Chronic glomerulonephritis. Chronic glomerulonephritis: forms, symptoms, diagnosis, treatment and prognosis Chronic diffuse process in the kidneys

One of the most common kidney diseases, difficult to treat and with a serious prognosis, is diffuse glomerulonephritis. The kidneys are a vital organ on whose normal functioning the entire body depends. Every process that occurs in humans is interconnected with the kidneys. Complexion, cheerful sparkle in the eyes, clear skin, clear mind, high performance - these are the qualities that we owe to the kidneys.

When glomerulonephritis begins, the body is gradually destroyed.

The essence of the disease is damage to the glomerular apparatus of the kidneys, which may have:

spicy;
subacute;
chronic course.

First, the glomeruli are affected, then the surrounding interstitial tissue, the process progresses, the kidneys become sclerotic with the development of chronic renal failure(CRF).

The trigger mechanism of the disease is the body's immune response to various provoking factors. The glomeruli are infiltrated by leukocytes and immune complexes, and inflammation of the glomerular apparatus of the kidneys develops.

Considering that all mechanisms in the body are interconnected, a violation of the filtration function of the kidneys entails changes in the acid-base composition, water and electrolyte balance of the body.

The kidney takes part in the metabolism of proteins, carbohydrates, fats, hormones, and vitamins. The preserved nitrogen excretory function of the kidneys ensures the removal of urea, creatinine, indican, and other waste from the blood.

Causesdiseases

Children more often develop acute diffuse glomerulonephritis after streptococcal infection, for example, a complicated course of sore throat, streptoderma.

The chronic process can develop at any age. Acute and chronic presentation of the disease is more common in men.

Previously, it was believed that these were diseases of men from unfavorable social strata. Now all segments of the population are susceptible to chronic diffuse glomerulonephritis, the following provoking factors are identified:

unfavorable environmental situation - background radiation;
use of toxic drugs;
vaccination;
consumption of low-quality alcohol and other poisons;
complicated course of childhood infections - chicken pox, infectious mononucleosis, mumps;
bacterial agents - streptococcus, staphylococcus, diplococcus, syphilis pathogen, enterococcus, toxoplasma, ureaplasma;
viruses - Epstein-Bar, herpes simplex, hepatitis B, cytomegalovirus;
systemic connective tissue diseases – systemic lupus erythematosus;
idiopathic option, when the cause of the disease is unknown.

The most diverse factors in nature lead to damage to the glomerulus, disruption of the filtration function of the kidneys, urine tests change, protein and red blood cells are observed.

The course of glomerulonephritis can be acute or chronic. When diseases develop as a result of complications of diseases of other organs and systems, then glomerulonephritis is called secondary, for example, with chronic illness connective tissue.

When diseases are limited only to the kidneys, edema, hypertension are caused by damage to the glomerular apparatus, then this is primary glomerulonephritis.

Primary and secondary glomerulonephritis is idiopathic when the cause is unknown.

Classification

Chronic diffuse glomerulonephritis can occur as:

latent form – changes in urine tests, patients have no complaints;
with hematuria;
With high blood pressure- arterial hypertension;
with the development of nephrotic syndrome, it consists of symptoms - loss of protein, as can be seen from a urine test - proteinuria, edema appears;
mixed variant, when a set of symptoms of all of the above conditions is observed.

The most insidious and most common, 60% of all chronic glomerulonephritis, is the latent form. There are changes in urine tests, there are no subjective complaints, edema, arterial hypertension are absent in patients, but the kidneys already have serious illnesses. This is why it is so important to periodically take blood and urine tests.

The latent form of chronic nephritis, when there is only urinary syndrome, in some cases ends in the development of renal failure.

In some cases, diseases have an undulating course. Exacerbations are replaced by remissions.

Development of the disease

Depending on which option, the form of glomerulonephritis predominates, includes different mechanisms development of the disease. But they all lead to kidney failure.

In patients, humoral immunity, which is provided by proteins dissolved in body fluids, is reduced. Allergens, or toxins, bind to these proteins rather than being eliminated through the kidneys. Large molecules are formed that settle on the walls of the glomeruli. Microcirculation suffers, ischemia is observed against the background of a perverted immune response - this is the main trigger for the development of glomerulonephritis. Further along the chain, phenomena such as:

Renal ischemia is regarded by the body as a threat, since it is a vital organ. The main carrier of oxygen, hemoglobin is found in red blood cells. With hypoxia of the renal tissue, an increase in the number of red blood cells is observed. An excess of blood cells leads to a decrease in fluidity and an increase in blood viscosity. The blood supply to organs throughout the body begins to suffer. Secondary hypoxic changes develop.
The body is trying to make the blood more fluid, to dilute it with liquid. This leads to sodium and water retention, and peripheral edema appears. The body's retention of sodium leads to loss of potassium and disruption of the heart. Excess sodium causes potassium deficiency. Without this microelement, the heart cannot work, which leads to catastrophically progressive heart failure.
An increase in water in the body against the background of increased blood pressure causes tachycardia. In order to pump an excess amount of blood, the volume of the heart muscle increases - myocardial hypertrophy develops.
The kidneys produce a substance that helps maintain normal blood pressure. Hypoxia leads to disruption of the production of this hormone. Patients have persistent arterial hypertension that cannot be treated with conventional antihypertensive drugs.
Large molecules, which are a combination of blood proteins with allergens, settled in the glomerular apparatus of the kidneys, are regarded by the body as a threat that must be eliminated. A large number of leukocytes rush to the kidneys. The vascular endothelium is damaged. An inflammatory response is observed, manifested by a violation of the permeability of the capillary wall. The liquid part of the blood leaves the vascular bed, the body retains the liquid even more to make the blood fluid, and a vicious circle closes. Swelling, symptoms of respiratory failure, heart failure, and disruption of the endocrine system appear and increase.
The formed elements of blood that clogged the glomerular apparatus gradually became sclerotic, the glomerulus was replaced by connective tissue. When this process affects more than 50% of the glomerular apparatus, glomerulonephritis is called diffuse.

Diffuse glomerulonephritis syndrome

Basic clinical syndromes diffuse glomerulonephritis:

nephrotic - the body loses protein due to disorders of the glomerular and vascular filters. There is an increase in the protein level in urine tests of more than 3.5, a decrease in the amount of blood protein less than 55, a violation of the ratio of protein fractions, edema, hyperlipidemia;
nephritic - the body’s reaction to aseptic inflammation of the glomerular apparatus of the kidneys - a certain number of red blood cells and protein appears in urine tests, edema, increased blood pressure (BP).
Urinary syndrome is manifested by minor changes in tests, in some cases it is an accidental finding.

Clinical picture

At first, patients only experience increased fatigue, dry hair, and brittle nails. Associating this condition more often with hypovitaminosis, they begin to take medicines, vitamin supplements, there is even greater disruption of kidney function.

The developed clinical picture is characterized by the appearance of:

decreased appetite;
weakness, malaise;
changes in laboratory data - protein, blood, leukocytes, casts in urine tests. increases due to large quantity squirrel. Reduced protein amount and dysproteinemia, lipidemia, hypercholesterolemia;
a tendency to increase blood clotting more often leads to the formation of blood clots of any location;
swelling;
disruption of the heart leads to heart failure;
pancreatic functions suffer, thyroid gland, .

