Download Treatment of patients with UA-hard problem, because it should be

Ministry of Health Republican Uzbekistan
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF "TRAINING GENERAL DOCTORS "
Lecture theme:
Differential diagnosis of nephrotic syndrome and tactics GP.
(Students Medical pedagogical faculty)
TASHKENT – 2016
2
MINISTRY OF HEALTH REPUBLICAN UZBEKISTAN
TASHKENT MEDICAL ACADEMY
DEPARTMENT OF "TRAINING GENERAL DOCTORS "
"APPROVED"
Dean of the medical pedagogical faculty
Professor Hamraev A.A.
____________________
____ ________ 2016 y.
Differential diagnosis of nephrotic syndrome and tactics GP.
TASHKENT – 2016
3
TECHNOLOGY TRAINING
Number of Students
The structure of the training session
Plan of the lecture
Time - 2:00
Lecture - in the form of presentation
13. Explain nephrotic syndrome
14. The main causes of nephrotic syndrome
15. Pathogenesis of nephrotic syndrome
16. Clinical signs of nephrotic syndrome
17. Typical signs edema in the nephrotic syndrome
18. Classification of nephrotic syndrome
19. Typical signs of options nephrotic syndrome
20. Changes in the internal organs of the nephrotic syndrome
21. Complications of nephrotic syndrome
22. Factors causing death by disease accompanied with
nephrotic syndrome
23. Treatment of nephrotic syndrome
The purpose of the training session: To provide students with information on the nephrotic syndrome,
the classification of nephrotic syndrome, the main diagnostic criteria for diseases associated with
nephrotic syndrome, complications, diagnosis, and education on prevention and emergency care.
Pedagogical objectives:
1. To provide full information to
students about classification, clinical
features and factors leading to
nephrotic syndrome. To deepen their
knowledge about the diagnosis and
emergency some help in the nephrotic
syndrome.
2.
Explained
to
PRINCIPLE
Differential diagnosis of diseases
accompanied by nephrotic syndrome
3. Achieve self-mastery of practical
skills in the nephrotic syndrome and
the disease is accompanied by
nephrotic syndrome
4. Explained to students the principles
of prevention
Teaching methods
Training forms
Training tools
Learning Environment
Learning outcomes:
GPs should know:
1. Be able to diagnose a nephrotic syndrome
2. Clinical symptoms of nephrotic syndrome
3. Acquire knowledge of the main causes of nephrotic
syndrome privodyashih
4. Able to determine the diagnostic criteria of diseases
accompanied by nephrotic syndrome
5. Able to identify the risk factors leading to sudden death
in the nephrotic syndrome
6. Complications of nephrotic syndrome
7. Principles of diagnosis and treatment of diseases
accompanied by nephrotic syndrome
8. Prevention and rehabilitation of diseases accompanied by
nephrotic syndrome
The text of the lecture, video, brainstorm, solve situational
problems, competition between groups, the technique the "yesno"
Laser projector, visual material on relations with specialized
equipment
Collective
Audience
4
Flow chart lectures
Stages, while
Stage 1
Input (5min)
Stage 2
Improve
knowledge (20
minutes)
stage 3
The main stage
(information)
(55 minutes)
Stage 4
final
(10 minutes)
Activities
Teacher
1. Tell theme intact and expected plans
2.1. Questions for students to improve their knowledge
1. Nephrotic syndrome, which means?
2. Key criteria for the diagnosis of nephrotic
syndrome?
3. List the group of diseases leading to nephrotic
syndrome?
4. The reasons leading to the development of sudden
death in the nephrotic syndrome?
5. Emergency medical care when complications
develop spontaneously in the nephrotic syndrome?
Conducts quick poll
2.2. Are referred to the purpose of the lecture
screening. Provide an explanation of the information
presented in lectures
Slide number 1, 2, ...
3.1. To familiarize with the essence of the lecture and
the criteria of forming spiritual identity
Improves students' knowledge about the topic of the
project and carry out the "brainstorming"
1 - plan question: Explain the nephrotic syndrome?
2 - plan question: List the clinical signs of nephrotic
syndrome?
3 - question the plan: the main cause of nephrotic
syndrome?
4 - Issues Plan: Causes of death in diseases
accompanied by the nephrotic syndrome?
5 - plan question: risk factors leading to the
development of complications in the nephrotic
syndrome?
6 - plan question: When options nephrotic syndrome
observed what changes?
7 - the question plan: Emergency aid in the
development of nephrotic crisis?
Suggest to stop and write down the main points lectures
4.1. The question is asked:
1. Explain nephrotic syndrome
2. Variants of nephrotic syndrome
3. The main causes of nephrotic syndrome
4. Complications of disease is accompanied by the
nephrotic syndrome
5. Complications in the nephrotic syndrome, and
emergency medical care
4.2. Writing assignments for independent discounts:
Nephrotic crisis and its treatment
Students
1. Listen
2.1. Answer questions
2.2. № 1 Familiarize with slides
2.3. Number 2 Familiarize with
slides
3.1. Ask questions and
discuss the materials specified
Writes highlights
4.1. answer questions
4.2. listen and write
5
Nephrotic syndrome (NS) - syndrome, which includes a number of clinical signs, most of
which are proteinuria greater than 3.5 g / day, swelling, as well as a number of specific metabolic
changes - violations, especially of protein and lipid metabolism (disproteinemia, hypoproteinemia,
hyperlipidemia). It is considered that the term "nephrotic syndrome" was introduced into the
literature W.Nonnenbruch (1949).The basis of the etiology of nephrotic syndrome are two types of
kidney changes - different versions of glomerular lesions and amyloidosis. In most cases, nephrotic
syndrome occurs in diseases of the kidney itself - acute and chronic glomerulonephritis. However,
kidney damage can be caused and systemic (systemic lupus erythematosus, hemorrhagic vasculitis,
periarteritis nodosa, scleroderma, rheumatic fever, etc.), infectious etiology (chronic suppurative
processes of the lung, bone, tuberculosis, syphilis, etc.), parasitic (malaria , schistosomiasis),
diseases of the liver disease, blood disorders, allergies, etc. The nephrotic syndrome may be induced
by drugs (antiepileptic drugs, drugs bismuth, gold, mercury, D-penicillamine, antibiotics, vitamins,
etc.).With all these diseases nephrotic syndrome is realized through the two above-mentioned
variants of renal - changes the type of glomerulonephritis and amyloidosis.Thus, the etiology is
diverse, but its clinical manifestations are the same type of non-specific nature, which, to some
extent conditioned by the common pathogenetic mechanisms.Modern views on the pathogenesis of
the National Assembly. based on a fundamental view of the kidney disease as immunological
nature. Immune disorders due to interaction of antigen with an antigen, complement activation, the
formation of immune complexes and their deposition on the basement membrane, is developing a
series of cellular reactions of immune inflammation (cellular infiltration of tissues, phagocytosis,
lysosomal enzyme output and other products of degranulation of white blood cells) as a result - is
affected basal membrane glomerular capillaries, increasing its permeability to plasma proteins while
reducing the ability of epithelial tubules reabsorb protein. All this leads to proteinuria and loss of
protein in the urine of more than 3.5 g / day. Up to a point protein deficiency is compensated gain
its synthesis in the liver, but when this process is a compensatory mechanism is exhausted,
hypoproteinemia develops. Developing hypoproteinemia aggravated intestinal protein loss,
enhanced catabolism of proteins of the body, including immunoglobulins, decreased reabsorption of
protein because protein block the tubules, kidneys and lymphatic edema, renal interstitium. As a
result, falls oncotic pressure, which leads to the development of nephrotic edema. While reducing
the protein content increased levels of blood lipids - cholesterol, triglycerides, phospholipids, Cio
due to the decrease of plasma lipolytic activity. When the National Assembly often develop changes
in anticoagulant system, thereby creating conditions hypercoagulable rovi by reducing the activity
of the anticoagulant and fibrinolytic factors, serum proteases, and activation of kinin-kallikreinovoy
system. Blood hypercoagulability may increase the morphological changes in the kidney
(fibrinogen-fibrin deposition in glomeruli, local intravascular coagulation), and cause further
decreased urine output up to anuria, and vascular thrombosis. Decrease oncotic plasma pressure to
the output of water and electrolytes into the interstitial tissue leads to hypovolemia, which is the
inclusion of compensatory mechanisms that regulate the amount of circulating plasma in the first
place, of aldosterone and ADH. As a result, increases the reabsorption of sodium and water by the
kidneys, increased tubular secretion of potassium, which can result in improved bicarbonate in the
blood. Shifts of water and electrolyte metabolism are often combined with a violation of calciumphosphorus in the form of hyperphosphatemia and hypocalcemia with the possibility of
osteoporosis. Inhibition of the function of phagocytes and antibody formation are accompanied by a
decrease in immunity. Count the NA hypertension is usually a sign of parenchymal lesions of the
kidneys - glomerulonephritis, pyelonephritis, polycystic kidney disease, renal disease, with
POLYSYSTEM diseases.The clinical picture of the National Assembly is very varied, as is made
up of a combination of symptoms of the underlying disease and the responses of the nephrotic
syndrome.When collecting history should pay attention to in the past transferred kidney and other
organs, capable of complicating the National Assembly, as well as food intolerances and
medications.Patients may bring a lot of non-specific complaints, but with the greatest constancy
indicate edema, which can develop gradually or rapidly, reaching overnight degree anasarca.With
slow development of the National Assembly first appears Morning swelling under the eyes, which
is due to the combined effect of a very low interstitial pressure in these areas and the temporary rise
6
in capillary pressure due to a long night of stay of the patient in a horizontal position. Further
swelling spread to the genitals, lower back and feet. In the later stages of the National Assembly the
distribution of edema obeys the law of gravity, which apply to all the subcutaneous tissue,
stretching the skin to form a pale band (strie distensae). Stretching bands are more common in the
lateral and lower parts of the abdominal wall, in the hips, lower back, that is, in areas of maximum
accumulation of edema fluid with variable stretching of the skin, breaking its elastic membrane, the
formation of scar connective tissue. At the height of the National Assembly, most patients have
transudaty in serous cavities: ascites, one-or two-sided hydrothorax, rarely hydropericardium.
