Details
Clinical diagnosis of the underlying disease:
Polycystic liver and kidney disease
urinary tract infection
Passport part
1. Patient I.
2. Gender female
3. Year of birth 1962, age 48
4. Permanent residence Moscow
5. Profession ultrasound doctor
6. Date of receipt 4.02.2011
Complaints
Complaints about fatigue, dizziness, general weakness, instability of blood pressure (130/90 mm Hg, with episodes of increase to 160/90 mm Hg).
Anamnesis morbi
He considers himself ill since 1992, when he notes the appearance of general weakness and increased fatigue.
In 1986, during the first pregnancy, a week before delivery, there were episodes of increased blood pressure up to 160/100 mm Hg. After delivery, blood pressure returned to normal.
In 1992, in the 2nd trimester of pregnancy, polycystic kidney and liver disease was diagnosed.
Since 2000, she has been experiencing episodes of increased blood pressure up to 160/100 mm Hg.
From 2007 to the present, therapy has been carried out: Concor, 2.5 mg / day. During treatment, blood pressure stabilized at 120/80 mm Hg.
In December 2010 - an outpatient examination at the polyclinic at the place of residence: an increase in the level of creatinine (164 μmol / m 2), in the general analysis of urine - protein (0.06 g / l), leukocytes (15 in the field of view). Therapy was carried out with kanefron (2 tab. 3 times a day), chimes (25 mg, 3 times a day)
Real hospitalization in the clinic for dynamic examination and correction of therapy.
Anamnesis vitae
Brief biographical information: was born in Moscow in 1962. The only child in the family. Married, two children.
Education: Higher medical (ultrasound doctor).
Labor history: career from 20 years to the present - an ultrasound doctor. Occupational Hazards: None.
Gynecological history: menarche at 14 years of age, then menstruation took place regularly, without complications.
1983 - diffuse uterine bleeding.
2006 - diagnosed with fibrocystic mastopathy.
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Pregnancy=5 |
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miscarriages=0 |
Household history: satisfactory
Nutrition: satisfactory
Bad habits: smoking, drinking, drug denies
Past illnesses: childhood diseases (chicken pox).
Widespread osteochondrosis.
Epidemiological history: contact with patients with acute viral hepatitis, tuberculosis, blood transfusion and its components denies.
Allergic history: drug intolerance - ampicillin - rash on the face.
Heredity
Mother, 81 years old, suffers from hypertension, multiple kidney cysts.
Father died at the age of 65, aortic aneurysm, coronary artery disease, arterial hypertension.
Children - sons 24 years old and 18 years old - duodenal ulcer.
Present state (Status praesens)
General inspection
General condition of the patient: moderate
Consciousness is clear
The position is active.
Build: normosthenic constitutional type, height 156 cm, body weight 55 kg, BMI = 22.9. The posture is straight, the gait is slow.
Body temperature: 36.7°C.
Skin and visible mucous membranes, pink, moist skin, reduced turgor, female-type hair. Nails of normal shape and color.
Development of the subcutaneous fat layer moderate.
There are no edema.
The lymph nodes: Occipital, parotid, cervical, submandibular, supraclavicular, axillary, inguinal lymph nodes are not palpable.
The calf muscles are painless on palpation.
The bones are painless when tapped, the joints are not changed.
Respiratory system
The shape of the nose is not changed, breathing through the nose is free, there is no discharge from the nose.
The chest is normosthenic, symmetrical, the intercostal spaces are moderately expressed.
NPV 17 min. The type of breathing is mixed.
On palpation: there is no pain, voice trembling is the same in symmetrical parts of the chest, it is not changed.
The elasticity of the chest is normal.
Bronchophony: the same over symmetrical areas of the chest.
With comparative percussion- a clear pulmonary sound is determined above the symmetrical areas of the lungs.
Topographic percussion:
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Topographic landmarks |
Right lung |
Left lung |
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Upper border of the lungs |
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Height of tops in front |
3 cm above the collarbone |
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Standing height of the tops at the back |
Spinous process of the VII cervical vertebra |
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Inferior border of the lungs |
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peristernal line |
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mid-clavicular line |
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anterior axillary line |
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Middle axillary line |
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Posterior axillary line |
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scapular line |
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Paravertebral line |
Spinous process of XII thoracic vertebra |
Spinous process XII thoracic vertebra |
Respiratory excursion of the lower edge of the lungs along the right and left scapular lines 2 cm.
Auscultation - weakened vesicular breathing with a hard shade over the entire surface of the lungs. There are no side breath sounds.
The cardiovascular system
Examination: the cervical veins are not changed, increased pulsation of the carotid arteries is not revealed. Apex beat, cardiac impulse, epigastric pulsation are not visually determined.
Palpation: The apex beat is palpated in the IV intercostal space 1.5 cm medially from the midclavicular line, not enhanced, not spilled.
Cardiac impulse, epigastric pulsation, trembling in the region of the heart are not determined.
Soreness and areas of hyperesthesia were not identified.
Percussion: Limits of relative cardiac dullness:
right - IV intercostal space on the right edge of the sternum,
left - IV intercostal space 1.5 cm medially from the midclavicular line,
upper - III intercostal space,
the width of the vascular bundle is 6 cm.
Auscultation of the heart: rhythmic heart sounds.
At 1 point of auscultation, 1 tone is muffled, not split, there are no additional tones and noises.
At the 2nd point of auscultation 2 tone of normal volume, the relative volume is not changed, not split, additional tones, no noise.
At the 3rd point of auscultation, the 2nd tone of normal volume, the relative volume is not changed, not split, there are no additional tones, no noise.
There is no 2 tone accent.
At the 4th auscultation point, tone 1 is muffled, not split, there are no additional tones and noises.
The rhythm is correct, 82 beats / min, the pulse of normal filling and tension,
BP 125/80 mm Hg
Digestive system
Appetite is normal. The tongue is moist, not furred. Teeth are sanitized. The act of swallowing is not disturbed.
The abdomen is of the correct form, painless on palpation, participates in the act of breathing. When examining the retraction, there is no visible peristalsis and pulsation. There is a bulging of the anterior abdominal wall due to the anterior surface of the left kidney.
Percussion: tympanic percussion sound over the surface of the abdomen.
On superficial palpation the abdomen is painless, the muscles of the anterior abdominal wall are not tense, Shchetkin-Blumberg's symptom is negative. The liver and left kidney are palpated.
Deep palpation data according to Obraztsov-Strazhesko: sigmoid colon - smooth, dense, painless, movable, non-rumbling cylinder about 3 cm wide, caecum - smooth, painless, slightly rumbling cylinder, 4 cm wide, transverse colon - smooth, painless, elastic cylinder about 3 cm wide , does not growl, the ascending and descending sections of the colon are painless, elastic cylinders, 4 cm thick. The large curvature of the stomach is not palpable. The gatekeeper is not palpated.
Topographic percussion of the liver: the lower edge of the liver along the right mid-clavicular line is located 5 cm below the level of the costal arch, along the anterior midline at the level of the lower third of the distance from the xiphoid process to the navel, along the left costal arch at the level of the left parasternal line.
The liver is palpable, on palpation dense, painless, with a bumpy surface, the lower edge of the liver protrudes from under the costal arch by 5 cm, dense, even.
The dimensions of the liver according to Kurlov: along the right mid-clavicular line 16/5 cm, along the anterior midline 14 cm, along the left costal arch 9 cm.
There are no symptoms of peritoneal irritation.
The spleen is not palpable. There is no ascites.
Chair: regular, normal.
urinary system
The kidneys are palpable on both sides, of a dense consistency, the surface is uneven (due to cystic changes). Pasternatsky's symptom is negative. Urination painless, regular.
Neuropsychic state and sense organs
Consciousness is clear. Contact. Hearing and vision preserved. There are no paralysis.
Endocrine system
The thyroid gland is not enlarged.
Provisional diagnosis:
Diagnosis of the underlying disease:
Polycystic liver and kidney disease
Diagnosis of complications of the underlying disease:
Arterial hypertension II degree, stage 1, risk 2
Chronic renal failure I degree
Concomitant disease diagnosis:
urinary tract infection
Examination plan:
1. Complete blood count
2. Biochemical blood test
3. Urinalysis
4. Chest x-ray
6. Rheumatic tests (SRP, Antistreptolysin-0)
7. Ultrasound of the kidneys, abdominal cavity
8. Daily urine for protein
9. Wasserman reaction
10. Sowing urine, determining the sensitivity of the pathogen to antibiotics
11. Urinalysis according to Nechiporenko
Data of laboratory, instrumental research methods and consultations of specialists
1. ECG 10\02\11
ECG conclusion: EOS is located vertically. The rhythm is sinus, correct.
2. Rheumatic tests 9/02/11
Within the normal range.
3. HBs AG, HCV ab 09/02/11
Within the normal range.
4. CSR for syphilis 09/02/11
Within the normal range.
5. Biochemical blood test 09/02/11
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Index |
Meaning |
Units |
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Transferrin |
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% sat. iron |
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total protein |
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Albumen |
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Creatinine |
mg/dl |
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Urea nitrogen |
mmol/l |
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Uric acid |
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total bilirubin |
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Rcreat.blood |
mg/dl |
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p E creat.urine |
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r B conc.index |
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o E daily diuresis |
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b R min. diuresis |
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a G filtering |
ml/min |
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And reabsorption |
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Urea extract |
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Sodium extract |
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Potassium excrement |
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total cholesterol |
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Triglycerides |
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Protein.frk.Alb. |
54.8-66.8 |
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Gamma |
11.8-17.8 |
Revealed excess of the norm indicators of creatinine, P creat.blood, urea nitrogen. A decrease in indicators of a G filtration, Belk.frk.Alb.
6. Complete blood count 09/02/11
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Index |
Meaning |
Norm |
Units |
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Leukocytes |
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red blood cells |
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Hemoglobin |
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Hematocrit |
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Average volume of erythrocytes |
femtoliter |
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platelets |
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Average hemoglobin concentration |
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Neutrophils |
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Monocytes |
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Lymphocytes |
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Basophils |
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7. General clinical analysis of urine 10\02\11
Protein was detected in the urine.
8. Immunoglobulins A, M, G 10/02/11
9. Complement 10/02/11
Within the normal range.
10. Tumor markers 10/02/11
Within the normal range.
11. Coagulogram 10/02/11
Within the normal range.
12. Ultrasound examination.
Liver enlarged, uneven contours, its echostructure is heterogeneous, increased echogenicity, multiple cysts from 10 to 40 mm in diameter are determined in the liver tissue. The main trunk of the portal vein is up to - 9 mm, the direction of blood flow is correct. Intrahepatic and extrahepatic bile ducts are not dilated.
Gallbladder and pancreas are not visualized due to the presence of a significant number of cysts in the abdominal cavity.
Spleen not enlarged, dimensions 96x40mm, uniform structure. The splenic vein is up to 4 mm in diameter, the direction of blood flow through it is correct.
kidneys enlarged, renal tissue is not visualized, the kidneys are represented by multiple cysts: on the left from 120 to 89 mm in diameter, on the right from 11 to 87 mm in diameter.
CONCLUSION: ultrasound - signs of multicystic changes in the echostructure of the liver and polycystic kidney disease.