Complications of symptoms included in nephrotic syndrome:

As fluid retention progresses, swelling increases and water accumulates in the abdominal cavity– ascites, in the pleural cavity – hydrothorax, pericardial cavity – hydropericardium.
Edema of the lungs, brain, retina.
Thrombosis, thromboembolism.
Ischemic heart disease, myocardial infarction.
Stroke.
As a result of a decrease in the volume of circulating blood, its accumulation in peripheral tissues, and protein deficiency, hypovolemic edema develops - a life-threatening condition.
The addition of infection causes peritonitis, pleurisy, pneumonia, and pleural empyema.

Clinical picture of nephritic syndrome

With a rapidly progressing process, in response to inflammatory changes of a non-bacterial nature, various combinations of specific, non-bacterial specific symptoms nephritic syndrome. Specific symptoms include:

the appearance of blood in urine tests;
increased blood pressure;
decrease in the amount of urine excreted per day;
swelling;
changes in immunological blood parameters.

Non-specific symptoms are often characterized by nausea, vomiting, and malaise.

Danger

Urinary syndrome is characterized by the appearance of small amounts of leukocytes, red blood cells, and protein in the urine. More often, urinary syndrome manifests itself as isolated proteinuria, microhematuria, and leukocyturia, which go unnoticed. There are no changes in the general condition of the patients. Arterial hypertension, no edema. If an increase in the level of leukocytes in the urine is accidentally detected, a person more often begins to independently treat for pyelonephritis, which causes even more harm. Consulting a doctor is necessary with any minimal changes in urine in the initial stages of the disease.

When can glomerulonephritis be diagnosed?

The list of manifestations that should alert you, urgently send sick to the doctor:

A few weeks after streptococcal or any other infection, swelling appears, an increase in blood pressure, protein, and blood cells in urine tests are noted. The latter are not visible to the naked eye. Important! 1-2 weeks after any infectious or viral disease take a urine test.
Suddenly detected arterial hypertension should immediately send patients to examine not only the heart, but also the kidneys to find the cause and prescribe adequate treatment.
Minor changes in urine tests accidentally discovered during a routine examination should alert you. Given the excellent compensatory abilities of the kidneys, severe disorders appear in advanced stages. Diseases must be identified at the very beginning. This will improve treatment results and significantly prolong life.
If there is hypertrophy of the heart muscle, along with a cardiac examination, it is necessary to undergo. There is heart damage, which is often secondary, against the background. Isolated treatment of the heart will not be effective.
Swelling of the face in the morning is one of the most dangerous symptoms of kidney disease.
More than 80% of waste, toxins, and end products of metabolism are removed from the body with urine. The appearance of skin itching and rashes is a reason to examine the kidneys.

Acute diffuse glomerulonephritis

Suddenly, acutely after an infection, intoxication or vaccination, swelling appears on the face, the amount of urine decreases to 400-500 ml per day, and its density increases. This is observed as acute diffuse glomerulonephritis. Some of the main symptoms are protein in the urine and a reduced amount of sodium. More often, patients pay attention to the appearance of blood in the urine, a rapid increase in body weight by 10-15 kg in a short period of time.

This form of glomerulonephritis rarely ends in anuria. For acute nephritis one of the most significant symptoms is arterial hypertension. Pain in the kidney area often develops with increasing size and tension of the capsule.

Against the background of an acute attack of diffuse glomerulonephritis, eclampsia or cerebral edema is more often observed. The second significant danger of acute nephritis is that arterial hypertension appears that is resistant to treatment. antihypertensive drugs.

The predominance of night urination over daytime urination, which does not happen normally, and low urine density should alert patients. At the slightest suspicion of acute nephritis, you should consult a doctor. Performing the Zimnitsky, Nechiporenko, Volgard tests will allow you to quickly make a diagnosis and begin adequate treatment of acute nephritis or a chronic process.

Important! Edema, impaired renal function in the form of protein, red blood cells in the urine, increased blood pressure require immediate medical attention. medical care, because they are symptoms characteristic of acute diffuse glomerulonephritis.

Chronic diffuse glomerulonephritis

urinary;
hematuric;
hypertension;
neurotic;
mixed.

Exacerbation of chronic nephritis is most often manifested by swelling of the face in the morning, change in the color of urine, decreased diuresis, increased blood pressure, headache, malaise, general weakness, and decreased performance.

Chronic diffuse glomerulonephritis may have a latent course, then there will be no clinical symptoms. Diseases in remission are also manifested by the absence of symptoms. In contrast to acute diffuse glomerulonephritis, in chronic glomerulonephritis there is always hypertrophy of the left ventricular myocardium. Violations of the nitrogen excretory function of the kidneys are more common, and many patients develop chronic renal failure within 1 year.

Diagnostics

A quick and accurate diagnosis will prevent the onset of chronic renal failure. Despite the similarity of clinical manifestations, the mechanism of development of kidney diseases is different, treatment will be different. To identify the predominant mechanism of development of syndromes, symptoms, and determine structural changes in kidney tissue, the following are performed:

biopsy;
immunological diagnostics;
blood and urine tests;

Differential diagnosis should be carried out with the following types of kidney diseases:

Pyelonephritis differs from acute glomerulonephritis by increased body temperature, absence of red blood cells, and a high content of leukocytes in the blood of patients.
pregnant women, characterized by severe urinary syndrome.
Tubulo-interstitial nephritis is characterized by the appearance of disease of the tubules, interstitium, in contrast to acute glomeruloneuritis.
Toxic, for example alcoholic kidney damage.
Amyloidosis is a disorder of protein metabolism throughout the body. At the initial stages of the disease, accumulation of amyloid protein occurs in all organs and tissues of patients, in contrast to acute or chronic glomerulonephritis.
Lupus nephritis in patients with systemic lupus erythematosus.
Periarteritis nodosa, or Kussmaul-Mayer disease, has a benign course, the cutaneous form of the lesion predominates. The kidneys are extremely rarely involved in the process, and the phenomena of chronic latent glomerulonephritis develop.
Wegener's granulomatosis in patients is characterized by autoimmune damage to the walls of small vessels of the bronchi, lungs, and eyes. The kidneys are the last to join when there is a generalized form of the lesion. The phenomena of intoxication, pain in muscles, joints, elevated temperature bodies. After this, the phenomena of acute glomerulonephritis occur and kidney function is impaired.
Goodpasture's disease is characterized by a set of symptoms - pulmonary hemorrhages, pneumonia, a form of damage with the development of glomerulonephritis. The course of the disease is unfavorable.
Hemorrhagic vasculitis in patients is characterized.
Urolithiasis disease.
Oncological diseases.
Hypersensitive vasculitis, Henoch-Schönlein disease in patients is characterized by thrombosis of small vessels after suffering streptococcal and viral infections. It differs from chronic nephritis and acute glomerulonephritis by the presence of skin rashes. The joint form is characterized by muscle and joint pain. The abdominal form is accompanied by gastrointestinal bleeding and hemorrhages in the abdominal organs. The phenomena of classic acute glomerulonephritis often occur when there is a fulminant form of the disease, which usually ends in death.
Hereditary nephritis - Alport's diseases. The disease begins to manifest itself at 5-7 years of age. The child has asymptomatic microhematuria and protein in the urine. They are detected by chance when there is a latent course of chronic glomerulonephritis. Along with pronounced urinary syndrome, there is a decrease in hearing, vision, swelling, additional external congenital anomalies development. Kidney function begins to suffer significantly by the age of 18-20 years, and chronic renal failure develops.