Conjunctival edema (chemosis) and are accompanied by retinal lachrymation, blurred vision. Due
to swelling of the genitals difficult urination. Edematous fluid in UA can seep through the cracks of
the skin surface. Nephrotic edema loose, easy to move and left a hole when pressed with a
finger.With the rise and spread of edema decreased diuresis. The urine often has a milky white color
because lipurii and strongly foaming due to high proteinuria.With long-term existence of the
complaint attached edema caused by trophic disorders: dry and flaky skin, dull hair, hair loss, brittle
nails with their thickening, transverse stripes.Usually varies significantly overall condition of the
patient: there are unmotivated weakness, fatigue, decreased ability to work. Patients lose their
appetite, there is dry mouth, thirst. During the development of ascites attached to anorexia nausea,
sometimes vomiting, bloating, diarrhea and persistent with an increase hydropericardium
hydrothorax and shortness of breath.Peculiar appearance of the patient - a combination of edema
and pale, dry skin. Typical complaints - drowsiness, hair loss, lethargy, physical examination
findings - a hoarse voice, bradycardia, heart sounds muted, data parakliniki - low voltage of all the
teeth of the electrocardiogram, reduced metabolic rate and the level of protein-bound iodine - all
this creates a typical picture of myxedema and has long been clinicians assumption of nephrotic
syndrome due to the state of hypothyroidism. This is a natural condition for HC hypothyroidism at
one time considered the main causative factor and recommended to treat it tireoidinom. Later it was
found that at least 25-30% of secreted into the blood thyroxine lost in the urine due to increased
permeability of the glomerular filter. In addition, the irreversible loss of serum proteins violate
traffic tireoidina and triiodothyronine, which leads to a lack of thyroglobulin. Initially, these losses
may stimulate thyroid function and to some compensated. However, over time the function of the
thyroid gland is exhausted, the more so that the shortage of protein and disrupt its metabolism
suffers activities of all endocrine glands, especially the pituitary hypo-secretion of its tropic
hormones, including thyroid. Thus, the loss of function of the thyroid gland in the National
Assembly is not seen as the cause, and as its consequence.
By the nature of the flow the following types of nephrotic syndrome
Type I - "debut" of kidney disease nephrotic syndrome.Such a beginning is observed more
often in acute glomerulonephritis, glomerulonephritis with minimal glomerular changes less
frequently - with membranous glomerulonephritis. In general, during the nephrotic syndrome as the
debut of the disease characterized by relative benign, and, with rare exceptions, this form ends more
or less long-term remission, which can last up to 8-10 years. Spontaneous remissions are rare, the
frequency range from 8 to 18% in different clinical forms of nephrotic syndrome in children - up to
26%. The duration of clinical signs for this option is measured from a few weeks to 1 year. In this
case, first of all wound edema and proteinuria, gradually decreasing and may persist for months.
Cases of recovery, re-confirmed renal biopsy are rare (often described in children). Renal function
in these patients maintained or fully restored along with the elimination of the clinical
manifestations of the syndrome.Type II - a chronic relapsing course.In patients for many years,
there has undulating increase or decrease in proteinuria, and edema, and the violent aggravation
replaced by a partial remission, which may last for months, sometimes years. Nephrotic syndrome
often arises. In this aggravation, usually on the third or fifth year of the disease, which is typical for
secondary nephrotic syndrome. The function of the kidneys is reduced gradually. Benign disease
flare-up is sometimes interrupted, each of which can be fatal, and quickly lead to renal failure. Each
subsequent relapse of nephrotic syndrome usually has a more severe course, and to eliminate it, a
more intensive therapy.Type III - relentlessly progressive course.There are two types of the
7
course.In the first version, in spite of active treatment, persistently kept nephrotic syndrome, and the
renal function over time is normal. Only after 8-10 years from the onset of nephrotic syndrome in
these patients (with no signs of deterioration) is formed by chronic renal failure. This option is set
for a membranous flow, and even mezangioproliferativnom fibroplasticheskom types of chronic
glomerulonephritis.The second option is observed in extracapillary, mezangiokapillyarnom
glomerulonephritis, focal segmental glomerular hyalinosis and when collagenosis, amyloidosis,
diabetic glomerulosclerosis, renal vein thrombosis. With progressive course of remission is not
observed, and even intensive therapy does not eliminate the symptoms of the disease after 1-3 years
there is chronic renal failure, and then the terminal uremia.Type IV - terminal nephrotic
syndrome.This is the rarest of all of the above variants of the extremely poor and the forecast.
Formed in the late stages of the disease in patients with chronic glomerulonephritis, and on the
background of secondary glomerulopathy. Is persistent, rapid progression of terminal uremia, loss
of patients at relatively low numbers creatinine, a higher frequency of various complications
predominantly inflammatory nature, the development of heart failure. Signs of nephrotic syndrome
in patients with preserved to death. The cause of the nephrotic syndrome terminal consider the
severity of exacerbation of the process in the kidneys, anemia, prolonged tissue hypoxia, venous
hypertension on the basis of heart failure, long-term prescription drugs.
The heart of the nephrotic
The heart of the nephrotic syndrome is involved in the disease process at an early stage,
which is associated with impaired protein metabolism accompanied by microcirculatory disorders,
vascular and tissue permeability, blood coagulation phenomena. This leads to perivascular edema,
hemorrhage, aneurysmal expansion of blood vessels, capillaries and zapustevaniyu intravascular
platelet aggregation up to the formation of microthrombi. Such changes apply to the myocardium.
Phenomenon of hypo-and dysproteinemia nephrotic syndrome cause myocardial degeneration and
qualify as "nephrotic (gipoproteinemicheskaya) cardiomyopathy." It is possible that, in addition to
vascular and degenerative disorders in the pathogenesis of myocardial damage in the nephrotic
syndrome are involved and autoimmune processes that contribute to changes in vascular
permeability and contribute to interstitial edema and serous impregnation infarction. All this leads
to functional reorganization in the myocardium and activation systems, specifically responsible for
the compensation of damage.Universal adaptive response to changes in the myocardium of the
internal environment is the phenomenon dystrophy with the subsequent development of
compensatory hypertrophyIn nephrotic syndrome, the tendency to increase the circulating plasma
volume to decrease in total peripheral resistance. Extracellular fluid volume increases. The analysis
of the phase structure of the systole of the heart indicates a violation of the contractile function of
the left ventricular myocardium and improve it in end-diastolic pressure. Heart size increased by
more than 77% of patients, mainly due to the left ventricle, at least - both. The vast majority of
patients I muted tone at the top, maybe I split tone. Approximately half of the patients at the top of
auscultated systolic murmur due to a hypervolemia and underlying anemia. The majority of patients
with advanced edema, hypovolemia occurs hyperkinetic type of circulation due to movement of
fluid from the bloodstream into the tissues and compensatory increase in heart rate. In patients with
hypervolemia in the absence of hemodynamic insufficiency observed persistent bradycardia, which
has adaptive nature and caused by vascular reflexes.Existed before the perception that no patients
with nephrotic syndrome propensity to atherosclerosis is now refuted. Found a significant increase
in the risk of progression of atherosclerosis and the occurrence of typical atherosclerotic
complications in patients with UA. There is evidence that in patients with nephrotic syndrome was
85-fold increased frequency of coronary artery disease.Investigation of apoproteins (apo) serum are
protein components of lipoproteins, identifies patients NA lipoprotein metabolism disorders, even
with a normal level of lipids in the blood, which increases the risk of coronary atherosclerosis. For
patients with nephrotic syndrome is characterized by the accumulation in the blood-rich VLDL and
LDL. In other words, the very nephrotic syndrome, regardless of its cause, is a pro-atherogenic
factor.Clinically nephrotic syndrome is classified into two forms: the so-called pure and mixed. Net
nephrotic syndrome is the main symptoms of the above without hypertension, hematuria, and renal
failure. With the combination of nephrotic syndrome with hypertension suggest a mixed
8
form. General symptoms of renal hypertension is different from hypertension symptoms in another
genesis. Clinical characteristics of renal hypertension varies widely - from unstable malosimptomno
to malignant hypertension hypertensive syndrome. To assess the severity of hypertensive syndrome
focus on diastolic, not systolic blood pressure. It is persistent and prolonged diastolic hypertension
results in a significant increase in heart size, ECG changes and a significant impairment of the
retina. Moderate hypertension (diastolic blood pressure less than 100 mm Hg) usually has little
effect on the clinical picture of the National Assembly. Heavy and especially malignant
hypertension with persistent high diastolic blood pressure, swelling of the retina, brain and heart
complications worsens the clinical course of the NA and accelerates the development of renal
failure
RESPIRATORY SYSTEM
The clinical manifestations expressed nephrotic syndrome include one-or two-sided
hydrothorax, frequency is 10-29,1%, and with a targeted X-rays of even 46.8%. At the same time
nephrogenic pulmonary edema described only in single patients with nephrotic syndrome and
adequate renal function. In the presence of hydrothorax patients may show changes in the shape of
the chest, its asymmetry, backlog in breathing affected part of the chest, the weakening or absence
of voice trembling. In marked accumulation of fluid percussion on the back of the chest reveals the
three zones of the apex defined clear lung sounds, from the base of the lungs - the absolute stupidity
and between a zone of relative deadened sound. Over the zone of absolute stupidity souffles are not
defined or sharply weakened. When a unilateral process bodies mediastinal shift away from the
affected side. Pleural fluid in the nephrotic syndrome consists mainly of transudate.
DIGESTIVE SYSTEM
Against the background-onset nephrotic syndrome, accompanied by a sharp and deep disturbances of
homeostasis, all exchanges is undergoing some changes and digestive system, its parenchymal organs.In patients with
nephrotic syndrome is formed nephrogenic gastropathy, not without some features. According fibrogastroscopy it early
enough and deeply affects antrum and faster than with other forms of chronic glomerulonephritis, is transformed into
total (common) atrophic gastritis with frequent erosion of the mucous membranes of the stomach and duodenum.