13. Study of urine according to Nechiporenko 10\02\11
Final diagnosis:
Clinical diagnosis of the underlying disease:
Polycystic liver and kidney disease
Diagnosis of complications of the underlying disease:
Arterial hypertension II degree, stage 1, risk 2
Chronic renal failure I degree
Concomitant disease diagnosis:
urinary tract infection
Substantiation of the diagnosis
The diagnosis of polycystic liver and kidneys was made on the basis of:
1) Data of the anamnesis of the disease: the diagnosis of polycystic liver and kidneys was made in 1992 (the diagnosis was confirmed by the data of an objective examination, the data of instrumental research methods: ultrasound - hepatomegaly, cysts in the liver and kidneys).
2) Data of an objective examination: on palpation, the liver is of a dense consistency, bumpy, its size is increased.
3) The diagnosis is confirmed by the results of additional research methods:
· Ultrasound examination - signs of multicystic changes in the echostructure of the liver and polycystic kidney disease.
Diagnosis Arterial hypertension II degree, stage 1, risk 2
placed on the basis of:
Anamnesis data (single episodes of increased blood pressure since 1986, then a systematic increase in blood pressure from 2000 to 160/100 mmHg)
Complaints about fatigue, dizziness, general weakness, instability of blood pressure (130/90 mm Hg, with episodes of increase to 160/90 mm Hg).
Stage I there are no organic lesions of target organs and associated clinical conditions.
Risk 2 based on an increase in blood pressure to 160/100mmHg. and the absence of other risk factors.
Diagnosis of chronic renal failure of the 1st degree
placed on the basis of:
· Biochemical analysis of blood: excess of the norm of creatinine, urea nitrogen was found.
Revealed a decrease in glomerular filtration rate (up to 54 ml / min)
A urinary tract infection is diagnosed based on:
Laboratory data: general clinical analysis of urine - revealed proteinuria (0.25 g / l), urine analysis according to Nechiporenko - leukocyturia (10000)
Treatment
Given the dynamics of the course of the disease, as well as data from additional research methods, it is advisable to continue maintenance antihypertensive therapy.
1. Concor, 2.5 mg / day - a selective beta-1-blocker, is used for arterial hypertension. When used in therapeutic doses, it does not have internal sympathomimetic activity and clinically significant membrane stabilizing properties.
Forecast
Favorable. According to the survey, there is stabilization in the course of the disease.
It is necessary to carry out dynamic monitoring of blood pressure to assess the effectiveness of antihypertensive therapy.
However, if the patient's attitude towards her disease is inadequate, chronic renal failure may develop and the general condition of the patient may worsen.
Karaganda State Medical Academy 503 gr. film director Minbaev Seid-Akhmet Full name: Dosmagambetova Aues
Age: born in 1974 (28 years old)
Nationality: Kazakh
Place of work: not working
Profession: -------
Home address: Karazhal st. Dzhambula, d.7
Date and hour of admission: 11.11.02, 9.00
Preliminary diagnosis: chronic glomerulonephritis, mixed form, exacerbation phase.
Clinical diagnosis of chronic glomerulonephritis, mixed form, exacerbation phase, CRF 1B. Secondary anemia of mild art. mixed genesis.
Complaints: constant dull, pulling, pulsating 2-sided pain in the lumbar region, swelling of the face in the morning, severe swelling of the lower extremities, pastosity of the lumbar region, anterior abdominal wall and upper limbs; decrease in urine output (2-3 rubles / day, in small portions), nocturia (1-2 rubles), periodic increase in blood pressure to 180/100 mm. rt. Art., pressing pains in the region of the heart with irradiation to the left subscapular region, arising from nervous strain, walking up to 100 m, climbing 2 flights of stairs, increasing blood pressure, stopping with nitroglycerin; shortness of breath with difficulty breathing when walking fast. Cough with white or yellow frothy expectoration. General weakness, loss of appetite, nausea, headache, dizziness, aggravated in a stuffy room and during physical exertion. Stool retention.
Anamnesis morbi: Considers herself ill since the age of 7, when she first noticed swelling of the eyelids, face - mostly in the morning, nocturia. She went to the clinic at the place of residence. According to the patient, protein was present in the urine in an amount of less than 1 g/l. No treatment was given. The edematous syndrome was transient, without a tendency to progression. In 1997 during the third pregnancy at 6 months. swelling of the face and eyelids appeared, then - on the lower extremities, later - throughout the body; BP increased to 140/100 mm. rt. Art., with crises up to 180/100 mm. rt. Art. The pregnancy was terminated for medical reasons for 7 months. After that, for 3 years, BP remained at the same level, there were crises; edema periodically appeared on the face, eyelids, upper and lower extremities. According to the patient, in urine tests during this period, proteinuria (3.3 g/l) and an increase in ESR (46 mm/hour) were observed. Regarding these exacerbations, she received treatment in a hospital (glucocorticoids, cytostatics) without much effect.
In 2000 blood pressure dropped to 120/80 mm. rt. Art., the frequency of crises decreased. The edematous syndrome became less pronounced, however, constant dull, pulling, pulsating 2-sided pains in the lumbar region, aggravated by physical exertion, joined. There were also pressing pains in the region of the heart with irradiation to the left subscapular region, arising from nervous overexertion, walking up to 100 m or when climbing 2 flights of stairs, increasing blood pressure, stopping with nitroglycerin; shortness of breath with difficulty breathing when walking fast.
The real deterioration began in early November 2002. with the appearance of edema of the face, lower extremities, pastosity of the lumbar region, abdomen, upper extremities; increase in blood pressure up to 140/90 mm. rt. Art., with crises up to 180/100 mm. rt. Art.
Anamnesis vitae: Born in 1974 in the Karaganda region, Karazhal, the first child in the family. Went to school at the age of 7. Secondary education. In 1996 she worked as a kindergarten teacher. Living conditions in childhood and now are satisfactory. Married, has 1 child. Of the transferred diseases: in 2000. - acute bronchitis. Tuberculosis, Botkin's disease, veins. denies the disease. Allergological history: polyvalent allergy (to glucocorticoids, ascorbic acid, citrus fruits), took suprastin. Heredity: the younger sister has pyelonephritis. The mother has pyelonephritis, a wrinkled kidney. Gynecological history: menstruation since the age of 13, regular, moderate, painless. 3 pregnancies, 1 birth (1993), 1 medical abortion. indications (1994), 1 stillbirth (induction of labor for 7 months) - 1997. Drinks alcohol in moderation (30 ml 1-2 rubles / month). I do not smoke.
Status praesens: The patient's condition of moderate severity, due to edematous syndrome, arterial hypertension and dysuria. The position is active. The patient is conscious, adequate.
Body type asthenic. Height - 165 cm, weight - 46 kg. The patient is undernourished.
The skin is clean, pale, dry, elastic. Turgor is increased due to edema. Edema is located on the lower extremities (up to the level of the upper third of the thigh), moderately dense, warm, when pressed, a hole remains, which lasts 10-15 minutes. Pastosity of the lumbar region, anterior abdominal wall, and upper limbs is observed. Hair and nails are dull. Adipose tissue is not expressed. Visible mucous membranes are pale pink, clean. Peripheral lymph nodes are not enlarged.
The muscles are somewhat atrophic. On the part of the osteoarticular apparatus, there are no deformations. Movement in the joints in full.
Respiratory system.
Breathing through the nose is free. The chest is asthenic, symmetrical. Both halves evenly participate in the act of breathing. Type of breathing - chest. NPV=19'. The chest is resistant, painless on palpation. Voice trembling is weakened in the lower sections of both lungs.
With comparative percussion of the lower sections of both lungs - dullness of percussion sound (from the level of 5,6,7,8,9 ribs along Linea medioclavicularis, Linea axillaris anterior, Linea axillaris media, Linea axillaris posterior, Linea scapularis, respectively)
Topographic percussion:
| The height of the tops of the lungs: | Left | On right |
| front | 3.5cm | 3cm |
| Behind | spinous process of cervical vertebra VII | -“- |
| Krenig margin width | 5cm | 4cm |
| Inferior borders of the lungs: | ||
| Linea parasternalis | - | 5 m/rib |
| Linea medioclavicularis | - | 6 rib |
| Linea axillaris anterior | 7 rib | 7 rib |
| Linea axillaris media | 8 rib | 8 rib |
| Linea axillaris posterior | 9 rib | 9 rib |
| Linea scapularis | 10 rib | 10 rib |
| Linea paravertebralis | Spinous process XI gr.vertebra | -“- |
| Excursion of the lower edge of the lung: | ||
| Linea medioclavicularis | - | 2 cm |
| Linea axillaris media | 4 cm | 4cm |
| Linea scapularis | 4 cm | 4cm |
Auscultatory: over the entire surface of the lungs, breathing is harsh, weakened in the lower sections due to the accumulation of fluid in the pleural cavity. There are no side breath sounds.
The cardiovascular system.
Neck veins are not visible. There is no visible pulsation on the carotid, radial arteries. There is no visible pulsation in the epigastric region. Varicose veins along the veins are not observed.
The area of the heart is not visually changed. There is no pathological pulsation in the region of the heart. The apex beat could not be palpated (due to hydrothorax).
The pulse on the radial arteries is rhythmic, weak filling, pulse rate = 70 beats / min. There is no pulse deficit. BP = 140/90 mm Hg. Art.
The right border of relative cardiac dullness is located in the IV m / rib 1 cm to the right of the sternum. Upper limit - III m / rib along linea parasternalis sin. The left border could not be percussed against the background of dullness of the lung sound. The width of the vascular bundle in the II m/rib = 7 cm.
The right border of absolute cardiac dullness is 4 m / rib along the left edge of the sternum. Upper - in 4 m / rib along linea parasternalis sin. The left border of absolute cardiac dullness could not be percussed.
Auscultatory: Heart sounds are muffled, the rhythm is correct. There are no pathological heart murmurs.
The digestive system.
The tongue is dry, not coated. Carious teeth. There is a crown on the upper left incisor. There are deposits of tartar. The mucous membrane of the oral cavity is pale pink. Swallowing is free. Zev is calm. Tonsils are bean-shaped, not enlarged. The abdomen is rounded and symmetrical. Participates in the act of breathing. Pastosity of the anterior abdominal wall is observed. The peristalsis of the stomach and intestines is not visible. Venous collaterals are not developed.
Palpation: the abdomen is painless, there are no signs of divergence of the muscles of the anterior abdominal wall. There are no peritoneal symptoms.
The sigmoid colon is palpable in the left iliac region. There is no pain on palpation. Width - 2.5 cm. The consistency is soft-elastic. The caecum is palpable in the right iliac region. On palpation it rumbles. Width - 3.5 cm. The consistency is soft-elastic. The ascending colon is palpable in the right lateral region. Width - 2 cm. Elastic, painless, rumbling. Descending colon - in the left lateral region. Width - 2 cm. Transverse colon, stomach - not palpable. Liver - on the edge of the costal arch. Its edge is rounded, dense-elastic consistency, smooth. The spleen is not palpable.
Percussion: The dimensions of the liver according to Kurlov are 9 cm, 7 cm, 6 cm. The dimensions of the spleen are: length = 8 cm, diameter = 5 cm.
Auscultatory: the lower border of the stomach is 3 cm above the navel.
The chair is decorated, not regular, without pathological impurities. The act of defecation is painless.
urinary system.
Visually, the area of the kidneys is edematous, symmetrical. The kidneys are not palpable. The symptom of effleurage is positive on both sides. Urination is free, painless, 2-3 rubles / day, in small portions. Nocturia (up to 2 p.). Urine is light yellow, cloudy.
Neuro-endocrine system.
The patient is conscious, adequate.