Complications

With glomerulonephritis, there may be complications that can be fatal:

development of acute renal failure;
stroke;
hypovolemic shock;
pulmonary embolism;
eclampsia;
diseases of the cardiovascular system.

Treatment

Treatment of acute glomerulonephritis is subject to the following goals:

recovery;
eliminate possible complications.

Treatment of chronic glomerulonephritis has the following objectives:

cause remission;
slow the progression of symptoms;
eliminate existing complications, prevent the emergence of new dangers.

With the rapid progression of chronic glomerulonephritis, it is necessary to reduce the rate of development of end-stage renal failure.

Non-drug treatment:

Active glomerulonephritis requires strict bed rest.
Following a diet with limited salt;
Consume enough protein and water.

Drug treatment of acute glomerulonephritis includes:

etiotropic therapy;
pathogenetic agents;
symptomatic drugs.

When installed infectious cause Acute glomerulonephritis is treated with antibiotics:

Penicillin.
Amoxicillin.
Cephalexin.
Doxycycline.
Cefaclor.
Roxithromycin.

For high blood pressure and edema, treatment of glomerulonephritis includes:

furosemide;
calcium channel blockers.

Additional treatment prescribed according to individual indications:

antihistamines;
calcium preparations;
vitamin C;
routine;
antiplatelet agents.

Drug treatment of chronic glomerulonephritis includes:

If the relationship between exacerbations of chronic glomerulonephritis and infections is proven, then antibacterial therapy is indicated.
Immunosuppressors: glucocorticosteroids, cytostatics to suppress the activity of glomerulonephritis.
Symptomatic treatment is prescribed according to indications: antihypertensives, antiplatelet agents, anticoagulants, lipid-lowering agents.

The latent form of chronic glomerulonephritis does not include immunosuppressive therapy.

The hematuric form of glomerulonephritis occasionally requires the use of drugs such as prednisolone and cytostatics. ACE inhibitors, dipyridamole, are commonly used.

Treatment of glomerulonephritis with ACE inhibitors:

enalapril;
lisinopril;
benazepril;
ramipril;
perindopril;
trandalopril;
zofenopril;
fosinopril

To achieve a nephroprotective effect, the following are prescribed:

losartan;
valsartan;
candesartan;
irbesartan;
telmisartan;
eprosartan.

Treatment of glomerulonephritis with calcium channel blockers:

verapamil;
diltiazem;
amlodipine;
lercanidipine.

Treatment of glomerulonephritis with selective β-blockers:

metoprolol;
nebivol;
carvedilol.

The hypertensive variant of chronic glomerulonephritis requires ACE inhibitors, cytostatics, and glucocorticosteroids.

Nephrotic and mixed forms of chronic glomerulonephritis give stable remission if treatment with steroids, cytostatics, and levamisole is used.

Treatment of glomerulonephritis with lipid-lowering drugs:

simvastatin;
atorvastatin;
rosuvastatin.

Such forms of chronic glomerulonephritis as hypertensive and nephrotic require the following:

hydrochlorothiazide;
furosemide;
indapamide;
spironolactone.

Any forms of chronic glomerulonephritis cannot be treated with motor therapy. Combinations of cytostatic and hormonal drugs are always used. How additional funds are used:

vitamin e;
heparin;
nadroparin calcium;
aspirin;
dipyridamole;
trental;
ticlopidine;
warfarin.

Rapidly progressive forms of chronic glomerulonephritis require hemodialysis, plasmapheresis, and ultrafiltration.

Surgical treatment of glomerulonephritis involves tonsillectomy for streptococcal infection. The malignant course of glomerulonephritis in end-stage renal failure may require transplantation.

Chronic diffuse glomerulonephritis- long-term (more than a year) immunoaldergic bilateral kidney disease, ending with their shrinkage and death of patients from chronic renal failure. Chronic glomerulonephritis can be either the outcome of acute nephritis or primary chronic, without a previous acute attack.

Symptoms, course are characterized by the same main points as acute glomerulonephritis: edema, arterial hypertension, urinary syndrome and impaired renal function.

During chronic glomerulonephritis there are stages:

a) renal compensation, i.e. sufficient nitrogen excretion function of the kidneys. It may be accompanied by severe urinary syndrome, but sometimes it is latent for a long time, manifesting itself only in slight albuminuria or hematuria;
b) renal decompensation, characterized by insufficiency of nitrogen excretory function of the kidneys. Urinary symptoms may be less severe. As a rule, high arterial hypertension is observed, edema is often moderate. At this stage, hypoisosthenuria and polyuria are expressed, which end in the development of azotemic uremia.

The following clinical conditions are distinguished: forms of chronic glomerulonephritis:

nephrotic form (see Nephrotic syndrome) is the most common form of secondary nephrotic syndrome. This form, in contrast to pure lipoid nephrosis, is characterized by a combination of nephrotic syndrome with signs of inflammatory kidney damage. The clinical picture of the disease can be determined for a long time by nephrotic syndrome and only then does glomerulonephritis progress with impaired nitrogen excretory function of the kidneys and arterial hypertension;
hypertensive form . Long time Arterial hypertension predominates among the symptoms, while urinary syndrome is less pronounced. Occasionally, chronic glomerulonephritis develops according to the hypertensive type after the first violent attack of glomerulonephritis, but more often it is the result of a latent form. Blood pressure reaches 180/100 - 200/120 mm Hg. Art. and can be subject to large fluctuations during the day under the influence of various factors. Hypertrophy of the left ventricle of the heart is noted, an accent of the second tone is heard over the aorta. As a rule, hypertension does not become malignant; blood pressure, especially diastolic blood pressure, does not reach high levels. Changes in the fundus of the eye are observed in the form of neuroretinitis; mixed form. In this form, there are simultaneously nephrotic and hypertensive syndromes;
latent form. This is a fairly common form, usually manifested only by mild urinary syndrome without arterial hypertension and edema. It can have a very long course (10 - 20 years or more), later leading to the development of uremia.
It should also be highlighted hematuric form, since in some cases chronic glomerulonephritis can manifest itself only as hematuria, not accompanied by either significant proteinuria or general symptoms(hypertension, edema).

All forms of chronic glomerulonephritis can periodically give relapses, very reminiscent or completely repeating the picture of the first acute attack of diffuse glomerulonephritis. They are especially often observed in autumn and spring and occur 1-2 days after exposure to an irritant, most often a streptococcal infection. In any course, chronic diffuse glomerulonephritis passes into its final stage - a secondary wrinkled kidney.

A secondary shrinkage kidney is characterized by a picture of chronic azotemic uremia (see Chronic renal failure).