Ulcerative defects in the stomach and duodenal bulb are rare.Are frequent complaints of heaviness in the epigastrium,
nausea, flatulence, and if the National Assembly expressed significantly, then the pain in different parts of the abdomen.
An objective study often distended abdomen, palpation it is often painful, but without a clear localization of pain. This
syndrome, which develops in the nephrotic syndrome, due to both structural changes in mucosa of the small intestine edema, atrophy of the villi, and the addition of infection, often opportunistic flora of Escherichia coli. A significant
decrease in the total suction surface of the small intestine due to edema, a violation of the adsorption properties of
mucous membranes, due to atrophy of lead, on the one hand, to a breach of hydrolysis in the small intestine (wall
suction), and on the other - to reduce the intensity of the absorption nutrients. Lack of absorption of nutrients, especially
protein, further adding hypoproteinemia already available in these patients. Violation of the protein contributes to the
increase in the balance of edema, and also leads to various trophic and metabolic disorders.Observed functional and
morphological changes in the liver. In hepatocytes reveal fatty, hyaline vacuolar degeneration, and sometimes necrosis.
Violation of the excretory function of the pancreas in the nephrotic syndrome accompanied by an increase in serum and
duadenalnom contents of lipase, amylase, trypsin, in some patients. Hyperproduction of the key enzymes of the
pancreas is likely adaptive functional and can be partly related to altered permeability of the cell structure of the
body.Some authors divide the nephrotic syndrome to full and part-time. Under incomplete nephrotic syndrome refers to
the absence of symptoms 2.1. This subdivision is very conditional, because the clinic is often a transition from one
version to another. The "fullness" syndrome does not depend on the severity and nature of the morphological changes
and usually the difference in the effectiveness of steroid therapy is absent.The extent of all forms of nephrotic syndrome
can range from mild to severe. Mild complaints patients may not present, or more often they are concerned about the
general weakness. The general condition is satisfactory, work capacity is preserved. No swelling, but in the morning can
be pastoznost face. Blood pressure is normal. The only manifestation of nephrotic syndrome in this case is high,
generally selective proteinuria (up to 5 g / l), which is often found by accident during routine inspections. In moderate
to severe observed a full-blown nephrotic syndrome. Dominated by symptoms such as widespread edema, oliguria,
edema fluid accumulation in the free body cavities.A kind of "watershed" moderate or severe nephrotic syndrome is the
serum albumin content of 20 ± 0,1 g / l. At the level of albumin less than 20 g / L in more severe manifestations of the
classic symptoms of nephrotic syndrome, high frequency and characteristics of complications, lower efficiency of
immunosuppressive therapy, the severity of the outcome. As the progression of nephrotic syndrome, a qualitatively new
system changes homeostasis, often irreversible. Formation of nephrotic syndrome can be lengthy and stormy.
9
Diagnosis and differential diagnosis
In identifying the NA may be useful "blister test Aldrich", introduced in the / skin isotonic
sodium chloride (0.2 ml) was absorbed in 1-2 minutes, instead of the 40-50 minutes. In the study of
urine determined increase in the proportion of urine, significant proteinuria - more than 3.5 g / day,
hyaline and granular cylinders, hematuria. Proteinuria was observed in the majority of renal disease
- acute and chronic glomerulonephritis, amyloidosis, kidney disease in systemic connective tissue
disease, renal vein thrombosis, hypertension, atherosclerotic nephrosclerosis, congestive kidney.
The main mechanism of proteinuria - increasing filtration of protein damage due to glomerular
basement membrane. Genesis of glomerular proteinuria should assume an average or severe
proteinuria, when combined with its cylindruria, hematuria. In identifying isolated proteinuria to
differentiate between amyloidosis, multiple myeloma, nephrotic form of chronic
glomerulonephritis. The combination of proteinuria with hematuria is typical of acute
glomerulonephritis, rapidly progressive glomerulonephritis, a mixed form of chronic
glomerulonephritis. When a latent form of chronic glomerulonephritis proteinuria and hematuria
expressed moderately.Diagnostic value of the cylinder is large enough. They are indicators of the
defeat of the nephron, as formed in the tubules and are therefore only of renal origin. They indicate
the presence of proteinuria, even if its level is not very high. They can be used to judge the degree
of destruction of tubular epithelium. In diseases such as kidney disease, acute and chronic
glomerulonephritis, diffuse connective tissue diseases, NA, nephrosclerosis urinary sediment is
usually combined - combined with hematuria cylindruria.In the blood analysis in the development
of the National Assembly may experience anemia due to dilution anemia, increased white blood
cells, neutrophils, erythrocyte sedimentation rate, as a result of activity of the process. An important
feature of the National Assembly - hypoproteinemia, disproteinemia to decreasing albumin and
increased number of alpha - and beta globulins, hyperlipidemia, hypercholesterolemia, increased inlipoprotein triglycerides. May increase the level of urea and creatinine, which also reflects the
active stage of the disease.When the National Assembly often develop changes in the state of
coagulation and blood prtivosvertyvayuschey systems, parameters of haemostasis, which is
reflected in the increase in the fibrinolytic activity and reduced fibrinogen, increased prothrombin
index, increased platelet aggregation as well as red blood cells. Immunological disorders are
expressed in reduction of T and B lymphocytes, the detection of circulating immune
complexes.Determined by ultrasound symmetrical enlargement of the kidneys, renal parenchymal
edema. Parameters radioisotope studies indicate parenhimiatozny type of violation.These additional
methods of study: systolic and diastolic blood pressure, blood pressure stable, hardly corrected
antihypertensives. On the ECG is usually detected pathology, mainly due to non-specific changes of
the myocardium (reduction of wave amplitudes T) and less - signs of left ventricular hypertrophy.
One third of the patients ECG defined indications for coronary pathology, whose frequency in
patients with nephrotic syndrome is much higher than in similar populations vozvrastnyh on
echocardiography - signs of left ventricular hypertrophy, hemodynamic, ocular fundus - angiopathy
and retinopathy.
Nephrotic syndrome in amyloidosis.
The appearance of the nephrotic syndrome in amyloidosis, which is expressed on average in
60% of patients with renal amyloidosis, marks the already difficult stage of amyloidosis. Nephrotic
syndrome is formed early, half of the patients - in the first 3 years. During this period, the patient
has edema occurring sporadically at first, but quickly spread and take stubborn, remaining
significant even in terminal uremic period. Development of nephrotic syndrome is usually gradual,
after proteinuric stage. Sometimes revealed "incomplete" nephrotic syndrome, when massive
proteinuria no edema, which may be associated with infiltration of amyloid adrenal glands and loss
of sodium. Some patients with amyloidosis formation of nephrotic syndrome can be a quick, often
triggered by intercurrent infection, vaccinations, etc. In this case, if the earlier stage of amyloidosis
was not timely identified, misdiagnosed acute nephritis or exacerbation of chronic
glomerulonephritis.Features of the clinical picture of nephrotic syndrome are related, on the one
hand, with the many manifestations of the disease, in which developed secondary amyloidosis, the
other - the very features of amyloidosis. Thus, in contrast to other renal disease, amyloidosis is
10
more characteristic hypotension, although high blood pressure can occur in 10-12% of patients,
hypertension differs benign course and has no prognostic significance. Characterized by disorders
of the gastrointestinal tract, diarrhea is often manifested as a result of dysbiosis, malabsorption
syndrome. The accumulation of amyloid in the liver and spleen does not violate their functions, but
in 60-70% of patients with an enlarged liver, among 35-40% of patients - spleen. Usually their
palpation painless, dense texture.Reliable sign of amyloidosis - increase the size of the kidneys in
the X-ray examination, which often do not decrease even with the development of renal failure. At
the stage of terminal renal failure in amyloidosis remains nephrotic syndrome. Patients with
secondary renal amyloidosis die at a relatively lower level of creatinine than in glomerulonephritis
from various complications.Peripheral blood reveals a sharp increase in erythrocyte sedimentation
rate, often greater than 50 mm / h, there is a tendency to anemia. In the urinary sediment, according
to the degree of proteinuria, detected cylindruria. Often found microhematuria and leukocyturia,
with amyloid lesions of the bladder may be a gross hematuria. Almost always reduced the
concentration of kidney function, which can be detected even in the proteinuric
stage.Dysproteinemia character may depend on the characteristics of a predisposing disease, which
led to the development of amyloidosis (rheumatoid arthritis, tuberculosis, etc.), but for most of
amyloidosis characterized by increased 2 and α
γ -globulins, fibrinogen serum.Lipid
metabolism may be significant, although not as high as in chronic nephritis, nephrotic type.
Immunologically may be a reduction in the total complement and increased IgAStudies have shown
that the 5-and 10-year survival of patients with secondary amyloidosis is respectively 77 and 44%,
life expectancy - 13.3 years. The closest prediction of secondary amyloidosis (in terms of 5-year
survival rate) is the same regardless of predisposing disease, while remote (10-year survival rate) is
determined by predisposing disease, significantly improved with the possibility of its effective
treatment, especially treatment. In 72% of patients with secondary amyloidosis the main cause of
death was uremia, in 28% of cases the cause of death was the progression of the disease
predisposing (especially in cases of tumor) or its complications. According to the same authors
amyloid nephropathy prognosis is less favorable in those cases where it first appears after the age of
30 years old and proceeds with clinical signs of generalization of amyloidosis, especially when
combined with diarrhea, kidney disease and / or hypotension. In the latter case, the average life
expectancy of patients, figured on the basis of life tables from the detection of proteinuria constant
was the lowest - 4.6 years.More pronounced changes in the digestive system are observed in
patients with nephrotic syndrome on the basis of hereditary amyloidosis in periodic disease. Various
dyspeptic disorders in the development of amyloidosis have been reported in 20-22% of cases, the
violation of the chair in 67% of patients, with the development of chronic renal failure clinical
manifestations gastroenteropathy becoming brighter. With the development of amyloidosis in
patients with periodic disease there is a significant parallel reduction of acid and enzyme
production, and according to the light-optical studies, such changes often ahead of the
morphological changes of the mucosa.Joining malabsorption and maldigestion worsens the
condition of patients with nephrotic syndrome and determines the prognosis of the disease. The
average life expectancy for patients with hereditary amyloidosis, was 6,8 ± 1,2 years, when
combined with the defeat of the intestine - 5,3 ± 1,4 years, with a combination of nephropathy,
intestinal lesions and hypotension - 2,3 ± 1, five years. Among the causes of malabsorption
syndrome in hereditary amyloidosis indicates a reduction of blood flow, damage to small blood
vessels of the mucous membrane, destruction of glandular tissue, due to the massive deposits of
amyloid in the mucosa, the defeat of the nervous system and the lack of segmented reductions
muscle membrane which results in the rapid evacuation of the intestinal contents, the deposition
amyloid in the capillaries of the villi and in the vessels, Entangling crypt. Almost half of the
patients with amyloidosis of the intestine revealed intestinal dysbiosis, with the development of
chronic renal failure dysbacteriosis detected in all patients.Reliable method of diagnosis of
amyloidosis is renal biopsy. In 75% of amyloid can be detected by a biopsy of the intestine, liver
50%, 20% gum.