There is no palpation pain along the nerve fibers and roots. Movement in the limbs in full. The patient in the Romberg position is stable, the finger-nose test is negative. Muscle tone is normal. Vision, smell, hearing are not impaired.
The thyroid gland is not palpable. There are no eye symptoms. Hair type - female. Adipose tissue is not expressed.
Mammary glands b/b on palpation, there are no pathological formations.
Graphological structure
| Symptoms, signs, treatment | 1981-1997 | March 1997 | 1997-2000 | August 2000 | 2000-2002 | November 2002 |
| swelling of the face hydrothorax | - | - | ||||
| Nausea, headache | 140(crises-180) | ++ | + | 140(crises-180) |
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| Dull 2-sided pain in the lumbar region | - | - | - | ++ | + | ++ |
| Oliguria Nocturia (1-2r/day) | + | 1-2r / d in small portions. | 3-4r / d in small portions. | + | 2-3r / d in small portions. |
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| Pain in the region hearts treated with nitroglycerin | - | - | - | |||
| Polyvalent Allergy | - | - | - | + | + | + |
| Enam - to lower blood pressure Methylprednisolone Chlorambucil Azathioprine | 150 mg/day | 75 mg/day. (6 months) |
In a supervised patient, the following clinical syndromes can be distinguished:
Edematous, expressed by swelling of the face, lower extremities, pastosity of the lumbar region, anterior abdominal wall and upper extremities, hydrothorax;
Arterial hypertension (BP - 140/90 mm Hg, history of crisis up to 180/100 mm Hg);
Dysuric (decreased urine output (2-3 rubles / day, in small portions), nocturia (up to 2 rubles), cloudy urine);
Painful, characterized by constant dull, pulling, pulsating 2-sided pain in the lumbar region;
Leading in the clinic of this patient is edematous syndrome, which determines the severity of the condition and was the reason for hospitalization.
Differential diagnosis of the 1st order.
With the leading edematous syndrome, the following diseases occur:
Myxedema
Circulatory insufficiency in a large circle due to stenosis of the right atrioventricular orifice
Chronic glomerulonephritis
Myxedema. With this disease, edematous syndrome is expressed by swelling of the face, especially in the eyes, lips, nose, tongue, as well as the neck, supraclavicular spaces, limbs; edema is dense, no fossa is formed when pressed, swelling of the mucosa is characteristic, while in the supervised patient, edema is located on the face, lower extremities, pastosity in the lumbar region, on the anterior abdominal wall and upper extremities; edema is moderately dense, a fossa is formed when pressed, there is no mucosal edema.
Pain syndrome, characterized by low back pain present in the supervised patient, can also be observed with myxedema.
Dysuric syndrome (decreased urine output (2-3 times a day, in small portions), nocturia (up to 2 times), cloudy urine), which is present in a supervised patient, is not typical for patients with myxedema.
Unlike myxedema, in which arterial hypotension is observed, the supervised patient has arterial hypertension syndrome (BP 140/90 mm Hg).
Cardiac syndrome in myxedema does not correspond to that of the supervised patient.
Myxedema is characterized by hypothermia (up to 34 0 C), which is uncharacteristic for the supervised patient.
In addition, with myxedema, there are neurological symptoms: voice change, hearing loss, lack of taste sensations, forgetfulness, drowsiness, slow speech, persistent headaches, neuralgia, tinnitus, a feeling of "goosebumps", which is uncharacteristic for the supervised patient.
All of the above makes it possible to exclude the diagnosis of myxedema at this stage of the differential diagnosis.
NK in a large circle due to tricuspid insufficiency. The edematous syndrome in NK in a large circle is manifested by edema on the lower extremities, feet, especially pronounced at the ankles; edema is cold, dense, the skin over the edema is thinned, bluish in color, when pressed, a hole remains, which disappears after 1-2 minutes; revealed ascites, hydrothorax. These manifestations are uncharacteristic for the supervised patient, because in our case, the edemas are warm, the skin over them is pale, the pit remains for 10-15 minutes when pressed.
With NK in a large circle, a dysuric syndrome may appear (due to a decrease in renal blood flow), manifested by oliguria, which is present in the supervised patient, however, nocturia observed in our patient is not typical for NK.
The pain syndrome present in the supervised patient (constant dull, pulling, pulsating 2-sided pain in the lumbar region) is not typical for NK.
Arterial hypertension in NK due to tricuspid insufficiency is accompanied by a predominant increase in diastolic pressure and, as a result, a decrease in pulse pressure, while in a supervised patient, blood pressure is 140/90 mm Hg, pulse - 50 mm Hg.
With NC due to tricuspid insufficiency, a cardialgic syndrome can be observed in the form of pressing pains in the region of the heart, which is present in the supervised patient.
Hepatolienal syndrome is a frequent and characteristic companion of NK in a large circle. The supervised patient has no enlargement of the liver and spleen (The dimensions of the liver according to Kurlov are 9 cm, 7 cm, 6 cm. The dimensions of the spleen are: length = 8 cm, diameter = 5 cm).
In addition, given that tricuspid insufficiency often develops with rheumatic heart disease, the history of the disease (pain in large joints after suffering a cold) will be characteristic. The supervised patient does not notice such manifestations.
Given the differences in the clinical picture of the disease under consideration and the pathological condition in the supervised patient, the diagnosis of NK in a large circle due to tricuspid insufficiency can be excluded.
Amyloidosis of the kidneys. The edematous syndrome in the supervised patient corresponds to that in amyloidosis, with the exception of a slight displacement of edema, which is not observed in our patient.
Pain syndrome, expressed in a supervised patient in dull, pulling, pulsating 2-sided pain in the lumbar region, is also characteristic of amyloidosis.
The dysuric syndrome present in the supervised patient (decreased urine output (2-3 times a day, in small portions), nocturia (up to 2 times), cloudy urine) can be observed with amyloidosis.
The syndrome of arterial hypertension present in the supervised patient (BP 140/90 mm Hg) is uncharacteristic of amyloidosis.
Cardialgic syndrome, which is expressed in the supervised patient by pressing pains in the region of the heart with irradiation to the left subscapular region, arising from nervous strain, walking up to 100 m, climbing 2 flights of stairs, increased blood pressure, which is stopped by nitroglycerin, rarely accompanies amyloidosis.
The hepatolienal syndrome characteristic of amyloidosis is absent in the supervised patient (Liver dimensions according to Kurlov - 9 cm, 7 cm, 6 cm. Spleen dimensions: length = 8 cm, diameter = 5 cm).
Dyspeptic syndrome, in amyloidosis, manifested by diarrhea, bloating, feeling of heaviness in the epigastrium after eating, is not observed in the supervised patient.
Guided only by clinical data, it is not possible to exclude the diagnosis of amyloidosis in a supervised patient without laboratory tests.
Chronic glomerulonephritis. The edematous syndrome in the supervised patient is manifested by facial edema, pronounced edema of the lower extremities, pastosity of the lumbar region, anterior abdominal wall and upper extremities. The same picture is observed in chronic glomerulonephritis.
The dysuric syndrome present in the supervised patient (decreased urine output (2-3 times a day, in small portions), nocturia (up to 2 times), cloudy urine) is characteristic of chronic glomerulonephritis.
Hypertension syndrome, present in a supervised patient (BP 140/90 mm Hg), often accompanies chronic glomerulonephritis.
Pain syndrome, expressed in a supervised patient in dull, pulling, pulsating 2-sided pain in the lumbar region, is also characteristic of chronic glomerulonephritis.
Cardialgic syndrome, which is expressed in the supervised patient by pressing pains in the region of the heart with irradiation to the left subscapular region, arising from nervous overexertion, walking up to 100 m, climbing 2 flights of stairs, increased blood pressure, which is stopped by nitroglycerin, may be present in patients with chronic glomerulonephritis.
Analyzing the above data, it is not possible to exclude chronic glomerulonephritis in the supervised patient.
Chronic glomerulonephritis seems to be the most probable of the listed diseases in the supervised patient (due to the similarity of the clinical picture).
Justification of the preliminary diagnosis.
The patient is exposed to a preliminary diagnosis: chronic glomerulonephritis, mixed form, exacerbation phase.
Glomerulonephritis is exposed on the basis of edematous syndrome, which is expressed by swelling of the face (more in the morning), lower extremities, pastosity of the lumbar region, anterior abdominal wall and upper extremities, hydrothorax; dysuric syndrome (decreased urine output (2-3 rubles / day, in small portions), nocturia (up to 2 rubles), cloudy urine); pain syndrome, characterized by constant dull, pulling, pulsating 2-sided pain in the lumbar region; and also taking into account the data of the differential diagnosis of the 1st order.
Aggravation phase: set on the basis of anamnesis data: at the beginning of November 2002. swelling of the face, lower extremities, pastosity of the lumbar region, abdomen, upper extremities appeared; increased blood pressure to 140/90 mm. rt. Art., with crises up to 180/100 mm. rt. Art.
Examination plan:
3. Ultrasound of the kidneys
4. Plain chest x-ray
5. Urinalysis according to Zimnitsky
6. Urinalysis according to Nechiporenko
7. Blood HD (creatinine, urea, total protein, cholesterol)
9. Examination of the fundus
10. Test with methylene blue
Laboratory and instrumental data.
Ultrasound of the kidneys. (11.11.02). Dimensions: left - 4.5x10.5 cm, right - 4.5x10.3 cm. The contours are clear, the parenchyma is homogeneous, edematous. CHLS is deformed. The mobility of the kidneys is preserved.
Conclusion: CHLS deformation in both kidneys, signs of edema of the kidney parenchyma.
Overview R-gram of the organs of the chest cavity. Lung fields of normal transparency. The sinuses are darkened, not differentiated. From the level of the 5th rib along the midclavicular line, a horizontal darkening (fluid level) is determined.
Examination of the fundus. There is a narrowing and tortuosity of the retinal vessels, swelling of the nipple of the optic nerve.
Differential diagnosis of the 2nd order.
After the 1st order differential diagnosis, due to the lack of laboratory data, we could not exclude the following diseases:
Renal amyloidosis, nephrotic stage
Chronic glomerulonephritis
Amyloidosis.
With amyloidosis, a detailed picture of nephrotic syndrome is observed, which is laboratory manifested by oliguria, increased urine density, massive proteinuria, severe hypoproteinemia, and hypercholesterolemia. In the supervised patient, urine density is normal, hypoproteinemia is insignificant (60 g/l), microhematuria (4-6-7 in p/sp) is observed, which is uncharacteristic of amyloidosis.
In OAM with amyloidosis in the sediment, the content of formed elements is poor, granular and hyaline ones predominate from the cylinders, pyuria is characteristic. The supervised patient has microhematuria, cylindruria (1-2 in p / sp, hyal.); no pyuria.
In the KLA with amyloidosis - a decrease in hemoglobin, leukocytosis, a sharp increase in ESR, while the supervised patient has leukopenia (3.2x10 9 / l), ESR is not sharply increased (21 mm / h), hemoglobin is reduced (108 g / l).
Ultrasound examination in amyloidosis with the development of renal failure and azotemia often shows enlarged kidneys, in advanced cases - wrinkled. In the supervised patient, the size of the kidneys was not significantly changed, there was a slight deformation of the CHLS, signs of parenchymal edema were observed.
Amyloidosis is not characterized by changes in the fundus observed in the supervised patient (narrowing and tortuosity of the arteries, swelling of the optic nerve papilla).
A test with methylene blue is pathognomonic in amyloidosis: amyloid absorbs methylene blue injected s / c (1% -1 ml), as a result of which the latter is not excreted and does not stain the urine blue. In a supervised patient, during a test with methylene blue, its excretion in the urine was observed, especially with the first two portions.