Diagnosis chronic glomerulonephritis. If there is a history of acute glomerulonephritis and severe clinical picture the diagnosis does not present great difficulties. However, in the latent form, as well as in the hypertensive and hematuric forms, its recognition can be very difficult. If there is no specific indication in the history of acute glomerulonephritis, then in case of moderately severe urinary syndrome it is necessary to carry out differential diagnosis with one of many unilateral or bilateral kidney diseases. The possibility of orthostatic albuminuria should be kept in mind.
When differentiating from hypertension, the time of appearance of urinary syndrome in relation to arterial hypertension is important. In chronic glomerulonephritis, urinary syndrome may long precede arterial hypertension or occur simultaneously with it. Chronic glomerulonephritis is also characterized by a lesser severity of cardiac hypertrophy, a lesser tendency to hypertensive crises (with the exception of exacerbations occurring with eclampsia) and a rarer or less intensive development atherosclerosis, including coronary arteries.

Chronic glomerulonephritis is supported by the predominance of erythrocytes over leukocytes in the urine sediment, the absence of active and pale (when stained according to Sternheimer-Malbin) leukocytes, as well as the same size and shape of the two kidneys and the normal structure of the pelvis and calyces, which is detected by x-ray urological examination. The nephrotic form of chronic glomerulonephritis must be distinguished from lipoid nephrosis, amyloidosis and diabetic glomerulosclerosis.

In relation to differentiation from renal amyloidosis, the presence of foci in the body is important chronic infection and amyloid degeneration of other localization.

The so-called congestive kidney sometimes gives rise to an incorrect diagnosis, because it can occur with significant proteinuria with moderate hematuria and high relative density of urine. It is often accompanied by edema, sometimes arterial hypertension. Congestive kidney is indicated by the presence of independent primary heart disease, liver enlargement, location of edema mainly in the lower extremities, less severe hypercholesterolemia and urinary syndrome, as well as its disappearance with a decrease in cardiac decompensation.

Treatment. It is necessary to eliminate foci of infection (removal of tonsils, sanitation of the oral cavity). Long-term dietary restrictions (salt and protein) do not prevent the transition of acute nephritis to chronic. Patients with chronic nephritis should avoid cooling, especially exposure to damp cold. A dry and warm climate is recommended for them. If the general condition is satisfactory and there are no complications, it is indicated Spa treatment in Central Asia (Bayram-Ali) or on the southern coast of Crimea (Yalta). Bed rest is only necessary during periods of significant edema or heart failure, as well as in cases of uremia.

For the treatment of patients with chronic glomerulonephritis, diet is essential, which is changed depending on the form and stage of the disease. In nephrotic and mixed forms (edema), the intake of sodium chloride from food should not exceed 1.5-2.5 g per day, for which they stop adding salt to food. With sufficient excretory function of the kidneys (no edema), food should contain a sufficient amount of protein - 1-1.5 g/kg in the form of animal protein, rich in complete phosphorus-containing amino acids. This normalizes the positive nitrogen balance and compensates for protein losses. In the hypertensive form, it is recommended to moderately limit the intake of sodium chloride ( table salt up to 3 - 4 g per day) with normal protein and carbohydrate content. The latent form does not require significant restrictions in the diet of patients; it must be complete, varied and rich in vitamins. Vitamins (C. complex B. A) should be included in the diet for other forms of chronic glomerulonephritis. It should be noted that a long-term protein-free diet without salt does not prevent the progression of nephritis and has a bad effect on the general condition of patients.

Especially great importance has corticosteroid therapy, which is the basis of pathogenetic therapy for this disease. For the course of treatment, 1500-2000 mg of prednisolone (prednisone) or 1200-1500 mg of triamcinolone are used. Treatment is usually started with 10-20 mg of prednisolone and the dose is increased to 60-80 mg per day (the dose of triamcinolone is increased from 8 to 48-64 mg), and then gradually reduced. It is recommended to carry out repeated full courses of treatment (for exacerbations) or small maintenance courses.

Sometimes intermittent courses of treatment with glucocorticoids are prescribed - 3 days a week daily, which reduce the severity of steroid Cushingoid syndrome and the frequency of steroid ulcers, while apparently maintaining the therapeutic effect of hormones.

While taking corticosteroids steroid hormones exacerbation of hidden foci of infection is possible. In this regard, treatment with corticosteroids is best carried out while prescribing antibiotics, or after removal of foci of infection (for example, tonsillectomy).

Contraindications to the use of corticosteroids in patients with chronic glomerulonephritis is progressive azotemia. For moderate arterial hypertension (180/110 mm Hg), treatment with corticosteroids can be carried out while simultaneously using antihypertensive drugs. High hypertension requires a preliminary reduction in blood pressure. If corticosteroid therapy is contraindicated or if it is ineffective, the use of non-hormonal immunosuppressants is recommended: azathioprine (imuran), 6-mercaptopurine, cyclophosphamide. These drugs are more effective treatment they are better tolerated by patients while taking prednisolone in moderate doses (10-30 mg per day), which prevents the toxic effects of immunosuppressants on leukopoiesis. In the later stages - with glomerular sclerosis and atrophy with high hypertension - immunosuppressants and corticosteroids are contraindicated, since there is no longer immunological activity in the glomeruli and continuation of such treatment only aggravates hypertension.

Drugs of the 4-aminoquinoline series - hingamin (delagil, resoquine, chloroquine), hydroxychloroquine (plaquenil) - have immunosuppressive properties.
Rezoquine (or chloroquine) is used 0.25 g 1-2-3 times a day for 2-3-8 months. Rezoquin can cause side effects - vomiting, lesions optic nerves Therefore, monitoring by an ophthalmologist is necessary.

Indomethacin, an indole derivative (metindole, indocid), is a non-steroidal anti-inflammatory drug. It is assumed that, in addition to providing analgesic and antipyretic effects, indomethacin affects mediators of immunological damage. Under the influence of indomethacin, proteinuria decreases. It is prescribed orally at a dose of 25 mg 2-3 times a day, then, depending on tolerability, the dose is increased to 100-150 mg per day. Treatment is carried out long-term, over several months. The simultaneous use of steroid hormones and indomethacin can significantly reduce the dose of corticosteroids with their gradual complete abolition.

The deposition of fibrin in the glomeruli and arterioles, the participation of fibrin in the formation of capsular “crescents”, and a mild increase in the plasma fibrinogen content serve as a pathogenetic rationale for anticoagulant therapy of chronic glomerulonephritis. By enhancing fibrinolysis and neutralizing complement, heparin affects many allergic and inflammatory manifestations: it reduces proteinuria, reduces dysproteinemia, and improves the filtration function of the kidneys. Heparin prescribed intramuscularly at 20,000 units per day or intravenously (1000 units per hour) can be used in combination with corticosteroids and cytostatics.