11
Nephrotic syndrome in diabetes mellitus.
It is important specific kidney in diabetes develops when insulin-like form, and in patients
suffering from non-insulin dependent diabetes mellitus.The first clinical signs of diabetic
glomerulosclerosis occur after 10-12 years after the occurrence of insulin-dependent diabetes
mellitus, but this complication is often found in patients who have diabetes prescription is less than
2 years at the same time may develop diabetic glomerulosclerosis against latent diabetes. The
severity of diabetes does not always correlate with the severity of diabetic glomerulosclerosis.The
earliest sign of diabetic glomerulosclerosis in the clinical stage of the disease is glomerular
proteinuria, the first time wearing a fickle and selective. In the future, the degree of selectivity is
gradually reduced. With a decrease in glomerular filtration rate 45 ml / min proteinuria gets mixed
(glomerular and tubular) character at the expense of protein reabsorption in the proximal
tubule. Massive proteinuria over 3.5 g / day in patients characterizes the development of nephrotic
syndrome, which is prognostically severe clinical sign of diabetic nephropathy. Advanced nephrotic
syndrome in diabetes occurs in 6-30% of cases and has a number of features. Usually it is formed
gradually, has all the characteristic clinical and laboratory findings. Edema in the nephrotic
syndrome are unusually high and refractory to treatment with diuretics, which may explain a more
pronounced delay of salt and water. Deterioration of renal function helps increase blood pressure,
which is found in 60-90% of cases of diabetic glomerulosclerosis degree of high blood pressure is
directly correlated with the severity of proteinuria. Thus, in the initial stage of the disease blood
pressure is usually in the normal range, then in clinical manifestations of its rise is detected in more
than half of patients. In the terminal stages of hypertension observed in all patients. There are
differences in the magnitude of hypertension - in clinical manifestations, it is typically less than
180/100 mm Hg, and in the terminal is higher than 200/110 mm Hg The pathogenesis of
hypertension in diabetes is not associated with activation of the renin-angiotensin-aldosterone
system, there are numerous data on the normal or more reduced plasma renin activity in patients
with insulin-dependent diabetes mellitus. A role in the development of hypertension is the primary
renal sodium retention with a subsequent increase in blood volume and the accumulation of sodium
in the vascular wall.Distinguish between slow and fast progressing versions of diabetic
glomerulosclerosis. The most common first one. In this case, the disease is characterized by the
slow development of symptoms. The first signs of disease appear gradually. Most often it appears
intermittently proteinuria, which in a few months, and sometimes years, becoming a stable, nonselective, the number lost by the urine protein. It has always found quite pronounced changes in the
retina. However, during this period, with good correction of diabetes may periods of relative
improvement, which show a decrease or even vanishing for a while proteinuria. In the future, these
periods of remission gradually reduced in length and identifies patients with less frequent, joins
progressive hypertension and can be displayed nephrotic syndrome. Relatively rare, but in young
patients, there are cases of rapid progression. These persons have badly adjusted (decompensated)
diabetes that requires the use of large doses of insulin. In patients with proteinuria increases rapidly,
which will soon become stable and nizkoselektivnoy. Already after 1-3 years from the first signs of
developing hypertension and edema occur. Usually this category of people is growing rapidly, and
progressive renal failure.With the constant proteinuria begins to steadily decline of glomerular
filtration rate of 1 ml / min per month. At this stage of the clinical manifestations of the correction
of hyperglycaemia can no longer stop the further increase in proteinuria, as morphological changes
become irreversible. Characteristic is the preservation of a high proteinuria, and edema, even in the
development of end-stage renal failure.In diabetic nephropathy, the mechanism of development of
hypertension includes a whole range of violations. All changes, developing diabetes with insulin
(endocrine, metabolic, and immune), contribute to the development of hypertension in diabetic
nephropathy, and the impact of these disorders is not so much direct as indirect. The value of the
morphological changes of the kidneys (glomerular sclerosis and interstitial renal juxtaglomerular
apparatus increased activity and reduced activity of interstitial cells medulla) is undeniable. Strong
influence on the development of hypertension in diabetes have not only glomerulosclerosis, but
generalized diabetic microangiopathy, culminating hyalinosis of microvessels, primarily arterioles.
Great value and a spasm of vascular smooth muscle cells, characteristic of diabetes appearance of
12
nephrotic syndrome, atherosclerosis, chronic pyelonephritis, and the accession of secondary
infections aggravate during diabetic glomerulosclerosis, leading to the rapid development of renal
failure. According to most researchers, chronic renal failure is the leading cause of death in patients
with insulin-dependent diabetes at the age of 40. Of the patients with advanced kidney disease die
from uremia 80%, of a heart attack - 10% and other causes - 10%.
Nephrotic syndrome in SLE
Lupus nephritis is a typical example immunocomplex kidney damage caused by the
deposition in the kidney of circulating immune complexes containing DNA and antibodies to
DNA.The clinical picture of lupus nephritis - from persistent minimal proteinuria does not affect the
well-being of patients and does not substantially affecting the prognosis to severe subacute nephritis
with nephrotic syndrome, hypertension, and renal failure, rapidly leading to death of the
patient.With a full-blown systemic lupus connection at some stage renal disease characteristic only
confirms the diagnosis, but often there are times when kidney in systemic lupus erythematosus
clinical acts to the fore in the absence or minimal expression of other symptoms of SLE.Lupus
nephritis is the most common monorgannym SLE onset, 10-25 percent of patients, it is one of the
first signs of the disease. Nephrotic syndrome usually develops in the first years of the current FCC.
Prognostic significance period elapsed prior to the development of renal NA, in patients who died
between the beginning of lupus nephritis and the emergence of the National Assembly was
significantly lower than that of the survivors. Involvement of the kidneys in the process depends on
the course of SLE: acute disease the development of lupus nephritis was observed in the first year
of the disease SLE, subacute - to 3-4 and chronic 8-10-year.Of the clinical features of the nephrotic
syndrome in lupus nephritis is worth noting rarity very high proteinuria, nonselective her character.
Pyuria may be a sign of inflammation in lupus kidney, and the consequence often joining secondary
urinary tract infections. Study leukocyte urine sediment helps to differentiate exacerbation of lupus
nephritis (with marked limfotsituriey) from secondary infection (prevalence of
neutrophils).Peripheral blood reveals leukopenia and lymphopenia with aneozinofiliya,
thrombocytopenia, accelerated ESR, or hemolytic hypochromic iron deficiency anemia.The
amendments proteinogram observed certain laws concerning the content of globulin fractions
having both diagnostic and prognostic value. In contrast to nephrotic syndrome in primary
glomerulonephritis and amyloidosis, which are highly hyper2 globulinemiya reaching 4050%, with lupus nephritis hyper2 globulinemiya usually expressed mild, average content of
16.8 %. The low content of
2-globulin is an unfavorable prognostic sign. Of gamma-globulin,
in contrast to other causes of nephrotic syndrome, however, increased, and it is also a bad
prognostic sign, reflecting greater activity of lupus nephritis.Feature of lupus nephrotic syndrome is
also a rare high-cholesterol hypercholesterolemia rarely exceeds 10,3-12,9 mg / dL. It is possible
that in SLE with her usual system defeats the development of high hypercholesterolemia, prevents
liver damage, responsible for the synthesis of lipids.Also characteristic of lupus nephrotic syndrome
is a frequent combination with hypertension and hematuria.Isolation of rapidly lupus nephritis with
nephrotic syndrome, hypertension (sometimes malignant), early development of renal failure is
dictated by a poor prognosis, the similarity of the clinical picture and course of other aggressive
type of jade, as well as the need to use massive therapy. The frequency of rapidly jade among all
cases of lupus nephritis is 10-12%. About 50% of patients die within the first two years of
onset.Thus, we can speak of certain clinical and laboratory features of lupus nephrotic syndrome
who have both diagnostic and prognostic value. They are:1) the development of nephrotic syndrome
in young women;2) for the type of subacute nephritis with a fast connection of hypertension and
renal failure;3) the severity of hematuria;4) non-selective nature of proteinuria;5) unusual for a
classical character dysproteinemia nephrotic syndrome - unusually high hyper2 globulinemii
and frequency of hyper-globulinemii;6) normal or moderately elevated serum
cholesterol.Prognosis of patients with lupus nephritis with nephrotic syndrome is very serious,
although it is better than the prognosis of patients with Bright's nephritis with nephrotic syndrome,
which can be explained, on the one hand, the greater the severity of immune mechanisms and,
therefore, greater efficacy of immunosuppressive therapy, and greater persistence in carrying
13
immunosuppressive therapy. On the other hand, may play a role, and some features of the nephrotic
syndrome in lupus nephritis, for example, reduces the risk of recurrence.