Given the data of the differential diagnosis of the 1st and 2nd order, we can completely exclude amyloidosis.
Chronic glomerulonephritis
In the KLA with CGN, a decrease in hemoglobin, erythrocytes and a color index, which is observed in a supervised patient (hemoglobin - 108 g/l, erythrocytes 4.0x10 12 /l, color index 0.82).
In OAM with a mixed form of CGN - moderately severe hematuria, significant albuminuria, cylindruria, a decrease in the specific gravity of urine (in moderate severity, as well as in the hypertensive form, an increase is possible). The supervised patient has microhematuria (6-7 p/s), massive proteinuria (3.05 g/l), cylindruria (hyal. 1-2), specific gravity is normal (1008).
Blood creatinine in CGN is normal or elevated, depending on the stage of CRF. In the supervised patient, blood creatinine is 0.139 mmol/l, which is typical for stage IV CRF (according to Ryabov, 2000).
With the development of chronic renal failure, an increase in blood urea is observed. In the supervised patient, blood urea is also increased (9.0 mmol/l).
In chronic glomerulonephritis, the Reberg-Tareev test: a decrease in glomerular filtration (depending on the severity of CRF), which is typical for the supervised patient (Reberg-Tareev test - 65 ml / min.).
Urinalysis according to Zimnitsky: CGN is characterized by the predominance of nocturnal diuresis over daytime, hypostenuria; the same changes are observed in the supervised patient (against the background of the treatment: I - 450 ml, density - 1012, II - 550 ml, density - 1010).
Nechiporenko test: CGN is characterized by a predominance of erythrocytes, or their equal ratio with leukocytes. In a supervised patient, leukocytes / erythrocytes = 1/1.
With CGN on ultrasound of the kidneys, a slight deformation of the CHLS is noted, signs of edema of the kidney parenchyma may be observed, which is typical for the supervised patient.
With CGN, the development of hydrothorax and hydropericardium is possible. On the survey radiography of the supervised patient, the sinuses are darkened on the left and right, and horizontal darkening (fluid level) is determined from the level of the 5th rib.
When examining the fundus of the eye in patients with CGN, narrowing and tortuosity of the arteries, single or multiple hemorrhages, and swelling of the optic nerve papilla are noted. Of these symptoms, the supervised patient has narrowing and tortuosity of the arteries, swelling of the optic nerve papilla.
Based on the differential diagnosis of the 1st and 2nd order in the supervised patient, we obtained the most similar clinical and laboratory data with chronic glomerulonephritis.
Substantiation of the clinical diagnosis.
The patient is given a clinical diagnosis: chronic glomerulonephritis, mixed form, exacerbation phase, CRF 1B. Secondary anemia of mild art. mixed genesis.
Glomerulonephritis is exposed on the basis of edematous syndrome, which is expressed by swelling of the face (more in the morning), lower extremities, pastosity of the lumbar region, anterior abdominal wall and upper extremities, hydrothorax; dysuric syndrome (decreased urine output (2-3 rubles / day, in small portions), nocturia (up to 2 rubles), cloudy urine); pain syndrome, characterized by constant dull, pulling, pulsating 2-sided pain in the lumbar region; in OAM: microhematuria (6-7 in p/s), massive proteinuria (3.05 g/l), leukocyturia (5-6 in p/s), cylindruria (hyal. 4-5); Reberg-Tareev test: decrease in glomerular filtration - 65 ml/min. Urinalysis according to Zimnitsky: I - 450 ml, density - 1012, II - 550 ml, density - 1010. Nocturia, hypostenuria. Nechiporenko test: the same ratio of erythrocytes to leukocytes: leukocytes / erythrocytes = 1/1; on ultrasound of the kidneys, there is a slight deformation of the CHLS, signs of edema of the kidney parenchyma; and also taking into account the data of the differential diagnosis of the 1st and 2nd order.
Chronic is exhibited on the basis of anamnesis data: she considers herself ill from the age of 7, when she first noticed swelling of the eyelids, face, nocturia. According to the patient, protein was present in the urine in an amount of less than 1 g/l. In 1997 during the third pregnancy at 6 months. swelling of the face and eyelids appeared, then - on the lower extremities, later - throughout the body; after that, edema appeared periodically on the face, eyelids, upper and lower extremities for 3 years. According to the patient, in urine tests during this period, proteinuria (3.3 g/l) and an increase in ESR (46 mm/hour) were observed.
Mixed form: exhibited on the basis of a combination of signs of nephrotic (edematous, pain, dysuric syndromes) form and arterial hypertension syndrome (BP - 140/90 mm Hg, history of crisis up to 180/100 mm Hg).
ECG shows sinus rhythm, medium voltage, left ventricular hypertrophy. In the study of the fundus - narrowing and tortuosity of the arteries, swelling of the nipple of the optic nerve.
The exacerbation phase is set on the basis of anamnesis data: in early November 2002. swelling of the face, lower extremities, pastosity of the lumbar region, abdomen, upper extremities appeared; increased blood pressure to 140/90 mm. rt. Art., with crises up to 180/100 mm. rt. Art.
CRF 1B is set on the basis of the patient's complaints of edema, decreased diuresis, weakness, headache, loss of appetite, and nausea. Data of the anamnesis of the disease about the duration and severity of the process. From laboratory data: Blood creatinine 0.139 mmol/l. Blood urea: 9 mmol/l. Reberg-Tareev test: decrease in glomerular filtration - 65 ml/min.
Secondary anemia of mild art. of mixed genesis is exhibited on the basis of complaints of sick weakness, headache, dizziness, aggravated in a stuffy room. History of long-term chronic kidney disease. Objectively: pale skin. As well as laboratory data: In the KLA: hemoglobin 108 - g / l, erythrocytes 4.0x10 12 / l, color index 0.82.
Etiology
Most often, chronic glomerulonephritis (CG) is a consequence of acute glomerulonephritis. Along with this, the development of primary chronic glomerulonephritis without a previous acute period is recognized. The main etiological factors of chronic glomerulonephritis are the same as in acute glomerulonephritis. Very often, the cause of the disease cannot be found. The role of genetic predisposition to the development of chronic glomerulonephritis is also widely discussed.
Pathogenesis
The mechanism of development of chronic glomerulonephritis is based on an immune inflammatory process, in the development of which the deposition of antibodies and complement fragments, the formation of a complement membrane-damaging complex, blood coagulation factors, leukotrienes, cytokines, neutrophils, platelets, macrophages, T-lymphocytes take part. IA Rakityanskaya (2000) emphasizes the great role of the genetic inferiority of the T-cell link of immunity in the development of chronic glomerulonephritis. At present, the doctrine of the trophic role of lymphocytes has been formed, which is performed mainly by early undifferentiated lymphoid precursors with a marker enzyme - terminal deoxynucleotidyl transferase (TdT cells). It has been established that these cells are able to participate in the processes of repair and physiological regeneration of glomeruli. It is assumed that TdT cells slow down the processes of sclerosis, support the regeneration of the basement membrane of glomerular capillaries and preserve its antigenic composition. With insufficient intake of these cells into the kidney, the physiological repair of the basement membrane of the glomerular capillaries is disrupted.
Detailed studies allowed I. A. Rakityanskaya (2000) to formulate a hypothesis of the origin of chronic glomerulonephritis, according to which, due to a genetic predisposition, there is an insufficient supply of early lymphoid (trophic) elements to the kidney, which disrupts the normal physiological repair of individual parts of the nephron and contributes to the formation of an inflammatory infiltration in the kidneys with the participation of T-lymphocytes, mononuclear cells, the release of a large amount of cytokines (IL-1, tumor necrosis factor, IL-4, IL-6, IL-10, etc.), which enhance the proliferation of glomerular cells, activate apoptosis, cause damage to all structures of the nephron, primarily the basement membrane, followed by the formation of immune complexes in situ.
Subsequently, the release of basement membrane antigens into the blood and the formation of immune complexes in circulation are observed, followed by deposition on the basement membrane and activation of the complement system, neutrophils, and macrophages.
Subsequently, against the background of attenuation of the proliferation of glomerular cells, activation of fibroblasts and the development of fibrosis are observed.
Non-immune mechanisms of progression are also of great importance, which include:
Development of progressive renal fibrosis;
Hemodynamic factors;
metabolic mechanisms;
coagulation mechanisms;
Tubulointerstitial sclerosis.
Development of progressive fibrosis in the kidneys
The immune-inflammatory process in the kidneys is accompanied by reparative changes, the outcomes of which are different: complete restoration of the glomerular structure is possible (usually under the influence of treatment or less often spontaneous) or, in an unfavorable course, the development of progressive fibrosis, which is the basis of chronic renal failure.
Progressive renal fibrosis is caused by hyperfunctioning of glomerular cells and blood cells that infiltrate the glomeruli of the kidneys, which is accompanied by excessive accumulation of the connective matrix and, at the same time, its insufficient utilization.
Role of hemodynamic factors
Hemodynamic disorders (systemic and arterial hypertension) are the most important factors in the progression of chronic glomerulonephritis.
Chronic progressive glomerulonephritis is characterized by the loss of functioning renal mass, which leads to compensatory hypertrophy and hyperfunction of the remaining renal
glomeruli. An increase in the function of the remaining glomeruli is always accompanied by a violation of intrarenal hemodynamics - intraglomerular hypertension and hyperfiltration, which ensures increased perfusion of the surviving nephrons. Activation of the renin-angiotensin-II system also plays an important role, which leads to spasm of efferent arterioles and increased pressure in the glomeruli. Increased intraglomerular pressure promotes mesangial cell proliferation and overproduction of the mesangial matrix.
The significance of intraglomerular hypertension in the progression of kidney damage is as follows. With an increase in intraglomerular pressure, the permeability of the basement membrane of the glomerular capillaries sharply increases, which contributes to the penetration of protein, lipids and other plasma components into the mesangium. These substances, being deposited in the mesangium, stimulate the proliferation of mesangial cells and hyperproduction of the mesangial matrix, which leads to sclerosis of the glomeruli.
Role of metabolic factors
Lipid shifts are of paramount importance among metabolic disorders in the progression of chronic glomerulonephritis. They are most commonly seen in individuals with nephrotic syndrome, but also occur in glomerulonephritis without nephrotic syndrome.
Changes in lipid metabolism most often consist in an increase in blood levels of cholesterol, triglycerides, low-density lipoproteins, non-esterified fatty acids, and an increase in the atherogenic coefficient. Dyslipidemia leads to the deposition of lipids in the kidneys. Lipid metabolism disorders are accompanied by a nephrotoxic effect, and when lipids are deposited in the renal structures, there is a simultaneous increase in the mesangial matrix, which indicates the fibrosogenic effect of lipid metabolism disorders. Of particular importance in this respect is the deposition of low-density lipoproteins in the kidneys. They can be captured by mesangiocytes, undergo oxidation in them, and oxidized forms of low density lipoproteins have a pronounced damaging effect on the kidneys.
Role of coagulation mechanisms
The most important mechanism for the progression of chronic glomerulonephritis is local intravascular coagulation of blood with the formation of microthrombi in the glomerular capillaries and the deposition of fibrin in them. The leading role in the development of intravascular hemocoagulation in the kidneys is played by damage to the endothelium by immune complexes, cytokines, inflammatory mediators, various endotoxins, and activated complement. This leads to a loss of thromboresistance by the endothelium, an increase in the production of procoagulant factors by the endothelium (von Willebrand factor, tissue thromboplastin, inhibitors of plasminogen activators) and a decrease in the synthesis of anticoagulant factors (nitrogen oxide and prostacyclin - vasodilators and antiaggregants).