For mixed forms of chronic glomerulonephritis(edematous and severe hypertensive syndrome), the use of natriuretics is indicated, as they have a pronounced diuretic and hypotensive effect. Hypothiazide is used 50-100 mg 2 times a day, Lasix 40-120 mg per day, ethacrynic acid (uregit) 150-200 mg per day. It is advisable to combine saluretics with the anti-aldosterone drug aldactone (veroshpiron) - 50 mg 4 times a day. The diuretic effect of hypothiazide is accompanied by the excretion of potassium in the urine, which can quickly lead to hypokalemia with the development of its characteristic general weakness, adynamia and impaired cardiac contractility. Therefore, Panangin or potassium chloride solution should be prescribed simultaneously. For persistent edema due to hypoproteinemia, it is possible to recommend the use of a high-molecular carbohydrate - polyglucin (dextran) in the form of a drip intravenous injection of 500 ml of solution, which increases the colloid-osmotic pressure of the blood plasma, promotes the movement of fluid from tissues into the blood and causes diuresis. Polyglucin works better during treatment with prednisolone or diuretics. Mercury diuretics should be avoided for renal edema, since their diuretic effect is associated with a toxic effect on the tubular epithelium and glomeruli of the kidneys, which, along with an increase in diuresis, leads to a decrease in the filtration function of the kidneys. Purine derivatives - theophyllia, aminophylline, etc. - are also ineffective in the treatment of renal edema.

In the treatment of hypertensive form of chronic glomerulonephritis antihypertensive drugs used in the treatment of hypertension can be used: reserpine; reserpine with hypothiazide, sympatholytics. Ganglion-blocking drugs, in particular hexonium and pentamine, can also be prescribed. However, sudden fluctuations in blood pressure and its orthostatic fall, which can worsen renal blood flow and filtration function of the kidneys, should be avoided. It is advisable to combine these antihypertensive drugs with reserpine, which reduces the tendency to sharp fluctuations in blood pressure and leads to a slower and more gradual decrease. In the hypertensive form of chronic glomerulonephritis, drugs that suppress the synthesis of catecholamines in the adrenal glands are indicated. This is alpha-methyldopa (aldomet, dopegit), which is prescribed at 0.75-1 g per day. In some cases, patients with arterial hypertension may be prescribed magnesium sulfate; when administered intravenously and intramuscularly in the form of a 25% solution, it can reduce blood pressure and improve renal function with a diuretic effect. It is especially indicated in the preeclamptic period and in the treatment of eclampsia, which can occur during exacerbation of chronic glomerulonephritis, as it helps reduce cerebral edema. For treatment in the final stage of chronic nephritis, see the section “Chronic renal failure”.

Forecast. The outcome of chronic glomerulonephritis is shrinkage of the kidneys with the development of chronic renal failure - chronic uremia. Immunosuppressive therapy significantly changed the course of the disease. There are cases of complete remission of the disease with the disappearance of both general and urinary symptoms.

Directory medical practitioner/ Ed. A. I. Vorobyova. - M.: Medicine, 1982

The content of the article:

Glomerulonephritis is a diffuse multifactorial disease of the glomerular apparatus of the kidneys of immune or allergic origin.

A chronic inflammatory process in the glomeruli leads to the loss of the functional ability of the kidneys to rid the blood of toxins.

Long-term pathology is always complicated by the development of chronic renal failure.

We talk about the chronicity of the process when immune inflammation in the kidneys exists for a year.

Code by international classification diseases ICD-10:

N03 Chronic nephritic syndrome

Pathogenesis

1. The following changes occur in the walls of the vessels of the renal glomeruli:

The permeability of the vascular wall of the renal glomerulus for cellular elements increases.

Microthrombi form, followed by blockage of the lumen of the vessels of the glomerular apparatus.

Blood circulation in the modified vessels is disrupted, up to complete ischemia.

Erythrocytes settle on important renal structures of the nephron: Bowman's capsule, renal tubules.

The process of blood filtration and the production of primary urine is disrupted.

Poor circulation in the renal glomerulus entails emptying of the lumen and gluing of the walls, followed by the transformation of the nephron into connective tissue. The gradual loss of structural units leads to a decrease in the volume of filtered blood (one of the causes of chronic renal failure). There are fewer and fewer nephrons capable of performing their work normally, which leads to poisoning of the body with metabolic products, while the necessary substances are returned to the blood in an incomplete volume.

Etiology and provoking factors

The etiology of CGN is as follows:

Infectious agents - bacterial (Str, Staf, Tbs, etc.), viral ( hepatitis B, C, cytomegalovirus, HIV)

Toxic agents - alcohol, drugs, organic solvents, mercury

The cause in most cases is group A beta-hemolytic streptococcus.

Diseases contributing to the development of pathology:

Sore throat and chronic tonsillitis,
Scarlet fever,
Infectious diseases hearts,
Sepsis,
Pneumonia,
Mumps,
Rheumatological diseases,
Autoimmune pathology.

Classification of chronic glomerulonephritis

Form of glomerulonephritis	Activity of the renal process	Kidney function status
1. Acute glomerulonephritis With nephritic (hematuric) syndrome - with nephrotic syndrome - with isolated urinary syndrome - with nephrotic syndrome, hematuria and hypertension	1. The period of initial manifestations (height) 2. Period of reverse development 3. Transition to chronic glomerulo-nephritis	3. Acute renal failure
2. Chronic glomerulonephritis Hematuric form - nephrotic form - mixed form	1. Period of exacerbation 2. Period of partial remission 3. Period of complete clinical and laboratory remission	1. Without renal dysfunction 2. With impaired renal function 3. Chronic renal failure
3. Subacute (malignant) glomerulonephritis		1. With impaired renal function 2. Chronic renal failure

Morphological classification of CGN

Diffuse proliferative

With "half moons"

Mesangioproliferative

Membrane-proliferative (mesangiocapillary)

Membranous

With minimal changes

Focal segmental glomerulosclerosis

Fibrillar-immunotactoid

Fibroplastic

The classification is based on the assessment of clinical and laboratory syndromes, pathogenesis (primary, secondary), functional ability of the kidneys (with loss, without loss, chronic renal failure) and morphology.

The course of hCG is:

Recurrent (remission is replaced by exacerbation).
Persistent (constant activity of immune inflammation in the glomeruli with preservation of the functional abilities of the nephrons for a long time).
Progressive (constant activity of the process with a tendency to renal failure, and a gradual decrease in glomerular filtration).
Rapidly progressing (the process is so active that after a short period of time, chronic renal failure is formed).

Clinical manifestations

In most cases, the pathology is characterized by slow development. Many patients cannot remember when it started and after what they got sick.

The most typical signs:

Diuresis depends on the severity of chronic renal failure: a decrease in daily diuresis (oliguria) by initial stage, with progression - polyuria (a lot of urine) leading to anuria in the terminal stage of chronic renal failure, in a clinical urine test there is a pathological content of protein and red blood cells.
Urination predominates, mainly at night: nocturia.
Swelling: from minor to severe, localization varies.
Weakness, fatigue.
Increased temperature response.
Development of persistent hypertension.
Thirst, the smell of acetone in the exhaled air, itchy skin indicate the advanced state of the disease and the progress of chronic renal failure.

There are several forms of chronic glomerulonephritis

Glomerulonephritis with isolated urinary syndrome

Isolated urinary syndrome is characterized by the following symptoms:

Asymptomatic hematuria

Asymptomatic proteinuria

No complaints

No edema, hypertension

The most common option is characterized by a benign course (aggressive treatment is not prescribed). The patient has no complaints with this form.

When examined, a small amount of protein and red blood cells are found in the urine.