The vast majority of patients with kidney disease was the direct cause of death. According to
various authors 10-year survival of patients with lupus nephrotic syndrome is 65-70% When
connecting hypertension prognosis worsens and the 10-year survival rate is 44-59%.
DRUG Nephropathy
The problem of drug therapy is extremely urgent and now attracts the attention of a wide
range of specialists. Continuous expansion of the arsenal of drugs over the past decade,
accompanied by a progressive increase in the number of cases with combined or isolated
involvement of different organs, resulting from the use of drugs in normal doses.As a result, a wide
spread of high pharmacological agents used in the treatment of patients, the most dangerous branch
of medicine has clinical pharmacology. According to various authors, 18-30% of patients who are
hospitalized, there are various side effects with the use of different drugs that are about a quarter of
them are fatal. Kidney, as a manifestation of medical complications, is less common than the
damage of the bone marrow or liver, but their appearance dramatically aggravates the
prognosis.Vulnerability buds due to a number of factors:1) high renal blood flow (about 25% of
cardiac output);2) high intensity, metabolic and transport processes in the tubular cells;3) most of
the drugs out of the body through the kidneys, the concentration of drug to be filtered at the
glomerulus, increases as the concentration of the glomerular filtrate, also highlights the kidney
drugs (like any other xenobiotics) by not only filtering and tubular secretion, significantly increased
the concentration of substances in the tubular cells;4) many drugs have a direct nephrotoxicity,
concentration of nephrotoxic agents increases with worsening renal function.Accordingly, various
mechanisms of effects on the renal parenchyma are the following variants arising during drug
therapy of renal changes:1) Drug kidney drug nephritis, kidney allergies, anaphylactic nephritis kidney disease of allergic origin, often combined with other forms of drug-disease;2) toxic
nephropathy or nephrotoxic nephritis - any violation of functional or morphological state of the
kidneys caused by the action of chemical or biological substances and agents that form toxic
products of the metabolism;3) Drug nephropathy - a combination of toxic and allergic processes or
predominance of one of them.Medicinal glomerulonephritis allergic genesis occur very rarely
following administration of serums and vaccines. Like other immune destruction, they are
associated with immune renal disease and the reactivity of the organism, often accompanied by
systemic manifestations (damage skin, joints, blood system, gepatolienalny syndrome serozity).
Nephrotic syndrome in this develops through the restructuring of the basement membrane antigen
and tubular epithelium in sensitized body upon repeated administration of antigen. Clinically
nephrotic syndrome in drug-disease appears most often edema and proteinuria, at least disproteinemia, hyperlipidemia and giperlipiduriey. The combination of these changes with other
well-known manifestations of the disease of drug facilitates correct assessment of nephrotic
syndrome.Nephrotic syndrome in medical nephropathy caused most often in the treatment of drug
gold, bismuth, anticonvulsants, captopril, develops most often gradual. Histologically, while often
revealed membranous nephritis, although there may be more severe cases with deposits on the
basement membrane, but without circulating immune complexes, suggesting a local - in situ - their
education. "Gold nephropathy" histologically characterized by different morphological variations
(often develops membranous nephritis, at least - minimal changes mezangioproliferativny
glomerulonephritis), different benign course with complete normalization of urine after an average
of 11 months after drug withdrawal gold.
Paraneoplastic nephropathy
The peculiarity of cancer pathology is the lack of typical symptoms of tumor in the initial
stage of the disease. Such common complaints as loss of appetite, fatigue, intermittent fever, often
interpreted as a result of overwork or any infectious disease, and in combination with pathological
findings in urine is usually diagnosed by an independent renal disease. However, has long been
known that malignant tumors of different localization, in addition to symptom caused by the direct
localization of tumor or its metastases, may be accompanied by clinical symptoms associated with
non-specific reactions caused by the tumor. These reactions are so-called paraneoplastic syndrome,
14
are extremely diverse - from local changes in the skin, arthralgia, fever, myalgia, hematological
disorders (anemia and polycythemia, thrombocytosis, and thrombocytopenia, leukemoid reaction)
to the expanded features of systemic disease resembling different diseases (rheumatoid arthritis,
dermatomyositis, and others).In paraneoplastic process involved and the kidneys, sometimes the
"isolation", so you need to keep in mind the possibility of "nephritic masks" of various
tumors.There are the following options for renal tumor diseases:1) amyloidosis;2) the type of
nephropathy glomerulonephritis (paraneoplastic nephropathy);3) metabolic acidosis and alkalosis4)
Electrolyte disturbances with the development of nephrocalcinosis and gipokaliemicheskoe
kidney;5) the metabolism of uric acid and urate renal tubular obstruction or the development of
interstitial nephritis;6) the toxic effect of Bence-Jones protein or blocked them tubules;7)
lizotsimuriya.The characteristic clinical feature of paraneoplastic nephropathy is nephrotic
syndrome, with all its typical characteristics and the rapid development of chronic renal failure. He
may be one of the first (and only kidney) symptoms of tumor, but often long regarded as a
manifestation of paraneoplastic process, although the formation of nephrotic syndrome in tumors is
not such a rare phenomenon.If paraneoplastic nephrotic syndrome detected simultaneously with the
tumor or after its discovery, in such cases, it is usually treated properly. However, the important fact
is the possibility of it long before the tumor itself manifest. Misinterpretation of paraneoplastic
nephrotic syndrome leads to inappropriate prescription corticosteroid therapy, reinforcing the
generalization process and to delay surgery. Timely antitumor treatment itself can cause regression
of the nephrotic syndrome.Morphological substrate of nephrotic syndrome in tumors may be renal
amyloidosis and paraneoplastic nephropathy (type of glomerulonephritis). Sometimes on the
specifics of the tumor can distinguish these options nephropathy. Thus, the more common
carcinomas (bronchogenic carcinoma, colon cancer, ovarian cancer) is usually accompanied by a
paraneoplastic glomerulopathy, a rare cancer (cancer of the renal parenchyma, Hodgkin) amyloidosis.Paraneoplastic renal amyloidosis in most cases shows a typical nephrotic syndrome,
which quickly (within a few weeks or months) replaces proteinuric stage. Among the pathogenic
mechanisms of paraneoplastic amyloidosis suggest immunosuppressive tumor growth, tumor decay
constant antigenic stimulation, the production of amyloid precursor directly by the tumor, infection
joining to cancer. With all the hypotheses of the pathogenesis of a direct relationship of tumor with
paraneoplastic amyloidosis confirmed by observations of regression of clinical manifestations of
amyloidosis after complete resection of the tumor, and recurrence of nephrotic syndrome in patients
operated on earlier in connection with the new formation may indicate a tumor recurrence or
metastasis. Appointment of corticosteroids in paraneoplastic amyloidosis dramatically accelerates
the course of amyloidosis and the development of chronic renal failure.Paraneoplastic nephropathy
(glomerulonephritis type) differs from the usual jade greater frequency of typical nephrotic
syndrome and rapid onset of renal failure. In such a quickly progressing for malignant renal disease
should always exclude it paraneoplastic genesis and conduct a targeted examination of the patient,
which is found in most cases a bronchogenic lung cancer, tumors of the gastrointestinal tract,
pancreas, gynecological. Pathogenesis of paraneoplastic glomerulopathy is not entirely clear: The
possibility of immunocomplex of membranous nephropathy with tumor antigen, suggests a
metabolic mechanism of paraneoplastic nephrotic syndrome (deficiency L-asparagine).
Morphological variants of paraneoplastic glomerulopathy diverse, while there are no laws of their
combination of features of the tumor. The most common kidney disease with paraneoplastic
membranous glomerulonephritis characterized мембранознопролиферативными or changes to the
typical subepithelial electron-dense deposits, Immunohistochemical study revealed deposits of IgG
and IgM and C3 fraction of complement.Thus, the selection "kidney masks" paraneoplastic
reactions is of great practical importance, since it allows a shorter time and more specifically
examine the patient and take appropriate treatment.Paraneoplastic etiology of renal disease can be
suspected sudden occurrence of nephrotic syndrome in a patient older than 40 years of rapidly
during nephropathy with a rapid succession of stages of renal lesions, detection of renal biopsy
membranoproliferative or membranous-proliferative or amyloidosis in the absence of reasons for
secondary amyloidosis.
Myeloma nephropathy
15
Multiple myeloma (multiple myeloma, generalized plasmacytoma, disease Rustitskogo
Calera) - the most common disease in the group paraproteinozov characterized by the proliferation
of a single clone (monoclonal) plasma cells with hyper homogeneous immunoglobulins or their
fragments.The disease occurs most often between the ages of 40 to 70 years, more often affects
women. Its frequency is 1:100,000 per year.Proliferation of plasma cells in the bone marrow leads
in most cases to razrusheniiyu bone as myeloma cells produce osteoklastaktiviruyuschy factor.
Destruction in the first place are flat bones, vertebrae and proximal long bones. The defeat of the
flat bones appears oval or round bone defect corresponding to form tumor nodules, without reactive
changes. Myeloma defects not replaced newly formed bone substance, so that frequent bone
fractures. In the diffuse distribution process osteoporosis. The result of bone is hypercalcemia and
hypercalciuria, hyperphosphatemia, and elevated blood alkaline phosphatase.The second
manifestation of multiple myeloma paraprotein is overproduction and their impact on the patient.