The role of tubulointerstitial sclerosis
It is believed that the epithelial cells of the renal tubules play a central role in the development of tubulointerstitial damage and sclerosis. They are activated and produce substances that contribute to damage to the renal interstitium and the development of fibrosis: macrophage chemotactic protein-1, angiotensin-II, endothelium, basic fibroblast growth factor, transforming growth factor p. Activation of renal tubular epithelial cells is mediated by cytokine production by cells involved in inflammation as well as protein reabsorption in the renal tubules. Persistent proteinuria has a toxic, damaging effect on the interstitium of the kidney.
The listed mechanisms of progression contribute to the development of a long-term inflammatory process, which flows in waves (with periods of exacerbations and remissions), which ultimately leads to sclerosis, hyalinosis, desolation of the glomeruli, and the development of chronic renal failure.
Treatment proposed in the literature.
Treatment program for chronic glomerulonephritis.
2. Etiological treatment.
3. Medical nutrition.
4. Pathogenetic treatment (glucocorticoids, cytostatics, NSAIDs, anticoagulants and antiaggregants).
5. Symptomatic treatment.
6. Phytotherapy.
7. Sanatorium treatment.
In chronic glomerulonephritis, hypothermia, excessive physical stress, psycho-emotional stress should be avoided. The patient is forbidden to work at night, in hot and cold shops, business trips are not recommended. It is advisable to rest for 1-1.5 hours. If colds appear, it is necessary to be released from work, bed rest at home, with exacerbation of chronic tonsillitis or other foci of nasopharyngeal infection - treatment with penicillin, erythromycin, when discharged to work, a control urine test should be done .
Patients with exacerbation of chronic glomerulonephritis should be hospitalized in the nephrological or therapeutic department with bed rest until the general condition improves, extrarenal symptoms disappear, and urine analysis improves.
Etiological treatment
Etiological treatment is possible only in a small number of patients. Etiological treatment consists in the use of antibiotics (primarily penicillin and its semi-synthetic drugs) and thorough sanitation of all foci of infection.
In most cases of chronic glomerulonephritis, etiological treatment does not play a significant role or is impossible.
Health food
With a mixed form of chronic glomerulonephritis, diet No. 7 is prescribed, taking into account the diet for nephrotic and hypertensive forms, i.e. the presence of arterial hypertension and edema and the associated need to limit the intake of salt and water.
In the hypertensive form of chronic glomerulonephritis, it is recommended to limit salt to 6-8 g per day. This is a predominantly dairy-vegetarian diet with the inclusion of potatoes, a large number of vegetables, fruits, and lean meat and fish are also allowed. With persistent and persistent arterial hypertension, fasting days are carried out (fruit-rice, potato, vegetable, etc.), which helps to reduce blood pressure.
With very persistent arterial hypertension, the amount of table salt can be reduced to 3-5 g per day. The complete exclusion of salt from the diet for a long time can lead to electrolyte disturbances (ripochloremia, hyponatremia) and cause deterioration of kidney function.
In the nephrotic form of chronic glomerulonephritis, the amount of salt is limited to 3 g per day, taking into account its content in food, special “kidney” bread is used without adding salt. The amount of proteins in the diet, according to modern concepts, should be 1 g per 1 kg of the patient's body weight. The amount of liquid consumed during the day, taking into account liquid meals, should not exceed 600-800 ml and depends on the amount of daily diuresis and the dynamics of edematous syndrome. In fact, the amount of fluid drunk during the day should not exceed the daily diuresis by more than 200-300 ml, taking into account the physiological loss of fluid through the respiratory system, skin, and gastrointestinal tract. The diet necessarily includes diuretic watermelon, pumpkin, melon, grapes, bananas.
Pathogenetic treatment
Pathogenetic treatment of chronic glomerulonephritis affects the main mechanism of the development of the disease - an autoimmune inflammatory process.
The mechanism of action of pathogenetic therapy means: pathogenetic treatment affects the damage to the basement membrane and mesangium by immune complexes and antibodies; on the release of inflammatory mediators and the activity of the kinin system; to changes in intravascular coagulation; on the function of phagocytosis.
Treatment with cytostatics
The therapeutic effect of non-hormonal immunosuppressants (cytostatics) is due to their immunosuppressive, anti-inflammatory and antiproliferative effects. The most important aspect of the action of cytostatics is the suppression of autoimmune inflammation.
The indication for treatment with cytostatics is a mixed form of chronic glomerulonephritis (a combination of nephrotic syndrome and severe arterial hypertension).
Cytostatics are effective in focal segmental glomerulonephritis (glomerulosclerosis begins exclusively in juxtamedullary nephrons, individual glomeruli are involved in the process - focal changes, individual segments of the vascular bundle are sclerosed in them - segmental changes) Positive results were obtained even with fibroplastic glomerulonephritis.
The following cytostatics are used: antimetabolites (imuran, azathioprine, 6-mercaptopurine), alkylating agents (chlorbutine, leukeran, cyclophosphamide), cyclosporine (sandimmune).
Azathioprine (Imuran) and mercaptopurine are prescribed 2-3 mg per 1 kg of patient weight (150-200 mg per day), cyclophosphamide-f 1.5-2 mg/kg (100-150 mg per day), leukeran - 0.2 mg each /kg for 4-8-10 weeks. In the future, maintenance therapy at a daily dose equal to "/2 or "/z of this dose is recommended for 6-12 months.
In the treatment of cytostatics, severe complications are possible: anemia, leukopenia, thrombocytopenia, agranulocytosis, pancytopenia, hemorrhagic cystitis, azoospermia.
Treatment with anticoagulants and antiplatelet agents
Heparin reduces intravascular coagulation, platelet aggregation, has anti-inflammatory, antidepressant and diuretic effects, and can lower blood pressure.
Indications for the appointment of heparin:
Nephrotic form of chronic glomerulonephritis (with glomerular filtration rate of at least 35 ml / min) in the absence of the effect of treatment with glucocorticoids and cytostatics;
Chronic glomerulonephritis with severe edema, moderate arterial hypertension (BP not higher than 160/90 mm Hg), as well as with incipient renal failure;
Heparin is injected under the skin of the abdomen at 5000-10,000 IU 4 times a day for 6-8 weeks, followed by a gradual dose reduction and drug withdrawal. Treatment with heparin is carried out under the control of blood clotting time (one should not strive to increase it by more than 2 times compared to the initial value).
After treatment with heparin, indirect anticoagulants (phenylin, pelentan, etc.) can be used at a dose that maintains the prothrombin index at 50-60% for 1-2 months. Antiplatelet agents are used much more often, most often courants in a daily dose of 225-400 mg (it is possible to increase the daily dose to 600-800 mg), the duration of the course is 8-12 months or more. Curantyl can be prescribed for almost all forms of chronic glomerulonephritis, except for hematuric.
Contraindications to the appointment of anticoagulants and antiplatelet agents are hemorrhagic diathesis, peptic ulcer of the stomach and duodenum. Heparin is contraindicated when glomerular filtration rate is less than 35 ml/min.
Passive immunotherapy with anti-HLA antibodies
Passive immunotherapy with anti-HLA antibodies also has an immunosuppressive effect, while the number of B-lymphocytes and the production of antirenal autoantibodies decrease, urine output increases significantly, proteinuria decreases, and an immunoregulatory effect is also manifested.
Indications for passive immunotherapy with anti-H1A antibodies are the nephrotic form of chronic glomerulonephritis and nephrotic syndrome of another origin. As a therapeutic drug containing anti-H1A antibodies, serum obtained from women whose sensitization to HLA antigens was the result of previous pregnancies that are incompatible according to the HLA system is used. The course of treatment consists of 2-4 intravenous injections of plasma, each with a volume of not more than 225 ml.
Symptomatic treatment
Treatment of arterial pshertensia
Arterial hypertension significantly worsens the prognosis in chronic glomerulonephritis, contributing to the progression of sclerotic changes and accelerating the onset of CRF. A persistent increase in systolic (160 mm Hg and above) and especially diastolic blood pressure (95 mm Hg and above) requires antihypertensive therapy.
In patients with CGN, a mixed nature of arterial hypertension is noted, i.e. in addition to the low-renin volume-dependent mechanism, a significant increase in peripheral resistance also takes part in the increase in blood pressure, therefore, in the treatment of renal arterial hypertension, both saluretics and sympatholytics and calcium antagonists are used.
Initially, diuretics are prescribed: hypothiazide (initial dose - 25 mg per day, maximum daily dose - 150 mg), brinaldix (from 20 to 60 mg per day), chlorthalidone or hygroton (from 25 to 100 mg per day), renez ( 0.5-2 mg per day).
Doses of saluretics (diuretics) depend on the severity of arterial hypertension and the dynamics of the decrease in blood pressure with increasing doses.
Together with saluretics, potassium-sparing diuretics are also used - aldosterone antagonists: veroshpiron (aldactone) in a daily dose of 50-100 mg (usually in two doses due to the short duration of action) or triamterene in the same dose.
When treating with saluretics, one should be aware of the possibility of developing hypokalemia, hypochloremia, hyperuricemia
In the absence of the effect of saluretics, it is advisable to add B-blockers to them, which reduce the minute volume of blood and renin production (it may increase during treatment with saluretics). Recommended propranolol (anaprilin, inderal, obzidan) 10-20 mg 3 times a day, trazikor 10-20 mg per day, whisken 10-15 mg per day.
If there is no effect, after 1-2 weeks, the doses of β-blockers are increased: anaprilin - up to 160-240 mg per day, trazicor - up to 120-160 mg per day, visken - up to 30-40 mg per day. After reaching the hypotensive effect, the dose is gradually reduced.
With the development of renal failure, it is advisable to combine treatment with powerful saluretics with the administration of dopegyt (methyldof), a sympatholytic of predominantly central action. The drug reduces peripheral resistance, cardiac output, reduces the activity of the renin-angiotensin-aldosterone system, at the same time it increases renal blood flow and glomerular filtration. The initial dose of the drug is 500 mg per day (1 tablet of 0.025 g 2 times a day), in the absence of effect, the dose is gradually increased to 750-1500 mg per day.
Instead of dopegyt, clonidine or hemiton can be used in combination with diuretics. Clonidine is a sympatholytic of central action, reduces cardiac output and peripheral resistance; unlike dopegit does not affect renal hemodynamics. The initial dose of the drug is 0.15 mg per day, the maximum daily dose is 2.4 mg. If necessary, stop taking the drug, the dose is reduced gradually, within 7-10 days, since a withdrawal syndrome with a sharp increase in blood pressure is possible.
For the treatment of arterial hypertension in patients with CGN, the sympatholytic drug reserpine can be used in combination with diuretics. The drug reduces peripheral resistance without affecting renal hemodynamics.
In arterial hypertension due to CRF, the postsynaptic sc-blocker prazosin is also effective, especially in combination with diuretics - thiazides. The initial dose of prazosin is 1 mg per day, the maximum is 10-20 mg per day.
Direct vasodilating drugs used in renal arterial hypertension include hydralase (it increases renal blood flow and glomerular filtration, is indicated for renal failure). In recent years, calcium antagonists have been used, with verapamil being preferred because it improves blood circulation in the kidneys. The drug is prescribed in a dose of 0.02-0.04 g 3-4 times a day.