Since the disease is secretive, and the progression of renal failure is slow but constant, sometimes all the laboratory and clinical signs of chronic renal failure are found in patients who first apply.

Latent form of chronic glomerulonephritis, despite the benign course of timely diagnosis, may cause kidney failure.

Nephrotic form of glomerulonephritis

Occupies just over 20% of cases. It is characterized by pronounced clinical manifestations, the leading symptom being the appearance of significant edema.

In a clinical urine test, the loss of protein (mainly albumin) is more than 3 g/day, which is why, on the contrary, there is a lack of protein substances in the plasma.

Increased levels of blood cholesterol, triglycerides and low-density lipoproteins.
The nephrotic form of glomerulonephritis is an indication for emergency hospitalization of the patient, since his condition is regarded as serious due to developed ascites, pleurisy, etc. against the background of massive edema. In addition, the patient has a risk of developing a secondary infection against the background of reduced immunity, osteoporosis, blood clots, hypothyroidism, atherosclerosis, heart attack, stroke.

All of the above pathology is a consequence of a violation of the water-electrolyte balance (loss of zinc, copper, vitamin D, calcium, thyroid-stimulating hormones etc.).

The most serious complications of the nephrotic form of glomerulonephritis are cerebral edema and hypovolemic shock.

Mixed variant or hypertensive form of glomerulonephritis

It is characterized by a combination of nephrotic syndrome and persistent hypertension (increased blood pressure). Typically rapid progression to chronic renal failure due to the detrimental effect of hypertension on the renal vessels.

Hematuric form of glomerulonephritis

Chronic glomerulnephritis in men often occurs in a hematuric form.

Swelling does not appear, there is no increase in blood pressure.

There is no pronounced proteinuria (no more than 1 g/day), but there is hematuria (red blood cells in the urine).

Factors that provoke hematuric chronic glomerulonephritis include:

Alcohol intoxication,
poisoning with any substances,
colds in Berger's disease.

Nephrologists note the following pattern: the brighter clinical manifestations, the greater the chances for full recovery functional capacity of the kidneys.

It must be remembered that any form of hCG, under certain circumstances, can go into an acute stage with a clinical picture typical of acute glomerulonephritis.

Chronic glomerulonephritis in the acute stage will be treated according to the regimen used in the treatment of acute immune inflammation of the kidneys.

How to diagnose chronic glomerulonephritis

Clinical and laboratory tests play an important role in the diagnosis of chronic hepatitis. During the conversation between the doctor and the patient, attention is paid to the presence of infectious diseases in the anamnesis, concomitant pathologies, in particular, systemic diseases, and the urological anamnesis is clarified.

General clinical urine analysis

Urine in chronic glomerulonephritis is variable, it depends on the morphology of the pathological process. Typically a decrease in specific gravity; the greater the amount of protein in the urine (up to 10 g/day), the more evidence for the nephrotic form.

Red blood cells are present: gross hematuria or microhematuria. In the urine sediment, hyaline and granular casts (nephrotic and mixed forms), fibrin are found.

The hypertensive form is characterized by a decrease in glomerular filtration.

Blood biochemistry

1. increased levels of cretinin, urea,
2. hypoproteinemia and dysproteinemia,
3. hypercholesterolemia.
4. increasing the titer of antibodies to streptococcus (ASL-O, antihyaluronidase, antistreptokinase),
5. decrease in the level of C3 and C4,
6. increase in all immunoglobulins M, G, A
7. electrolyte imbalance.

Urine culture for flora and sensitivity to drugs.
Zimnitsky's test.
Nechiporenko's test.
Rehberg's test.

Instrumental diagnostics

Kidney ultrasound with Doppler
On initial stages Ultrasound diagnostics does not reveal pronounced changes.
If chronic glomerulonephritis progresses, sclerotic processes in the kidneys are possible with a decrease in their size.

Survey and excretory urography, radioisotope scintigraphy make it possible to assess the function of each kidney separately and the general condition of the parenchyma.

ECG
If the patient has persistent hypertension, electrocardiography will confirm hypertrophy (increase in size) of the left ventricle.

Fundus examination

Symptoms are similar to those of hypertension:

1. narrowing of the arteries,
2. dilatation of veins,
3. pinpoint hemorrhages,
4. microthrombosis,
5. swelling.

To determine the morphological component of the form of hCG, a diagnostic biopsy is possible. Based on the results of the morphological conclusion, treatment tactics are selected.

The procedure is considered invasive and has a number of contraindications:

Single kidney or lack of collateral kidney function.
Coagulopathies.
Right ventricular failure.
Infectious processes.
Hydronephrosis.
Polycystic disease.
Thrombosis of the renal arteries.
Kidney cancer.
Heart attacks, stroke in acute stage.
Confusion.

Differential diagnosis is carried out with the following diseases:

Chronic pyelonephritis,
hemorrhagic fever with renal syndrome,
nephrolithiasis,
hypertension,
tuberculous lesions of the genitourinary organs, etc.

Treatment for chronic glomerulonephritis

The treatment regimen will depend on the form of the disease, clinical manifestations, concomitant pathology, the presence of complications.

The main aspects of treatment for chronic glomerulonephritis are to normalize blood pressure, eliminate edema and maximize the pre-dialysis period.
It is recommended to normalize the work and rest schedule, avoid hypothermia and work with toxic substances.

Pay attention to the timely sanitation of areas of possible infection: caries, tonsils, throat, etc.

Diet for chronic glomerulonephritis

Proper diet is important.

Chronic renal failure leads to disruption of the electrolyte balance of the blood, self-poisoning of the body as a result of the accumulation of toxic substances.

Properly selected nutrition can correct the adverse effects of toxins on the body at the initial stage of chronic renal failure. And at all other stages of chronic renal failure, you can’t go without a diet.

What can you eat with glomerulonephritis - unites diet (table No. 7).

Its main points:

Refusal of salt.
Reducing the amount of fluid consumed.
Introduction to the diet of foods with a high content of potassium and calcium.
Limiting the consumption of animal proteins.
Introduction of vegetable fats and carbohydrates into the diet.

Proper nutrition during hCG will allow you to live longer without hemodialysis or kidney transplantation

Medicines for chronic glomerulonephritis

Immunosuppressive drugs

First-line drugs are immunosuppressive drugs. Due to the suppressive effect on the activity of the immune system, pathological processes in the glomerular apparatus of the kidney are slowed down.

Steroids

The dosage of prednisolone is calculated individually, 1 mc/kg per day, for 2 months, with a gradual reduction to avoid withdrawal syndrome. Pulse therapy is periodically prescribed (injection of corticosteroid drugs in a high dose for a short time). With irregular dosage, incorrect dosage, untimely initiation of therapy and severe immune disorders, the effectiveness decreases.

The following conditions are contraindications for treatment with nonsteroidal hormones:

Active tuberculosis and syphilis,
viral ophthalmic diseases,
infectious processes,
lactation,
pyoderma.

Steroids are used with caution in diabetes mellitus, thromboembolism, herpes,
systemic candidiasis, hypertension, Itsenko-Cushing's disease, severe chronic renal failure.

Cytostatics

Used for progressive forms of chronic pyelonephritis in men and women, and in all cases where there are contraindications to the prescription of steroid drugs, or the appearance of complications, or in the absence of effect from therapy.