One manifestation is paraproteinemii paraprotein deposition in tissues and development
paraamiloidoza. In contrast, secondary amyloidosis, paraamiloidoz organs affected, rich collagen
(skin, periarticular tissue, etc.). The clinical picture is characterized paraamiloidoza macroglossia,
skin infiltrates. Syndrome protein pathology manifests dryness of the skin, against the peripheral
blood flow in the form of Raynaud's syndrome. Develops hyperproteinemia by paraproteins. A
characteristic feature is the presence in the plasma and urine unusual body proteins - M-proteins,
which are the product of the modified plasma cells and their physical and chemical properties
similar to normal immunoglobulin and differ from them only in structural construction. Specific for
multiple myeloma is the Bence-Jones protein, consisting of the light chains with a molecular weight
of from 25,000 to 40,000, which is why it is easy to pass urine.The third manifestation of multiple
myeloma - Hematology - anemia, leukopenia, thrombocytopenia due to growing tumor in the bone
marrow.The fourth clinical syndrome - kidney disease, which is the most common visceral
pathology in multiple myeloma and largely determines the prognosis. The frequency of multiple
myeloma nephropathy, according to different authors, from 30 to 50% and even up to 80%, and in
the terminal stage of the disease is detected in almost all patients.In the development of kidney
disease in multiple myeloma following act as pathogenic factors:1) pathological overproduction of
immunoglobulin light chains and their accumulation in the distal tubule, possibly with a direct toxic
effect on the cells of the proximal and distal tubules;2) hypercalcemia distortionary concentrating
ability of the kidneys, nephrocalcinosis;3) hyperuricemia.Most early and constant symptom
myeloma nephropathy - proteinuria, which is revealed in 70-90% of cases. Characterized the steady
progression of proteinuria, sometimes reaching high values without developing hypoalbuminemia
and hypercholesterolemia. Formation of nephrotic syndrome is very rare and only in the
development of amyloidosis. Histologically detected with mesangial and subendothelial amyloid
deposition in the glomeruli. Electron microscopy revealed typical amyloid fibril structure.
Amyloidosis occurs in multiple myeloma, according to various sources, in 10-14% of patients. The
main cause of amyloidosis - neoplastic transformation of cells synthesizing abnormal
immunoglobulins. Amyloid fibrils are composed of fragments of immunoglobulin light chains.
During the nephrotic syndrome in multiple myeloma is often complicated by a variety of infections
due to impaired immune status of these patients, progressively increases renal failure.
Complications of nephrotic syndrome.
Nephrotic syndrome rarely occurs without complications, it can be considered a kind of a
risk factor for various complications. Complications of nephrotic syndrome can be divided into
spontaneous and iatrogenic, that is provoked by the activities of physicians.Spontaneous
complications depend on the severity of renal disease, the nature of the underlying disease and the
severity of the nephrotic syndrome. The frequency of infections were in doantibakterialnuyu era
leading cause of death in patients with nephrotic syndrome due to a sharp drop in immunity and
resistance to infection due to the loss of immunologically active proteins in the renal filter,
including the diversion of circulating antibodies of complementary proteins. Reduced immunity
compounded using immunosuppressive therapy. Among the most frequent infectious complications
of recurrent respiratory infections, pustular skin lesions, pneumonia, pleurisy (often encysted),
transformed from recurrent hydrothorax, especially after repeated evacuations pleural fluid, with the
16
possible development of pleural empyema. Infection may contribute to the development of
disorders of the skin tselostnosti (cracks edematous skin, injection site). One of the most serious and
severe complications is pneumococcal peritonitis, which currently is extremely rare due to the
timely administration of antibiotics. Bacterial peritonitis must be differentiated from abdominal
nephrotic crisis - one of the initial symptoms of hypovolemic shock.
Nephrotic called crisis of sudden development peritonitopodobnyh symptoms with fever
and rozhepodobnymi skin changes, dramatically worsening the condition of patients with severe
nephrotic syndrome (anasarca, dropsy of serous cavities, hypoproteinemia to 35 g / L,
hypoalbuminemia to 8.4 g / l), with the progression of which develops hypovolemic shock with
collapse and the possibility of a fatal outcome. Nephrotic crisis complicates the course of nephrotic
syndrome of various etiologies, but most often occurs in patients with lupus nephritis and Bright.
The main pathophysiological link nephrotic crisis is hypovolemia. In the pathogenesis of nephrotic
crisis predominant role given to the accumulation in the blood and edema fluid of vasoactive
substances that cause vasodilation, which increases vascular permeability, and also leads to the
progression of hypovolemia. Perhaps in the early stages of the nephrotic syndrome in the initial
increase in vascular permeability, the role belongs to the cellular factors (leukocyte) and
biologically active amines (histamine), but later, when, in response to the massive proteinuria
synthesize increased amounts of precursor proteins (prekallikreinogen) and kininogenov, conditions
to activate the kinin system, the final product of which (bradykinin) increases vascular permeability
and gives painful effects. Hypovolemic shock nephrotic feature is the connection sharp decrease in
blood volume with increased vascular permeability and plazmorragiey while increasing the
extracellular fluid volume in the body. Since the process of extravasation occurs gradually, the
clinical picture of hypovolemic shock is usually preceded by several stages of nephrotic crisis. The
first signs of nephrotic crisis are anorexia, nausea, vomiting unmotivated. Next in sequence or
simultaneously an intense abdominal pain and rozhepodobnye migratory erythema. Often the
symptoms of nephrotic crisis combined with a variety of clinical disorders of hemostasis (local
intrarenal intravascular coagulation, peripheral phlebemphraxis, during shock with DIC), which
complicates the differential diagnosis of nephrotic crisis and its treatment. Nephrotic crisis observed
in 6.2% of cases of nephrotic syndrome of various etiologies. Its development may be triggered by
intercurrent infection, fatigue, injury, thrombotic complications of nephrotic syndrome.The clinical
picture of abdominal pain crisis creates great diagnostic difficulties as abdominal pain have no strict
localization. Palpation of internal organs is difficult because of the large ascites. There may be mild
symptoms of peritoneal irritation. Occurrence of abdominal pain accompanied by fever (intermittent
or subfebrile). The patient is conscious, anxious, may be vomiting and diarrhea. There is marked
leukocytosis, leukocyturia, sometimes strengthening microhematuria. These features require a clear
differential diagnosis with a number of urgent conditions that arise in the nephrotic syndrome,
particularly for the glucocorticoid and cytotoxic therapy: bacterial peritonitis, perforated gastric
ulcer, acute appendicitis, ovarian cyst rupture, thrombosis of mesenteric vessels, renal veins or other
branches of the inferior vena veins, tuberculosis mezadenitom, abscess and carbuncle kidneys, acute
crisis of local intrarenal intravascular coagulation, and the main of which is the earliest
manifestation of acute renal failure. Many issues such a wide differential diagnosis can be removed
diagnostic abdominal puncture. In patients with a true crisis of nephrotic peritoneocentesis provides
a transparent foaming from the presence of protein in it and slightly opalescent on the presence of
lipids sterile liquid with all the properties of a transudate, which identifies high levels of histamine,
serotonin and bradykinin.Great difficulties arise in the differential diagnosis of renal vein
thrombosis, and other branches of the inferior vena cava, the more that can be accompanied by
acute thrombosis of shock and consumption coagulopathy, and therefore attach great importance to
determine the volume of circulating blood. BCC reduction to 60-55% of normal to diagnose
developing hypovolemic shock and take the necessary therapeutic measures. Signs of shock are
weakness, tachycardia, low body temperature, oliguria, acidosis, hypoxia, hypotension progressing
up to the collapse. Hypovolemic shock, exacerbated by massive diuretic therapy, sometimes
becoming irreversible fatal character, despite all the modern methods of treatment.In addition to
abdominal pain, a manifestation of nephrotic crisis can be rozhepodobnye migratory erythema,
17
occurs suddenly on the belly skin, in the abdominal or chest wall, the front of the thigh, leg. The
appearance of erythema associated with a high fever. Skin erythema in a pale pink color, without a
sharp transition at the boundary with normal skin, hot to the touch, with symptoms of hyperesthesia.
Erythema can spot a few hours spontaneously disappear in one place and appear in another.