With persistent arterial hypertension, an ACE inhibitor, capoten (captopril), can be recommended in a daily dose of 25 to 100 mg.
Stages of treatment of arterial hypertension in chronic glomerulonephritis:
1. Restriction of sodium and the appointment of diuretics (hypothiazid, with renal failure - furosemide); if necessary, use potassium-sparing diuretics.
2. In combination with diuretics, the following are prescribed: -blockers (obzidan, inderal, etc.); dopegit (for renal failure), hemiton or reserpine.
3. Hydralazine or apressin (in combination with diuretics or O-blockers); prazosin.
It should be emphasized that sympatholytics (dopegyt, clonidine, reserpine, octadine) retain sodium and water and should be combined with diuretics. In severe arterial hypertension, it is advisable to connect ACE inhibitors to the treatment.
With the development of a hypertensive crisis, treatment is performed by intravenous administration of sodium nitroprusside, diazoxide, dibazol, clonidine, rausedil, furosemide
Treatment of edematous syndrome
Edema in chronic glomerulonephritis is associated with hypoalbuminemia and a sharp decrease in the ability of the kidneys to excrete sodium and water.
With severe edema, fasting days are recommended: sugar (150g per 1-2 cups of boiled water with lemon in 4-5 doses), vegetable (1.5kg of vegetables in the form of salad without salt), watermelon (300g 5r / day), fruit or berry (250g 6 r/day)
Phytotherapy:
Infusion of birch buds.
A decoction of lingonberry leaves.
Infusion of black elderberry flowers.
Infusion of cornflower flowers.
Infusion of herb knotweed (knotweed).
Decoction of burdock root.
Infusion of kidney tea leaves (orthosiphon).
As a rule, treatment with medicinal plants lasts 1-2 months or longer.
If the edema does not disappear, diuretics are prescribed that do not have a nephrotoxic effect: hypothiazide 50-100 mg per day; furosemide 40-80 mg per day; uregit 50-100 mg per day; triampur-compositum (combination of hypothiazide and triamterene) 1 tab. 2-3 r / d; veroshpiron 75-200 mg per day. Diuretics are prescribed in short 3-5-day courses, if necessary, combine 2-3 drugs.
The program of differentiated therapy for chronic nephritis
Mixed form of chronic glomerulonephritis
Significant restriction of the regime and ability to work, often the solution of the issue of disability of III or II group.
Diet with restriction of salt and water.
Diuretics and antihypertensive therapy.
Treatment with heparin and chimes.
With pronounced activity of glomerulonephritis - cytostatic therapy, pulse therapy with cyclophosphamide.
Phytotherapy.
Sanatorium-resort
and physiotherapy treatment
The main therapeutic factor for patients with chronic glomerulonephritis in resorts and sanatoriums is the effect of a warm and dry climate, insolation.
The effectiveness of climatic treatment is enhanced by the simultaneous use of grape therapy, fruit diet. Treatment of patients with chronic glomerulonephritis should be carried out at these resorts in the warm season for 2-4 months.
In the complex therapy of CGN, physiotherapy is also used. Inductothermia and ultrasound on the kidney area are recommended. These procedures have an anti-inflammatory effect, increase diuresis.
Thermotherapy is an effective treatment for CGN.
Indications: mixed form of CGN with moderate edema, proteinuria within 3-4 g per day without impaired renal function and blood pressure not more than 170/100 mm Hg. Art.
Under the influence of thermotherapy, glomerular filtration improves, nitrogen excretion function of the kidneys, blood pressure decreases, and edema is significantly reduced.
Contraindications for all types of physiotherapy and sanatorium treatment are a pronounced exacerbation of glomerulonephritis and a significant impairment of the functional ability of the kidneys, high arterial hypertension (above 180/110 mm Hg), severe edema, hypoproteinemia in the nephrotic form, macrohematuria.
Treatment proposed by the curator.
3. Pathogenetic therapy:
Therapy with corticosteroids is not possible (due to the presence of an allergy to corticosteroids). There is also a contraindication to the appointment of cytostatics - leukopenia (3.2x10 9 / l)
Immunosuppressive therapy:
Rep: Tab. Batrideni 0.1
S.: ½ tab. 2 r / d, regardless of food intake.
This drug from the group of immunosuppressants is used in kidney allotransplantation and in chronic glomerulonephritis. Contraindicated in pregnancy, infectious, purulent diseases. Possible activation of chronic foci of infection. With a decrease in the level of leukocytes below 3.0x10 9 /l, it is recommended to reduce the dose of the drug. It should not be combined with cyclophosphamide, imuran and other antimetabolites.
Antiplatelet therapy:
Rp: Tab.Curantyli 0.025
S.: 1-2 tab. 3r/d.
Stimulates the synthesis of prostacyclin and inhibits - thromboxane. Effects: prevents the formation of blood clots in the vessels, dilates the coronary vessels, slightly reduces blood pressure, improves cerebral circulation. Improves kidney function in patients with chronic glomerulonephritis. Contraindication - common atherosclerosis.
4. Treatment of edematous syndrome:
Rep: Sol. Lasix 1%-2ml
D.t.d. No. 5 in amp.
5. Treatment of arterial hypertension:
Rep: Tab. Apressini 0.01
S.: 1 tab. 2 r / day after meals
It has a direct antispasmodic effect on myofibrils of arterioles (hydrazine group delays the inactivation of the endothelial relaxing factor). Improves blood supply. brain, kidneys. Contraindications - idiosyncrasy, disseminated lupus erythematosus, peripheral neuropathy.
6. Phytoapplications on the lumbosacral region in order to improve blood circulation in the kidneys, anti-inflammatory, antispasmodic:
Pour hot water for 1 hour, drain the water, spread the raw materials on gauze (4-6 cm thick layer), apply to the kidney area. On top - oilcloth and a blanket. For 40 min. Apply before bed.
Treatment offered at the clinic.
For patients with chronic glomerulonephritis and CRF, bed rest is necessary.
2. Diet 7 with fluid restriction (400.0) and salt. Control of blood pressure, diuresis.
3. Treatment of edematous syndrome:
Rep: Sol. Natrii chloridi 0.9% - 200ml
Sol. Acidi Ascorbinici 5% - 6 ml
D.S.: in / in, cap., at the end of the system - Sol. Lasix 1%-2ml
Lasix reduces the reabsorption of sodium, chloride, potassium and water in the loop of Henle, does not reduce glomerular filtration.
Not associated with neurological pathology. Probably there are violations of mineral metabolism, renal rickets. Cardiologist. Date: 11/10/1996 No pathology. Urologist. Date: 11/10/1996 Diagnosis: urinary tract infection in question, perinatal CNS lesion. An ultrasound of the kidneys is recommended. ENT. Date: 11/13/1996. Sulfur plugs removed. A slight hyperemia of the posterior pharyngeal wall was noted. ...
Animal history (Anamnesis) Life history (Anamnesis vitae) Domestic cat, not neutered. Feeding is mainly fish, mainly pollock, rarely saffron cod, haddock, raw or boiled. History of the disease (Anamnesis morbi) In the last 3 days, blood has been observed in the urine of the cat, diuresis is painful, difficult. The appetite is preserved, in general, the behavior and condition in the opinion of the owners are unchanged, although ...
DIAGNOSIS OF THE MAIN DISEASE:
Primarily - chronic glomerulonephritis, nephrotic syndrome, stage of renal failure, progressive course, remission phase, CRF III st.
COMPLICATIONS:
Chronic renal failure, severe stage, symptomatic renoparenchymal hypertension.
ACCOMPANYING ILLNESSES:
pancreatitis, latent, mild course, remission phase, secondary bilateral pleurisy, chronic course.
Complaints: the patient complains of general weakness, shortness of breath during exercise, periodic rises in blood pressure, nausea, periodic vomiting, headaches, loss of appetite.
Status praesents subjectivus
The mood is good, attention, memory, sleep are not disturbed, periodic headaches, no fainting, no changes in the sensitivity of the limbs. By evening, the patient notes difficulty in movements in the limbs. Vision, hearing, smell are not impaired.
During the illness, the patient notes a change in the color of the skin.
(took a yellowish color), skin moisture is moderate. There were no rashes or itching during the illness. The shape of the nails did not change. There was no increase in body temperature, the presence of chills, night sweats denies.
Breathing through the nose is free. The presence of pain in the chest, cough denies. There was no sputum discharge, hemoptysis during the period of illness. The patient notes mixed shortness of breath during physical exertion, attacks of suffocation denies. The presence of pain in the region of the heart denies, there are no palpitations, interruptions in the work of the heart. During the illness, there were swelling in the legs, there was also swelling of the brain and lungs.
Diuresis is adequate to the given load. Appetite is reduced, the amount of water is dosed, there is no pain when eating. With periodic exacerbations of the disease, the patient notes nausea, vomiting (last time 10 days ago),
vomiting can be on an empty stomach, as well as after eating. The volume of the abdomen during the disease did not change. The stool is normal, no pain, no tenesmus.
Urination is free, painless, adequate to the given load. The daily amount of urine is greater than the nighttime, there is no bleeding during urination.
There are no pains in the joints, no pains in the spine, no muscles, no swelling, no deformities of the joints, no disturbance of their function.
Anamnesis morbi
The patient first fell ill 5 years ago, when the diagnosis was made during the examination - primary - chronic glomerulonephritis, nephrotic syndrome, CRFIIIArt. In 1997, the patient's condition deteriorated sharply, edema appeared on the lower extremities, shortness of breath during physical exertion, loss of appetite, nausea, vomiting, anemic syndrome, severe asthenia. The patient was hospitalized by ambulance with swelling of the brain and lungs to the regional hospital, where the diagnosis was confirmed. In July - August 1999, the last hospitalization in the regional neurological department, where intensive infusion therapy, detoxification therapy was carried out, diuretics, antiplatelet agents, antihypertensives were prescribed. Currently hospitalized for the imposition of an arterio-venous fistula on the left arm for the purpose of program hemodialysis.
Anamnesis vitae
He was born and developed normally. Sexual, neuropsychic, physical development corresponded to age. Diseases of viral hepatitis, malaria, sexually transmitted diseases, tuberculosis, helminthiasis denies. Notes frequent respiratory diseases. History of pancreatitis. In 1973 he underwent surgery for paraproctitis. There were no injuries or contusions. His mother had a history of diabetes mellitus, and his father had a cardiac pathology. Close relatives denies tuberculosis, syphilis, mental illness, malignant diseases, alcoholism. Living conditions are satisfactory, meals are regular, he follows the prescribed diet (for the last 3 months), fractional meals.
Since 1965, he began working at the plant, the work is associated with neuropsychic stress (engineer), there were no breaks in work due to health conditions. I smoked for 30 years and quit in 1992. Alcoholic drinks, drugs does not accept.
Status praesents objectivus
The patient's condition is satisfactory, consciousness is clear, active position in bed. Normosthenic body type, height - 175 cm, weight - 80 kg. The skin is pale yellowish in color, the visible mucous membranes are pale pink, subcutaneous fat is evenly developed, excessively, there are no edema, pastosity of the legs and feet. Lymph nodes are not palpable. The head is of a normal shape, the face is symmetrical, the reaction of the pupils to light is normal. There is no swelling in the neck area, the dimensions are normal, the thyroid gland is not enlarged.