Sometimes the treatment regimen includes both hormonal drugs and cytostatics.

Contraindications: pregnancy and active phase of infectious processes.

With caution: severe dysfunction of the liver and kidneys, blood pathology.

List of cytostatics for chronic glomerulonephritis in men and women:

Cyclophosphamide,
Chlorambucil,
Cyclosporine,
Azathioprine.

Complications: hemorrhagic cystitis, pneumonia, agranulocytosis (pathological changes in the blood, inhibition of hematopoiesis).

With developed side effects Cytostatic therapy for chronic glomerulonephritis in men and women is canceled.

Nonsteroidal anti-inflammatory drugs

It was believed that Indomethacin, Ibuklin, Ibuprofen are capable of suppressing the autoimmune response. Not all nephrologists prescribe NSAIDs, since drugs from the NSAID group have a toxic effect on the kidneys and often provoke the development of drug-induced nephropathy even without glomerulonephritis.

Anticoagulants and antiplatelet agents

Helps improve the rheological properties of blood. Prevents the processes of thrombus formation in the renal glomeruli and the adhesion of blood vessels. Heparin is most often used for a course of 3 to 10 weeks in individual dosages, which depend on many factors, including coagulogram parameters.

Symptomatic therapy

Symptomatic therapy depends on the clinical manifestations of chronic glomerulonephritis and includes:

Antihypertensive drugs.
Diuretics.
Antibiotics.

Antihypertensive drugs

Some forms of GM are characterized by a persistent increase in blood pressure, therefore the prescription of antihypertensive drugs from the group of ACE inhibitors is justified:

Captopril,
enalapril,
ramipril

Diuretics

To activate fluid flow in the nephron, diuretics are used:

Antibacterial drugs

Sometimes hCG occurs against the background of some kind of infection, in this case it is prescribed antibacterial drugs to prevent secondary infection. Protected penicillins are more often prescribed, since the drugs have less toxicity and are effective against group A beta-hemolytic streptococcus.

If you are intolerant to penicillins, cephalosporin antibiotics can be used. The use of antibiotics is justified when there is a proven connection between the development of glomerulonephritis and an infectious process, for example, in a man or woman, glomerulonephritis after streptococcal tonsillitis appeared 14 days later.

The outcome of chronic diffuse glomerulonephritis is always secondary kidney shrinkage and the onset of chronic renal failure.

If chronic renal failure has led to significant disturbances in the functioning of the body, program hemodialysis is indicated when the creatinine level reaches 440 µmol/l. In this case, it is justified to refer the patient for a disability examination. The diagnosis of CG in itself, without impaired renal function, does not give the right to disability.

For hypercholesterolemia, statins are prescribed to lower cholesterol levels.
There are good reviews of the use of plasmapheresis for glomerulonephritis.

Chronic glomerulonephritis in children

In pediatrics, glomerulonephritis in children ranks second after infections urinary tract. Children aged 3 to 9 years are most often affected by the disease.

Boys experience immune inflammation in the kidneys 2 times more often than girls. In some cases, pathology develops 10-14 days after a childhood infection. Just like in adult men and women, chronic glomerulonephritis is the outcome of an acute immunological process in the kidneys.

Clinical manifestations, forms, signs are identical.

Treatment is less aggressive due to age.

Chronic glomerulonephritis in children is treated by a nephrologist.

Prevention of exacerbations in chronic glomerulonephritis comes down to timely sanitation of foci of inflammation, regular monitoring of clinical and laboratory parameters, adherence to diet, avoidance of hypothermia, and timely completion of therapy.

Prognosis for chronic glomerulonephritis depending on the morphological variant

GN of minimal changes - preservation of kidney function after 5 years - 95%;

Membranous GN - preservation of kidney function after 5 years - 50-70%

FSGS - preservation of kidney function after 5 years - 45 -50%

Mesangioproliferative - preservation of kidney function after 5 years - 80%

Membranous-proliferative - preservation of kidney function after 5 years - 45 - 60%

Life expectancy depends on the clinical variant of the disease and the characteristics of the functional state of the kidneys.

Favorable prognosis for the latent variant (subject to timely treatment), questionable for hematuric and hypertensive variants.

The prognosis is unfavorable for nephrotic and mixed forms of glomerulonephritis.

The kidney is a complex apparatus that performs a number of vital functions important functions ensuring the normal functioning of the body. Each structural element of this organ participates in the process of filtration of blood plasma, as a result of which a waste product is formed - urine. There are many kidney diseases, the chronic or acute course of which has a damaging effect on one or another structural element, causing diffuse changes kidney

Kidney structure

To understand what diffuse changes are, it is necessary to understand the functional structure of the renal apparatus.

When studying the structure of the kidney, the parenchyma (the main renal tissue) and the pyelocaliceal system (PSS) are first distinguished. In the structure of the parenchyma, one should distinguish the cortex, consisting of nephrons (glomeruli, surrounded by a capsule) and the medulla, consisting of urinary tubules, this is where urine is formed. The pyelocaliceal system serves to accumulate and remove the resulting urine.

Arterial blood passes through long and thin arteries that form the glomerulus, where primary filtration occurs, and then enters the urinary tubules, which provide absorption (reabsorption) of the filtered useful substances(glucose, vitamins, minerals). Thus, maximum plasma purification is achieved while minimizing the loss of useful substances.

Any changes in the structure of the kidney, in 90% of cases, are the result of pathological processes leading to disruption of their functions. Therefore, detection of diffuse abnormalities in tissues during ultrasound or other diagnostic procedures, it is necessary to perform a set of diagnostic measures aimed at identifying the reasons that caused these changes.

Important! From 150 to 180 liters of fluid pass through the kidneys every day, forming 1.5–1.8 liters of urine as a result of reabsorption.

Types of changes

Depending on the zone of localization of diffuse changes, the following structural disorders are distinguished:

kidney bodies;
parenchyma;
sinuses;
pyelocaliceal system.

A significant role, in terms of diagnosis, is played by the nature of structural changes, which makes it possible to make an initial diagnostic verdict, which does not, however, exclude further comprehensive examination. For example, the following deviations may be observed:

change in kidney size;
asymmetry of kidney contours;
thinning or thickening of the renal parenchyma;
formation of foci of increased or decreased density in the parenchyma;
disturbances in the structure of the sinuses;
changes in the structure of the collecting system;
fluid in the collecting system;
seals in the structure of the renal vein.

Important! An increase in the volume of the pyelocaliceal system in a newborn child is not a pathology, since it occurs as a result of the forced accumulation of metabolic products within one’s own body, during the period of intrauterine existence.

The lobed structure of the kidney in children is also not a pathology, as it returns to normal by 2-3 years of life

Ultrasound diagnostics

Ultrasound, today, retains its primacy among all diagnostic procedures due to its accessibility, high information content and the absence of contraindications for conducting an unlimited number of studies. The method is based on the properties of soft tissues to resist the penetration of ultrasonic waves.

In this case, some waves are reflected, and some pass through the tissues, being absorbed by them. The more ultrasound is reflected (hyperechoic area), the lighter the shade on the monitor screen and, accordingly, the greater the density of the organ or its inclusions.