Dimensions erythema often in hand, sometimes more. The maximum duration of erythema in one
place 1-3 days. Titles protivostreptokokkovyh antibodies in the serum were normal. Antibiotic
therapy is not effective. In the edema fluid from the area close to the rozhepodobnoy erythema,
found histamine, serotonin, bradykinin. The differential diagnosis of erythema rozhepodobnoy
should be primarily mug, always flowing in patients with nephrotic syndrome, hard, often
protracted. By the development of erysipelas - an acute infectious process - in the nephrotic
syndrome predisposes immunosuppression, decreased phagocytic function of white blood cells and
macrophages of the skin, suppression interferonobrazovaniya, degeneration and fissures of the
epidermal sheet. It is also necessary to carry out the differential diagnosis of acute phlebitis
superficial veins, deep vein phlebemphraxis limb.Nephrotic crisis should be differentiated from the
crisis as a local or disseminated intravascular coagulation. In nephrotic syndrome, with deposition
of immune complexes and / or in situ formation of the glomerulus, inflammation with increased
vascular transudatsiey procoagulant proteins on the one hand, the functional contribution of the
kidneys is lost in hemostasis, the other - a process of local activation of coagulation with
intravascular coagulation it at certain stages able to go into disseminated process. Changes in
hemostasis in this lead to the development of acute renal failure and disseminated intravascular
coagulation. It is important to remember iatrogenic factors which cause the crisis of local and
disseminated intravascular coagulation. Thus, the occurrence of DIC causes prednisolone, aadrenostimulyatorov, e-ACC and other drugs that cause platelet aggregation, increases blood
clotting and reduces its anticoagulant and fibrinolytic potential, especially when combined
applications; misuse of anticoagulant doses causing depletion provision of antithrombin III and the
fibrinolytic system.The clinical picture of the local crisis intravascular coagulation characterized by
the appearance of pain in the stomach and waist area, gross hematuria, a sharp decrease in blood
pressure and rapid development of acute renal failure.Term DIC indicated nonspecific General
pathological process associated with entering the bloodstream activators of blood coagulation and
platelet aggregation, the formation there thrombin activation and depletion of plasma enzyme
systems (coagulation, kallikrein-kinin, fibrinolytic, etc.), education levels set microbunches and
aggregates of cells that block the circulation in the organs, leading to the development
trombogemorragy, hypoxia, acidosis, malnutrition and deep organ dysfunction, intoxication protein
decomposition products and other metabolites and often rise to secondary profuse bleeding. During
DIC may be acute, protracted, recurrent, chronic and latent.There are 4 stages of DIC:Stage I hypercoagulable state with intravascular platelet aggregation;Stage II - transition, with increasing
coagulopathy and thrombocytopenia, multi-directional changes in the overall coagulation tests;III
stage - the stage of deep anticoagulation. Characterized by the depletion mechanism of blood
clotting and the development of uncontrolled bleeding;IV stage - the stage of origin. Degenerative
changes in the organs.Clinic DIC made by symptoms of the underlying disease that caused its
development gemokoagulyatsionnogo shock (acute forms) with a fall in blood pressure, hemostatic
disorders from hyper-to gipokoagulyalyatsii, blockade of microcirculation in the target organs
(lungs, kidneys, stomach, intestines) their dysfunction and degeneration. The sharper the DIC, the
more transient and ephemeral phase of hypercoagulability and the worst of the severe
anticoagulation and bleeding. When protracted course of DIC observed in immune-disease, the
process usually begins with a long period of hypercoagulability phlebemphraxis with
thromboembolic and ischemic events in the organs. In the absence of control of the system, these
initial hemostasis disorders characterized by hypercoagulability high spontaneous aggregation of
platelets, parakoagulyatsionnymi positive tests (ethanol, protaminsulfatny), increased fibrinolysis
products and other violations inherent first phase of DIC often viewed, or are associated with local
thrombosis . And when it is the terminal period, manifested either massive and multiple thrombosis,
or acute anticoagulation and massive bleeding mainly from the gastrointestinal tract, treatment is
usually effective.The change of parameters of coagulation and anticoagulation systems in the
18
development of DIC goes through several stages. In the initial stage there is blood
hypercoagulability. Most bolnyx reduced platelet count in the blood (the acute form in 82% of
cases, chronic - in 55% of cases), increased their adhesion and aggregation properties, increased
concentration of fibrinogen, soluble complexes of fibrin-fibrinogen degradation products fibrinfibrinogen (FDP ), shortened the clotting time of blood - blood clots are often already in the needle
for blood sampling. Reduced levels of antithrombin III, decreased fibrinolytic activity of blood. In
stage II, during the fall of blood clots in the blood vessels, some coagulation tests reveal more
hypercoagulability, whereas others - hypocoagulation. Parakoagulyatsionnye (ethanol,
protaminsulfatny) tests remain elevated, elevated levels of fibrin degradation products, fibrinogen
(FDP), decreased platelet count, fibrinogen concentration decreases. Fibrinolytic activity of the
blood usually increased. Steadily decreasing levels of antithrombin III, which is one of the most
important changes in the blood coagulation system and is essential to the effective conduct of
pathogenetic therapy.In hypocoagulation stage dramatically lengthened thrombin time and violated
to some extent other coagulation parameters - clumps of small, loose or are not formed.
Exacerbated by thrombocytopenia, platelet function dramatically impaired. Parakoagulyatsionnye
tests often become negative. At this stage may develop hemorrhagic syndrome with catastrophically
severe, not controlled by therapy, bleeding. By laboratory signs of DIC include the reduction in the
number of platelets, fibrinogen and antithrombin III, increasing the time of fibrinolysis.No less
dangerous, such vascular complications of nephrotic syndrome, ischemic heart disease, pulmonary
embolism, stroke, peripheral phlebemphraxis etc. As mentioned above, in patients with nephrotic
syndrome, a significantly increased risk of progression of atherosclerosis with the typical
appearance of atherosclerotic complications. Thus, in patients with nephrotic syndrome is described
by 85-fold increased frequency of coronary heart disease, which contributes not only atherogenic
dyslipidemia direction but also naturally developing fibrinosis. Strokes in patients with nephrotic
syndrome developed in secondary fibrinolysis cerebral vasculitis and accession malignant
hypertension, often in the terminal stage.
Therapy of nephrotic syndrome
Treatment of patients with UA-hard problem, because it should be connected to the
nosological forms (etiology HC) and renal function, a term of the National Assembly, the
peculiarities of course, complications.All patients with UA to be hospitalized in the Nephrology
Unit. They are assigned to bed rest (horizontal position, to improve renal blood flow), diet number
7, 7a with fluid restriction and salt to 5 g / day., During edema up to 1-2 g / day.
Etiological principle of treatment is the most progressive. Removal of the causative factor,
infection control, removing the source of chronic abscesses, tumors, tuberculosis, diabetes itself can
cause regression of the National Assembly. Unfortunately, the etiological treatment does not always
give the desired effect and the need arises for pathogenetic therapy. For the treatment of
autoimmune genesis of the National Assembly are widely used methods and tools
immunodepresivnoy therapy.
Immunosuppressants - the means used to suppress the immune response, which in a number of
pathologic processes, including the kidneys zaboleaniyah become perverted nature, such as autoimmune
reactions. Drugs - immunosuppressive depending on the mechanism of action are combined into several
groups:
Hormonal – glucocorticoids
Alkylating agents - cyclophosphamide, melphalan, hlorbutin, tiofosfamid, mielosan.
Antimetabolites - folic acid antagonists - methotrexate, purine antagonists - mercaptopurine,
azathioprine, pyrimidine antagonists - fluorouracil, cytosine arabinoside.
Antibiotics - actinomycin, mitomycin, adriamycin.
Drugs of different mechanism of action - vinblastine, vincristine, L-asparaginase, cisplatin.
Glucocorticoids
Glyukortikoidy in nephrology administered parenterally and inside. Glucocorticoids are used
most often in the nephrotic syndrome in the 3 or 4-component circuits in patients with chronic
glomerulonephritis, SLE, lipoid nephrosis, and requires long-term therapy.3-component scheme:
GCS, antiplatelet agents, anticoagulants.Four-component scheme: SCS, cytostatics, antiplatelet
19
agents, anticoagulants. In the appointment of GCS is always important to be sure that this patient as
reasons NA excluded amyloidosis, tuberculosis, diabetes divabet, vascular thrombosis.Appointed
forms for oral administration: hydrocortisone, prednisone, dexamethasone. These drugs can be
administered orally or parenterally. Main dose corticosteroids designate rate of 1-2 mg / kg,
followed by a decline after the effect. Tablet dosage forms of drugs and easy to switch from one
drug to another by the number of tablets. Glucocorticoids are used up quickly or intermediateacting. Depending on the severity of the pathological process are appointed medium, or high doses
of hormones, the positive effect is achieved, after which the dose is reduced to an effective but
minimal maintenance. Optimal dose is 5-10 mg / day. In the period of dose reduction, the closer it is
to the maintenance, the slower it is necessary to reduce the dose of glucocorticoids.There are three
modes or three schemes of long-term treatment with glucocorticoids. Continuous treatment - taking
medication every day, but here it is necessary to take into account the circadian rhythm of
endogenous release of glucocorticoids. Their activity is minimal in the morning, increasing during
the day and in the evening rise. Therefore, two thirds of the daily dose should be appointed in the
morning, 1/3 - in the afternoon, in the evening - only for special reasons. Alternating treatment,
supporting twice the dose is taken once a day in the morning. This treatment regimen can
significantly reduce the incidence of side effects. Intermittent therapy, glucocorticoids are appointed
by short courses of 3-4 days followed by a break of 4 days. In / in is used for urgent care - "pulse
therapy." Indications yavlyutsya: high activity of rapidly form glomeruli and lupus nephritis,
nephrotic, lupus crises. The introduction of corticosteroids may be single or repeated over several
days. You can use high, even toxic doses, but cancel them immediately, because in these cases there
are no withdrawal symptoms. Methylprednisolone 500 mg diluted in normal saline or 5% glucose
injected into / in 30 minutes, repeat infusion every 12 hours. Course - 3 days. After the end of pulse
therapy, if achieved a positive effect, prescribe prednisone 50 mg 2 times a day to stabilize the
patient's condition, and then gradually reduce the dose. In appointing SCS possibility of side effects.
Immunosuppressants - cytostaticsIn nephrology of cytotoxic drugs are most often used
azathioprine and cyclophosphamide, and a new immunosuppressant cyclosporin A. They are
appointed in the case of contraindications to steroid therapy (HC with hypertension, NA
rezistenntny to steroid therapy, depending on the development of GCS), no effect on Sustainable
Integrated pathogenetic therapy development of nephrotic crisis.
Azathioprine - refers to the antimetabolites, purine antagonists, when used as an
immunosuppressant quickly progressing glomerulonephritis with the development of the National
Assembly, lupus glomerulonephritis, severe forms of chronic glomerulonephritis. The drug is
administered in a dose of 1.5 - 2.0 mg / kg per day is long enough, often in combination with
prednisone, antiplatelet and anticoagulation. In the treatment should be carefully monitored blood
count (leukocytes, platelets).
Cyclophosphamide - drug alkylating action as immunosuppressant inhibits proliferation of
lymphocyte clones involved in perverted immune response. The usual dose in these cases, 50-100
mg / day. During treatment, the blood test should be performed at least two times a week.
Cyclosporine A is a fungal peptide with a strong immunosuppressive effect. Basically it has
an effect on the early stages of activation of T-helper cells. Used mostly for kidney transplantation
and is usually combined with glyukortikoidami. The initial dose of the drug is administered in / for
4-12 hours prior to renal transplantation and continue in / infusion over 2 weeks. Then move on to
oral maintenance therapy. The initial dose is the introduction of non 3-5 mg / kg / day when
administered 10-15mg/kg/sutki. Further doses are selected by daily radioimmunoassay
determination of cyclosporin A in the blood. Side effects: renal, liver, gastrointestinal tract,
leukopenia, thrombocytopenia, fluid retention, addition of a secondary infection, infertility.
Antiplatelet agents and anticoagulants, especially applications in nephrology.
Antiplatelet agents and anticoagulants used in nephrology in the four-component scheme for
severe glomerulonephritis, when given prednisone, one of the cytotoxic drugs, heparin and
antiplatelet as chimes. Patients with chronic pyelonephritis, in some cases, it calls tiklid or
pentoxifylline. Renal vein thrombosis shown aspirin. Aspirin as an antiplatelet agent is now widely
used in ischemic heart disease, cerebrovascular disease, for the prevention of venous thrombosis.