The shape of the chest is normosthenic, breathing through the nose, respiratory rate - 20 per minute. There is no pain on palpation of the chest, voice trembling is not intense, symmetrical in both parts of the chest. Resistance is expressed moderately. With comparative percussion, the nature of the percussion sound is the same in symmetrical areas of the chest, in the Traube space - tympanitis. With topographic percussion, the position of the upper borders of the lungs is 3 cm above the clavicle in front, behind - at the level of the spinous process of the VII cervical vertebra. The width of the Krenig fields is 6 cm. The lower borders of the lungs are normal.
| Place of percussion | Right lung | Left lung |
| Linea parasternalis | VI rib | |
| Linea medioclavicularis | VI intercostal space | |
| Linea axillaris anterior | VII intercostal space | we don't percuss |
| Linea axillaris media | VIII intercostal space | |
| Linea axillaris posterior | IX intercostal space | |
| Linea scapularis | X intercostal space | |
| Linea paravertebralis | spinous process of 2nd thoracic vertebra |
The mobility of the lower edges of the lungs is normal, for the right lung:
on line medioclavicularis
on line axilaris media
on linea scapularis on inspiration - 2, on exhalation - 2, total - 4
For the left lung:
on line medioclavicularis do not define
on line axilaris media on inspiration - 3, on exhalation - 3, total - 6
on linea scapularis on inspiration - 2, on exhalation - 2, total - 4
Auscultation revealed vesicular breathing over the lungs. There are no side breath sounds. Bronchophony in symmetrical areas of the chest is equally pronounced. There are no protrusions in the region of the heart in the region of the heart, there is no pulsation in the region of the heart in the jugular fossa, subclavian region, along the edges of the sternum, in the epigastric region. On palpation, there is no cardiac impulse, the apical impulse is determined in the fifth intercostal space 1 cm medially from the linea medioclavicularis. The width of the apex beat is 2 cm, high, reinforced, resistance is moderate. Cat purring is not defined. Percussion limits of relative cardiac dullness comply with the norm:
- right border - in the IV intercostal space 1 cm medially from the right edge of the sternum
- upper limit - in the III intercostal space 1 cm to the left of linea parasternalis sinistra
- the left border is in the 5th intercostal space 1 cm medially from the linea mediaclavicularis sinistra.
Limits of absolute cardiac dullness:
- right border - along the left edge of the sternum
- the upper limit is in the IV intercostal space 1 cm to the left of the linea parasternalis sinistra.
- the left border is in the V intercostal space 2 cm medially from the linea mediaclavicularis sinistra.
Diameter of relative cardiac dullness - 14 cm. The boundaries of the vascular bundle on the left and right along the edges of the sternum in the II intercostal space, its diameter is 6 cm.
On auscultation, the heart sounds are muffled, the accent of the third tone is over the aorta. The activity of the heart is rhythmic. Pulse on both hands - 80 beats. in min. The pulse is rhythmic, symmetrical on both hands, good filling, not tense, of medium size. On the carotid arteries, stop arteries, the pulse is satisfactory. BP on the brachial arteries 160/90 (maximum 230/90 mm Hg).
The mucous membrane of the oral cavity is pale pink, the tongue is without features. The teeth are healthy, the gums are pale pink, they do not bleed.
The abdomen is rounded, no protrusions, no visible peristalsis. On superficial palpation, the abdomen is soft and painless; With deep palpation according to Obraztsov - Strazhesko sigmoid, cecum, segment of the ileum, ascending, descending, transverse colon are palpated in the form of moderate density, painless cylinders, the caecum rumbles on palpation (normal). The lower border of the stomach is located at 2 cm of the navel, it is determined by percussion, according to the splash noise. With deep palpation, the edge of the liver is soft and painless. With percussion, the size of the liver according to Kurlov: according to lin. mediaclavicularis dextra - 0, according to lin. mediana anterior - 9 cm, along the left costal arch - 8 cm. The spleen is not palpated. On percussion, the diameter of the spleen is 5 cm, the length is 7 cm. The pancreas is not palpable.
Examination of the urinary system showed no edema, Pasternatsky's test was negative. The kidneys are not palpable. Percussion determines the dullness of the sound above the pubis due to the full bladder.
There are no pathological changes in the spine, no joint deformities. Muscle tone is normal, there is no pain on palpation.
Brief summary and preliminary diagnosis:
Based on the patient's complaints (general weakness, shortness of breath during physical exertion, periodic rises in blood pressure, nausea, periodic vomiting, headaches, loss of appetite.), subjective and objective data (pale yellow skin, increased blood pressure, emphasis III on the aorta), anamnesis diseases (previous hospitalizations), a preliminary diagnosis can be made: Primary chronic glomerulonephritis, CRF - II-III degree, progressive course.
Survey plan
1) Complete blood count
2) Urinalysis
3) Biochemistry of blood, study of hemostasis
4) Sample according to Nechipurenko, Zemnitsky
5) Ultrasound examination
6) X-ray examination
Clinical laboratory and instrumental studies
1) Complete blood count - 09/07/99
Hb - 64 g / l, Erythrocytes - 2.31 g / l
Color indicator - 0.83
Leukocytes - 9.3 g / l
Neutrophils - 78%
Segmented - 32%
Platelets — 323 g/l
Reticulocytes - 0.43
Hypohemoglobinemia, anemia, mild leukocytosis
2) General analysis of urine - 09/07/99
Color - pale yellow
Transparency - cloudy
Specific gravity - 1008 (reduced)
Reaction - sour
Protein - not found
Glucose - not detected
Leukocytes - 1-4 in the field of view
Erythrocytes - single
3) Nechipurenko test
Leukocytes - 1500
Red blood cells - 500
Cylinders - no
4) Biochemistry of blood - 09/07/99.
Total protein — 59.0 g/l
Urea - 19.6 increased
Creatinine - 0.78 mmol / l increased
Thymol reaction - 2.0 units
Bilirubin - 9.5 mmol / l
direct -
indirect - 9.5 mmol / l
5) Hemostasis - 09/07/99
Prothrombin index - 89%
Fibrinogen - 5.35 g / l increased
The liver is slightly enlarged, the pancreas is not enlarged. The gall bladder is not changed. Fibrin threads are present in the right pleural cavity. There is not much fluid in the left pleural cavity. There is no free fluid in the abdominal cavity. Kidneys of heterogeneous echostructure. In the left kidney along the outer contour, subcapsular cyst 30 mm. There is no stasis of urine in the kidneys.
Conclusion: Chr. Glomerulonephritis. Secondary bilateral pleurisy. consequences of pancreatitis.
Differential Diagnosis
Chronic glomerulonephritis should be differentiated from chronic
pyelonephritis. Chronic glomerulonephritis is indicated by the predominance of erythrocytes over leukocytes in the urine sediment, as well as the same size and shape of the kidneys, as well as the normal structure of the pelvis and calyces (which is confirmed by instrumental studies). Unlike chronic glomerulonephritis, chronic pyelonephritis is not characterized by hypertension.
Primary - chronic glomerulonephritis should be differentiated from hypertension, where the time of occurrence of the urinary syndrome in relation to arterial hypertension matters. In primary chronic glomerulonephritis, the urinary syndrome may appear long before the development of arterial hypertension or may occur simultaneously with it (which is observed in this patient). Chronic glomerulonephritis is also characterized by a lesser severity of cardiac hypertrophy, a lesser tendency to hypertensive crises, less intensive development of atherosclerosis, including coronary arteries (as can be seen from the anamnesis and studies of the patient).
In the nephrotic form of chronic glomerulonephritis, it is differentiated from amyloidosis. Kidney amyloidosis is characterized by the presence in the body of chronic foci of infection in the form of suppurative processes in the lungs, osteomyelitis, tuberculosis, etc. This is not observed in the patient.
Substantiation of the diagnosis
Based on the patient's complaints about general weakness, shortness of breath during physical exertion, periodic rises in blood pressure, nausea, periodic vomiting, headaches, decreased appetite, Subjective and objective data, medical history (primary chronic glomerulonephritis, previous hospitalizations), clinical course of the disease, medical history (history of chronic pancreatitis, diabetes mellitus in the mother - a predisposition to renal pathology), clinical and laboratory data (anemia, hypohemoglobinemia, leukocytosis, decreased specific gravity of urine - impaired concentration function of the kidneys), conducted diff. diagnosis, the main diagnosis can be made: primary - chronic glomerulonephritis, nephrotic syndrome, progressive course, remission phase, CRF IIIArt.
Complications: CRF severe stage, symptomatic renoparenchymal hypertension.
Accompanying illnesses: chronic pancreatitis, secondary bilateral pleurisy, chronic course.
General principles of treatment
The patient should be assigned a semi-bed rest, table number 7, a diet is very important - the content of sodium chloride is reduced to 1.5 - 2.5 g per day.
important in the treatment of patients hormone therapy
Rp.: Tab. Prednisoloni 0.005 № 20
D.S. PO two tablets 6 times a day
The patient should also be given:
Rp.: Heparini 5 ml
- S. 20,000 U/day IV (5000 U 4 times a day)
Rep.: Tab. Furosemidi 0.04 № 10
D.S. 1 tablet 2 times a day
Rp.: Rheopolyglucini 500 ml
- S. B/in drip
Rp.: Reserpini 0.0001 No. 20
D.S. 1 tablet 2 times a day after meals
Rp.: Anaprilini 0.01 No. 40
D.S. 2 tablets 2-3 times a day
This patient is also indicated for surgical intervention on the imposition of an arterio-venous fistula on the left arm for the purpose of program hemodialysis.
Diary of the course of the disease
| the date | Patient status | Appointments |
| 6.09.99 | The patient's condition is satisfactory. Complaints of loss of appetite, shortness of breath with little physical exertion. Objectively, there is a pulmonary sound above the lungs, vesicular breathing, muffled tones, Р — 78 beats BP - 160/90 mm Hg |
Rp.: Heparini 5 ml S. 5000 units 4r per day |
| 7.09.99 | The patient's condition is satisfactory. There are no complaints. Objectively, there is a pulmonary sound above the lungs, vesicular breathing, muffled tones, Р — 78 beats BP - 160/90 mm Hg The abdomen is soft and painless on palpation. |
Rp.: Heparini 5 ml S. 5000 units 4r per day IV drip reopoliglyukin 400 ml |
2015-04-19 08:22
On March 23, 2015, Alfiya and her husband Sergey came to our clinic for Chinese medicine treatment. Alfiya came from Novosibirsk, Russia. She recalled her medical history and treatment and told us that 5 years ago she was diagnosed with chronic glomerulonephritis. After being diagnosed, she took active treatment and multiple medications. She was always treated according to the doctor's prescriptions, but the condition gradually worsened and uremia still arrived. 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 Alfiy 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 latent hematuria ++, creatinine in the blood 180 mmol/l. The local doctor diagnosed her with CKD (chronic kidney disease) and prescribed Moxonidine, Methyldopa, and Hydrochlorothiazide. These 3 medicines reduce blood pressure, meaning local doctors have experienced treating CKD by controlling blood pressure. In this chronic renal failure at a decompensated degree.
Second hospitalization:
After being discharged from the hospital, Alfiya always took medication regularly, but there was swelling in the lower extremities, creatinine increased to 250 mmol/l. In 2012, the cutting condition worsened and Alfiya was in the hospital for the second time. Then the pressure was 220/120 mm Hg, hemoglobin up to 98 g/l, proteinuria +++, latent hematuria ++, creatinine 400 mmol/l. Then hypertension and anemia were. Amlodipine and an 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 treatment effects were not so ideal, creatinine was over 600 mmol/L. One day in 2014, severe shortness of breath arose and the third hospitalization began. The pressure was 230/110, creatinine was crying up to 800, and there was also coronary heart disease, myocardial ischemia and other diseases. And then the dialysis began, 3 times a week.
