 78*33, parenchyma 9 mm. Differentiation of layers is difficult. The pyelocaliceal system is a rough, stringy structure. In the CLS projection, small hyperechoic structures with a diameter of up to 2-3 mm are visualized. The kidney parenchyma is dense and poorly differentiated.

BLADDER: empty.

CONCLUSION:

PLEURAL CAVITY: On the right - fluid, 10 mm thick, posterior sinus is visualized. On the left - fluid, 12 mm thick, is visualized in the posterior sinus.

Electrocardiogram from29.02 .1 6 .

Conclusion: sinus rhythm, heart rate 98 beats/min. EOS - normal position. Amplitude signs of left atrial hypertrophy. Left ventricular hypertrophy.

Echocardiogram from 17.0 2 .1 6 .

Conclusion: Signs of hypertrophy of the left atrium and left ventricle.

Examination by an ophthalmologist on 09.28.13.

The surrounding tissues and appendages of the eyes are apparently not changed. Full eye movements. The anterior segment of the eyes is not changed. Optical media are transparent. Fundus of the eye: optic discs are pink, the boundaries are clear, the vessels are not changed, the macular area is not changed, the periphery is without features.

Conclusion: no pathology was detected in the fundus.

Clinical diagnosis and its rationale:

Primary: End-stage renal failure. Chronic kidney disease 5 - outcome of nephropathy of mixed origin (ischemic + hypertensive nephroangiosclerosis)

Related: Atherosclerotic lesions of the aorta, aortic valve leaflets, and main arteries. Cardiogenic cirrhosis of the liver. Arterial hypertension grade 3, high risk, CHF 2B, FC 3, pulmonary hypertension.

This diagnosis was made based on:

Complaints: general weakness, increased fatigue, swelling in the lower extremities, headache;

History of the disease: In 2012, the patient was in the surgical department of the Republican Clinical Hospital with a diagnosis of left-sided inguinal hernia. A routine renal ultrasound revealed signs of terminal renal damage. A biochemical blood test revealed an increase in creatinine and urea. He was sent to the nephrology department of the Republican Clinical Hospital, where a diagnosis of CKD stage 5 was made - the outcome of nephropathy of mixed origin (ischemic + hypertensive nephroangiosclerosis). Readmission to the nephrology department in February 2014:

urea 9.0 mmol/l, creatinine 490 mmol/l, anemia, after which a decision was made to transfer the patient to hemodialysis. The patient has been on hemodialysis for 2 years.

Laboratory data: anemia in the UAC (HGB - 83g/l (N=114-134g/l)). In biochemical analysis: Hypercholesterolemia. Elevated levels of creatinine (487 mmol/l) and urea (8.8 mmol/l), which indicates a severe impairment of the filtration and reabsorption function of the kidneys.

GFR=11 ml/min/1.73 m2 (MDRD). The indicator corresponds to CKD stage 5.

Data instrumental methods research:

Ultrasound of the kidneys: signs of end-stage renal failure.

Ultrasound of the liver: signs of liver cirrhosis.

ECG: sinus rhythm, heart rate 98 beats/min. EOS - normal position. Amplitude signs of left atrial hypertrophy.

Echocardiogram: signs of hypertrophy of the left atrium and left ventricle.

Differential diagnosis: Chronic kidney disease should be differentiated from acute renal failure.

The criteria for CKD are:

1) Proteinuria;

2) Persistent changes in urine sediment (erythrocyturia, leukocyturia, cylindruria);

3) Changes in the kidneys with imaging studies (changes in kidney size);

4) Changes in the composition of blood and urine (changes in serum and urinary concentrations of electrolytes, changes in CBS);

5) Persistent decrease in glomerular filtration rate less than 60 ml/min/1.73 sq. m;

6) Pathomorphological changes in kidney tissue identified during lifetime nephrobiopsy (sclerotic changes in the kidneys, changes in membranes);

7) Arterial hypertension (persistent, high);

8) The ECG shows signs of left ventricular hypertrophy in combination with changes caused by electrolyte disturbances.

OP criterionNare:

1) A sudden decrease in urine output below 500 ml/day within 24 hours after exposure to an etiotropic factor.

2) Low specific gravity of urine with severe oliguria.

3) An increase in the level of residual nitrogen in the blood plasma with corresponding symptoms from the central nervous system.

4) Arterial hypertension is rare.

5) The ECG shows signs of electrolyte disturbances.

In favor of CKD with its differential diagnosis with acute renal failure indicates:

1. History of kidney disease. The patient suffered from pyelonephritis in childhood(gradual development).

2. Arterial hypertension with left ventricular hypertrophy. According to ECG and echocardiography, the patient has signs of hypertrophy of the left heart (there are morphological changes).

3. Reduction in kidney size according to ultrasound (78*33 in the patient, while the norm is 100*50).

4. Colorless urine.

Treatment:

1. ACE inhibitor: enalapril 2.5 mg * twice a day.

2. Antiplatelet agents: acetylsalicylic acid 125 mg at night.

3. Renal replacement therapy (hemodialysis).

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Abstracts on medicine Acute renal failure: causes, stages of development, intensive care. Medical history chronic renal failure End stage renal disease medical history

Complaints

morbi

vitae

praesens communis

Occurrence of the disease Acute renal failure

Course of the disease Acute renal failure

Pathological anatomy

Symptoms of the disease Acute renal failure

Treatment of the disease Acute renal failure

History of the development of the present disease. Diseases suffered during the patient's life. General condition of the patient. Results of laboratory and instrumental studies. Clinical diagnosis and its rationale. Criteria for chronic kidney disease. Treatment plan.

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