20
Antiaggregant as it acts in small doses (0.125 - 0.25). However, the side effects of the drug,
especially ulcerogenic, still manifests. In this regard comes mikristin - granular microcrystalline
drug aspirin, enclosed in a sheath of polyvinyl acetate. Sulfinpyrazone is briefly in the application
(up to a week) reversibly inhibit platelet aggregation function, as a long - is irreversible and it is
restored when the drug and the emergence of new generations of blood platelets. Chimes increases
the production of prostaglandins in the kidney, thereby increasing their depressor function.Heparin
in nephrology is mainly used in the 4-component therapies of patients quickly progressing and
some forms of chronic glomerulonephritis. The mechanism of action, reduction of autoimmune
inflammation, reduction of cell permeability of capillaries, reducing proteinuria, decreased
aggregation and adhesion reduction in all phases of coagulation natridiureticheskoe action. The
duration of action of heparin and efficiency depend on the route of administration. At / in a duration
of 2-6 hours, the maximum efficiency; / m administration - the duration of 2-8 hours, the effect of
medium strength, § / to the introduction - the duration of 4-12 hours, the efficiency is low.As a
direct anticoagulant heparin anticoagulation to achieve recommended for use in the following way:
first in / injected 15-20 thousand units., Then a / m to 5 thousand units 4 hours or s / c at the same
dose after 6 hours. To achieve other therapeutic effects of heparin can be administered in smaller
doses - 5 thousand units 2-3 times / m or m / k Control in the treatment of heparin is through regular
study time, blood clotting, and (or) of the activated partial thromboplastin time. Both of these
figures should be 1.5 to 2 times, and on these figures should be supported. The patient should be
aware of the need to immediately inform the doctor about the slightest sign of bleeding. Regularly,
usually every other day examined the urine, in time to reveal hematuria.
Side effects. The most serious and dangerous - bleeding, at least - an allergic reaction.
Prevention of complications in the treatment of heparin consists, first, in a strict view of the
absolute and relative contraindications for the use of heparin, and second, strict and regular
monitoring of the therapy. Absolute contraindication is bleeding or hemorrhage.Edema in UA
gipoalbuitnemy associated with a sharp decline in the ability and kidneys excrete sodium, which
can be reduced by the elimination of hypoalbuminemia, albumin, fresh frozen plasma, plasmasolutions, increasing OTsKi main prescriptions, promotes the excretion of sodium.
Diuretics - especially applications in nephrology
By diuretics (diuretics) were currently the drugs that increase urine output by blocking the
reabsorption of sodium and water. Caused by the nature of diuretic effects of diuretics may be
divided as follows:
I. Osmotic diuretics (manitol, urea). Introduced into the bloodstream, they significantly
increase the osmotic pressure, increased CBV, glomerular filtration, and, due to the high
osmotic pressure in the urine provisionally, significantly reduces the reabsorption of
water and very mild Na +.
II. Saluretiki (thiazides, furosemide, Uregei, chlorthalidone, Klopamid) drugs that
increase urine output by blocking the reabsorption of sodium, at the same time blocking
the reabsorption of K +, chlorine, phosphorus.
III. Potassium-sparing drugs that moderately reduce the reabsorption of sodium, but at the
same time reduce the excretion of K + (veroshpiron, amiloride, triamterene).
The speed of the onset of diuresis, its magnitude and duration of diuretics differ as follows:
Strong diuretics: furosemide, Uregei, bumetamid, osmodiuretiki. Medium strength: thiazides,
amiloride, triamterene. Weak diuretics: veroshpiron, chlorthalidone.
On the preferential localization of the diuretics are divided:
I. Diuretics acting on the proximal tubule segment: diakarb, osmodiuretiki.
II. Diuretics acting on the cortical segment of the loop of Henle: thiazides, chlorthalidone,
Klopamid.
III. Diuretiki operating throughout the loop of Henle: furosemide, Uregei, bumetamid.
IV. Diuretics acting on the distal tubule: veroshpiron, amiloride, triamterene.In nephrology
diuretics used to treat edema and symptomatic renal hypertension. Dose in the first case
to be significantly higher. Mainly used saluretiki - hydrochlorothiazide group and more
21
powerful loop diuretics - furosemide, ethacrynic acid. It is better to use one of diuretics,
cocktails saluretics recommended for edema refractory to conventional therapy.
Saluretiki useful to combine with potassium-sparing diuretics - veroshpirona and
triamterenom. It should be borne in mind that the first drug has antialdosterone acting and is best
given in hyperaldosteronism. Saluretiki usually appointed by a broken circuit (2-3 days of
reception, 2 day break), potassium-sparing drugs - daily. In nephrotic syndrome, a good effect is
achieved with the combined use of diuretics and glucocorticoids in patients with refractory edema
advisability of aminophylline / v, albumin or poliglyukina / in, and then in / Lasix. Osmotic
diuretics are currently used primarily for the prevention of acute renal failure. It should be
remembered that they are assignable, with adequate numbers of blood pressure with a saved filter in
the renal glomeruli.
Side effects
Osmotic diuretics – hypervolemia
Thiazides, klopamid, chlorthalidone - hypokalemia, hyperuricemia, dyspepsia, allergic
reactions, photosensitivity, increased LDL, pancreatitis, vasculitis.Loop diuretics (furosemide,
Uregei, bumetamid) - hypokalemia, hyperuricemia, cochlear neuritis, allergic reactions.
Potassium-sparing diuretics (veroshpiron, triamterene) - hyperkalemia, gynecomastia,
impotence, holectaz, gastroduodenal bleeding.
IAP - application in nephrology
The main application of the IAP in nephrology, until recently, was the genesis of renal
hypertension, renovascular hypertension. Caution should be observed in patients with bilateral renal
artery lesions and signs of chronic renal failure in these situations can cause elevated IAP
nitrogenous wastes. There have been reports about the possibility of IAP in nephropathies without
hypertension, but severe parenchymal, early manifestations of chronic renal failure.
IAP - mechanism of action of developing or converting enzyme in the body contributes to
the conversion of inactive angiotensin I to active angiotensin II (ATII). In addition, converting
enzyme, in fact, is kininazoy, ie degrading enzymes kinins. Converting enzyme inhibitors - IAP helps reduce the content of ATII, which leads to a decrease in OPS and blood pressure, as well as to
a reduction in aldosterone in the adrenal glands. Reduced secretion of aldosterone increases sodiumedge, lower edge of potassium, decreased blood volume and blood pressure. Decreases as the
concentration of sodium in the wall of resistance vessels, which is controlled by aldosterone, which
also leads to a decrease in blood pressure. Raising kinins and prostaglandins in the kidney increases
their depressor function. IAP in the affected kidney, where, with a reduced number of nephrons,
develops hyperfiltration in glomeruli unaffected, and normalize the process. Thus, they have a
protective effect in patients with diffuse nephropathies.IAP - characteristics of drugs
Captopril (Capoten, Tenziomin) applies inside of 25-75 mg 2 times a day, but the initial dose
can be 25 - 12.5 mg 2 times a day.
Enalapril (Enap, Enam, Renitec) used inside 2.5 to 5 mg per day in 1 or 2 doses, 1.25 mg
intravenously every 6 hours.
Lisinopril (Dacre, Prinivil, Sinokril) is assigned inside of 10-40 mg 1 time per day.
Ramipril (Alteys, Tritatse) appointed interior of 2.5-20 mg / day in 1-2 reception.
Side effects. Are rare, mainly in the long run. Note the skin rashes, taste disturbances, and
cough. May develop proteinuria. In the treatment of renovascular hypertension with bilateral renal
artery stenosis may develop azotemia.
Interaction. IAP well with beta-blockers, diuretics and calcium antagonists. They should not
be combined only with potassium-sparing diuretics.
Treatment of complications of nephrotic syndrome
Treatment of complications NA includes pulse therapy with corticosteroids or cytotoxic
drugs, supplementation of circulating blood volume., The introduction of protein drugs, dextran,
and the use of antihistamines antikininovyh, antibiotics, heparin, anticonvulsants.The peculiarity of
this group of patients is the timely detection of signs of NA in the outpatient setting, which is
possible in a systematic medical observation. This primarily refers to the features detected in the
22
urine sample. Need further dieting and proper mode of treatment. It should be remembered that the
addition of infection, frequent colds state abrupt withdrawal of the drug should cause concern in
terms of worsening of the underlying disease and the accession of the National Assembly. It is
advisable to periodically monitor the indicators reflecting the known side effects of drugs.Disability
issues should be resolved individually, should consider the impact of negative factors hypothermia, excessive exercise. The plan may be discussed further rehabilitation spa treatment
REFERENCES
1. Симченко Н.И. Вероятность совпадения результатов бактериологического
исследования мочи в разные сроки при почечной патологии /Здравоохранение Белоруссии,
1990, N7, с.30.
2. Рябов С.И. идр. Диагностика болезней почек. Л. Медицина, 1979, 255 с.
3. Рябов С.И. Болезни почек. Руководстве для врачей. Л. Медицина, 1982, 430 с.
4. Кухтевич А.В., Русских А.В., Киреева В.И. Транзиторная протеинурия как
проявление миеломной болезни /Тер.архив, 2000, N6, с.65-66.
5. Диагностика и лечение внутренних болезней. Под ред.Ф.И.Комарова и
А.И.Хазанова. М. Медицина, 1999, Т.2, с.512.
6. Б.И.Шулутко. Внутренняя медицина /Руководство для врачей. Т.1, Санкт-Петербург,
1999, с.410-511.
7. Нефрология. Руководство для врачей. Под ред.М.Е.Тареевой. М., Медицина, 1995.
8. Окороков А.Н. Лечение болезней внутренних органов. М., Медицина, 2004, т.2.
9. Терапевтический справочник Вашингтонского Университета. Под ред.М.Вудли и
А.Уэлан, Пер. с английского, Москва, Практика, 1995 г.
10. Дж.Мерта. Справочник врача общей практики. Перевод с английского. Москва,
Практика, 1998 г.