Alfiya did not understand why in 5 years she never stopped treatment, but her condition still gradually worsened?
Alfiya received program treatment from us:
Kidney disease is caused by the accumulation of multiple harmful substances in the blood. With the circulation, various wastes and toxins increase the burden on the kidneys and accumulate in the kidneys, causing damage to the kidneys. And so it is necessary to cleanse the blood of waste and toxins from the blood and kidneys.
Conducted Blood Pollution Therapy, Enema, Micro-Chinese Medicine Osmotherapy, Medicated foot bath and others.
After 21 days, Alfiya returned home with satisfaction.
This is a sudden onset and rapidly progressive impairment of renal function, manifested by oligoanuria, azotemia, and disturbances in water and electrolyte balance.
The onset of the disease Acute renal failure
The causes of acute renal failure are manifold. E. M. Tareev identifies the following groups of causes: 1) shock kidney, 2) toxic kidney, 3) acute infectious kidney, 4) vascular obstruction, 5) urinary tract obstruction.
Traumatic shock, electrical injury, burns, massive blood loss, crush syndrome with muscle crush, operational shock, transfusion of incompatible blood, pregnancy toxicosis, myocardial infarction, exhausting vomiting can lead to the development of a shock kidney. Toxic kidney occurs when poisoning with heavy metal salts, primarily mercury salts, organic poisons (carbon tetrachloride, dichloroethane, acetic acid, methyl alcohol, etc.), some drugs (barbiturates, quinine, pachycarpine), plant and animal poisons origin (snake, mushroom venom and insect venom).
Acute infectious kidney occurs with sepsis of various origins, primarily with 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 due to mechanical obstructions to the outflow of urine in nephrolithiasis, compression of the ureters.
Course of the disease Acute renal failure
Given 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 is the ischemic factor.
With a significant decrease in the work of the heart, 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. Violation of the renal circulation inevitably leads to a decrease in filtration and a violation 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 impaired renal circulation in various types of shock is a spasm of the renal vessels due to neurohumoral effects on the vessels of the kidneys of histamine and serotonin released during shock or destruction of blood cells and tissues in pathological conditions.
The ultimate mechanism of renal ischemia is anoxia of the renal tissue, to which the latter is very sensitive. However, a decrease in 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 reduce 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 basement membrane of the tubules, the glomerular filtrate can directly contact the interstitium of the kidneys and is easily absorbed back into the blood and lymph.
Another important factor is nephro-toxins. Various nephrotropic poisons disrupt the enzymatic processes in the renal tissue, and by damaging the lysosomal cell membranes, they can lead to necrosis. According to current 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 cortical layer 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 characteristic, for a shock kidney, damage to the basement membrane of the tubules with fragmentation of the main membrane, referred to as tubulo-rhexis. In the epithelium of the tubules, swelling of the cytoplasm, granular, vacuolar, less often fatty degeneration are noted. Electron microscopic examination reveals swelling, edema and disintegration of mitochondria. Morphological changes in acute renal failure undergo rapid dynamics. The necrotic epithelium is desquamated and rejected, the edema of the interstitial tissue decreases, and the regeneration of the epithelium begins along the remaining main membrane. However, where there was a rupture of the basement membrane, complete recovery 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) recovery of diuresis with an initial diuresis phase and a polyuria phase, and finally 4) a recovery period. In the first period, the symptoms of the underlying disease, which led to acute renal failure and shock, are most pronounced. There is tachycardia, a decrease in blood pressure, which, however, may be transient. In 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, the state of health of patients improves for a while, despite the absence of urine. Gradually, they begin to complain of weakness, loss of appetite, headache. There are nausea, vomiting. With the progression of the disease during breathing, the smell of ammonia is determined.
Disorders of the central nervous system are diverse. Most often there is apathy, but sometimes the patient may be agitated, poor orientation in the environment, confusion. Hyperreflexia and convulsive seizures are often noted.
In cases where acute renal failure was a consequence of sepsis, herpetic eruptions around the mouth and nose can be noted. The nature of skin changes in acute renal failure, which developed as a result of allergic reactions, can be varied: fixed erythema, urticaria, toxicoderma. The pulse is over 100 beats per minute. The boundaries of the heart are expanding. Especially defiantly, the expansion of the heart is determined on radiographs. Above the apex of the heart, a systolic murmur is heard, an accent of the II tone, 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 blockade, mainly associated with disorders
electrolyte metabolism and acidosis. There may be fibrinous pericarditis with a pericardial friction rub, pain in the heart, changes in the electrocardiogram. Interestingly, the symptoms of pericarditis are aggravated after hemodialysis.
Nausea and vomiting, loss of appetite are observed in almost all patients. Less common are diarrhea and melena. Especially often the phenomena from the digestive organs are observed in hemorrhagic fever with renal syndrome. The occurrence of gastrointestinal lesions is associated primarily 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 clinically poorly recognized and is diagnosed mainly by chest x-ray. At the same time, bilateral, symmetrical, with fuzzy contours darkening in the root zone is detected.
The predominant clinical sign at this stage is oligoanuria. The amount of daily urine ranges from 20 to 300 ml at a density of 1003-1008. Urine is cloudy, dark brown or bloody. The sediment is large, contains many erythrocytes, leukocytes, lumps of cylinders impregnated with hemin. There is a lot of protein in the urine. The excretion of urea and creatinine in the urine is reduced. In the blood, high leukocytosis, a pronounced shift in the leukocyte count, anemia, and an increase in ESR are noted.
Anemia in acute renal failure develops constantly. Anemia is most pronounced in cases where acute renal failure is preceded by intravascular hemolysis. Anemia, growing during the period of oliguria, reaches a maximum in the initial phase of diuresis recovery and persists during the recovery period.
Pronounced violations of homeostasis develop. The content of residual nitrogen increases from 14-26 to 140-260 mmol/l (from 20-40 to 200-400 mg%). Urea nitrogen rises to a greater extent than residual nitrogen in general. The level of creatinine increases more rapidly than urea, especially in patients with massive muscle lesions. The content of ammonia in the blood also increases sharply, especially with combined renal and hepatic insufficiency. The concentrations of uric acid and indoxin increase not so significantly. Metabolic acidosis develops, usually uncompensated. For acute renal failure
sufficiency is characterized by hyperkalemia and hypermagnesemia, manifested by an electrocardiographically high T wave, a decrease or disappearance of the U wave, a violation of atrioventricular and intraventricular conduction. High potassium levels are explained by the appearance of such pathological neuromuscular symptoms 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. At the same time, the electrocardiogram shows a decrease in the ST segment, a decrease in the voltage of the T wave, a high Q wave. The S-T interval is significantly lengthened.
During the period of oligoanuria, as a rule, hyperhydration is observed with a decrease in hematocrit. *
Liver damage in acute renal failure is almost constant. Clinically, liver lesions are manifested by scleral icterus 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, methods of active = therapy for renal failure are required to maintain the life of the patient.
An increase in diuresis can begin a few days after oliguria and occurs gradually. At first, the amount of urine exceeds 500 ml, and then, gradually increasing, it is more than 2000 ml / day. From this time begins the third period of acute renal failure.
In this period, clinical improvement does not develop immediately, and sometimes the condition of patients may worsen. At the beginning of the diuretic period, the level of azotemia may increase, hyperkalemia may increase. The concentration ability of the kidneys remains low. The patient loses weight during polyuria. The period of polyuria usually lasts 4-6 days. In patients, appetite improves, pathological changes in the nervous system and the circulatory system disappear.
Conventionally, it is considered that the recovery period begins from the day of the disease, 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 concentration ability of the kidneys, and tubular secretion gradually increase.
However, within 1-2 years, signs of functional insufficiency of individual organs and systems (heart, liver, etc.) may persist.
Acute renal failure, if not fatal, results in gradual recovery without a tendency to develop chronic kidney disease.
After 6 months, more than half of the patients fully recover their ability to work, although some of the patients by this time have limited ability to work, and they are recognized as disabled of group III. In many ways, the working capacity of patients depends on the underlying disease that caused acute renal failure.
Treatment of the disease Acute renal failure
Measures aimed at reducing the action of nephrotoxins and preventing circulatory disturbances reduce tubular damage. Early removal of the poison from the body, the appointment of specific antidotes and the use of drugs that prevent and eliminate circulatory disorders are also measures for the prevention of acute renal failure.
In cases where there is a risk of developing acute renal failure, in order to prevent it, mannitol can be administered intravenously in a 10% solution 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. In the stage of oliguria, the use of mannitol is ineffective and impractical.
It should be noted that the 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 replenish the loss of fluid and electrolytes.
The appointment of large amounts of fluid to the patient during the period of oliguria and anuria in the hope of stimulating diuresis and reducing the concentration of nitrogenous slags does not give results. It enhances hyperhydration, reduces the effective osmotic pressure of plasma and enhances water "intoxication".
In the initial period of the disease, the most effective therapeutic agent is an exchange transfusion of blood. With its help, part of the non-dialyzed plasma hemoglobin is extracted, the bloodstream is replenished with red blood cells, and 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 blood volume.
Measures are being taken to combat shock and blood loss. In cases where there is a picture of shock and compensation for blood loss does not eliminate hypotension, the use of corticosteroids (30-60 mg of prednisolone or 100 mg of hydrocortisone intravenously) is indicated. However, the expediency of such therapy is limited to the very initial period of the disease.
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 makes it necessary to reduce the dosage and frequency of antibiotic administration. Antibiotics such as streptomycin, monomycin, neomycin are best not used in acute renal failure due to their nephrotoxicity.
Due to the risk of urinary tract infection, attention should be paid to the fact that the introduction of an indwelling catheter, especially in men, in order to accurately control diuresis is dangerous due to the development of urethritis, prostatitis and cystitis, followed by pyelonephritis.
During the first three periods of the disease, protein is completely excluded from the patient's diet. You can give the sick cream, sour cream, syrups. With porous dyspeptic disorders, the patient eats parenterally.
To combat acidosis, a 5% solution of sodium bicarbonate is used from the initial calculation of 0.5-1 ml per 1 kg of weight under the control of determining indicators of acid-base balance.
To correct protein catabolism, anabolic steroid hormones are administered: methyl androstenediol, nerobol, retabolil.
Effective intravenous infusion of hypertonic solutions of 40% glucose (up to 100 ml / day). At the same time, insulin is used at the rate of 1 unit per 3-4 g of glucose.
Long-term gastric lavages are shown to flush out nitrogenous wastes; this relieves patients of indomitable nausea and vomiting. Parenteral administration of calcium salts is necessary, especially with the development of convulsive seizures.
Acute renal failure, not amenable to conservative treatment, 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 not advisable, since in a significant part of cases, conservative treatment can restore kidney function. Hemodialysis is indicated at blood creatinine levels above 114 mmol / l (15 mg% "), urea above 49 mmol / l (300 mg%), residual nitrogen above 113-140 mmol / l (160-200 mg%), potassium 6, 5 mmol / L. Indications for hemodialysis should be evaluated only in conjunction with the clinical picture.Contraindications for hemodialysis are septic process, acute thromboembolism, myocardial infarction, gastrointestinal bleeding, severe heart and liver failure.
The issue of sanatorium treatment is decided in each case individually and not earlier than 6 months after discharge from the hospital.
The resorts of Bayram-Ali, Bukhara, the southern coast of Crimea are shown.