The classification of diffuse changes in the structure of the kidneys, from the point of view of ultrasound, includes the following types of changes:

clear;
fuzzy;
moderate;
weak;
expressed.

Diffuse changes in the renal pelvis caused by deformation of the renal pelvis or sinuses due to formed stones will appear on the ultrasound machine monitor as hyperechoic areas. Tissues with low density will appear on the ultrasound monitor as darker areas called hypoechoic. Liquid located in the structure of an organ, for example, a cyst, is characterized as an anechogenic formation.

Diffuse changes in the kidneys with ultrasound examination will have the following symptoms:

darkening in the parenchyma;
hyperechoic zones in the CLS;
lack of clear contours in the parenchyma;
darkening of the contours of the renal arteries
anechogenic areas in the parenchyma or CLS;
deformations of the contours of the pelvis and renal capsule.

Ultrasound can be used to examine functional state kidneys in the fetus in the last stages of pregnancy

Causes

The reasons for the deterioration of the kidney structure may lie in a wide variety of pathologies or anatomical changes, congenital or acquired. For example, a congenital bend of the ureter or curvature as a result of its compression during pregnancy by a growing fetus can lead to the development of hydronephrosis.

An increase in the volume of the pyelocaliceal system, which is a direct sign of the disease, during diagnosis is defined as “diffuse changes in the pelvis”. Also, structural changes in the maxillary sinus and renal sinuses can cause:

cystic formations in the cavity of the pelvis or calyces;
stones in the jaw;
tumor formations.

Damage to the kidney sinuses is often accompanied by pain in the heart and increased blood pressure

Inflammatory and sclerotic processes are of great importance in the development of structural disorders of the kidney sinuses, causing swelling (in the case of inflammation) or atrophy (in the case of atherosclerotic changes) in the vascular surface of the sinus. Often, inadequate treatment of an inflammatory disease leads to the development of atrophic processes.

Important! Characteristic feature, accompanying the course of the acute stage of diseases is an increase in the organ, while the chronic course, on the contrary, is its decrease.

Diffuse changes in the renal parenchyma can have various manifestations, due to the structural features of the parenchymal tissue. The list of diseases that cause disruption of the normal structure of kidney tissue includes:

parenchymal cyst;
pyelonephritis;
glomerulonephritis;
nephrosclerosis;
tuberculosis.

Parenchymal cyst

A renal parenchymal cyst is a congenital or acquired pathology in which, directly in the main tissue of the organ, a cavity space filled with serous or hemorrhagic exudate is formed. A cyst can form in the kidney in a single instance (solitary), but multiple cystic lesions can also be observed (polycystic).

The mechanism of cyst formation is of great diagnostic importance. If the cystic cavity is formed as a result of injury or a violation of the outflow of fluid from the nephron canal due to obstruction by uric acid crystals, then, as a rule, such a formation is benign and can be easily removed using the laparoscopic method. When diagnosed, a cyst is defined as a single cavity, round or oval in shape with clear boundaries, filled with liquid contents.

Overlapping the lumen of the tubule with polyps or dysplastic changes, for example, proliferation of connective tissue, leads to the formation of a multilocular cyst, which is a multi-chamber cavity formation with clear contours.

A multilocular cyst is considered to be a cystic form of cancer.

Pyelonephritis

Inflammatory kidney disease, accompanied by damage to the underlying renal tissue and renal pelvis. Most often, the disease affects both the right and left kidney and can have an acute or chronic course.

The reasons for the development of pyelonephritis can be:

Prostate adenoma. An enlarged gland prevents the timely outflow of urine from the kidneys, promoting the development inflammatory process. Infection of the kidney by pathogenic microorganisms developing in the prostate gland also plays a certain role;
Vesicoureteral reflux. In most cases, the development of pyelonephritis is preceded by cystitis or urethritis. As a result of the long course of these diseases, the mechanism that prevents the return of urine into the ureters is disrupted, which is the cause of kidney infection;
Urolithiasis disease. In addition to disrupting the outflow of urine, stones damage the mucous membrane of the pelvis, facilitating the penetration of pathogens into the kidney tissue.

When visualizing the condition of the kidneys on an ultrasound monitor, when acute course disease, there is an increase in the thickness of the parenchyma, a discrepancy in the size of both kidneys, and in chronic cases - uneven contours, heterogeneity (due to scar formation) and thinning of the structure of the underlying tissue. At chronic pyelonephritis extensive diffuse changes in the parenchyma are observed.

Glomerulonephritis

As a rule, glomerulonephritis occurs as a result of previous infectious diseases:

angina;
otitis;
scarlet fever;
pneumonia.

The immune restructuring of the body, provoked by bacterial microflora, causes the kidneys to perceive their own tissues as foreign, exposing them to attack by protective complexes. IN healthy body immune complexes must be neutralized in the liver, but if this does not happen, the vessels of the renal glomeruli are subject to destructive effects.

With glomerulonephritis, the kidney is usually of normal size, but may be enlarged. The structure of the parenchyma is uneven, due to the enlargement of the renal glomeruli, the vascular system is poorly defined, multiple hemorrhages and microscopic exudative cavities may be present.

Hematuria is one of the diagnostic signs glomerulonephritis

Nephrosclerosis

Nephrosclerosis is a disease associated with insufficient blood supply to the kidneys due to sclerotic damage to the vascular system. Impaired blood supply leads to the gradual death of the functional components of the kidney - the glomeruli - and their gradual replacement with connective tissue.

Due to the fact that the interstitial tissue has a denser structure, the intensity of the shade during ultrasound examination has some differences, due to which extensive diffuse changes are determined. In addition, with nephrosclerosis, atrophic changes occur, leading to a decrease in the size of the organ (wrinkling) and thinning of its membrane.

The stages of nephrosclerosis are divided into:

primary;
secondary.

Atherosclerotic changes in blood vessels are the main cause of the development of primary nephrosclerosis

If in custody medical examination, there is the wording “primarily shriveled kidney” - which means that the pathological processes are caused by atherosclerotic damage to the vascular system. A secondary wrinkled kidney is the result of chronic inflammatory processes that cause irreversible damage to the parenchyma:

glomerulonephritis;
tuberculosis;
pyelonephritis.

Important! With nephrosclerosis, the kidneys have a fine-grained surface, as a result of which, when performing an ultrasound, the contour has unclear outlines, in some cases, pronounced tuberosity is determined.

Tuberculosis

Tuberculous kidney damage, depending on the stage of development, can have a variety of manifestations:

multifocal damage to the entire volume of parenchyma, accompanied by the formation of capsules filled with necrotic masses. With ultrasound, the capsules are defined as multiple cystic formations, filled, unlike cysts, not with exudate, but with denser masses (caseous);
isolated single foci of parenchymal damage;
multiple scar changes (areas with increased echogenicity). This process is observed during the restoration of an organ after an illness;
partial or complete replacement of one of the segments of healthy kidney tissue with encapsulated foci of necrosis;
damage to more than 70% of organ tissue.

Important! In addition to the formed capsules, ultrasound reveals a deformation of the pyelocaliceal system, which has certain similarities with a similar deformation during the development of a parenchymal cyst.

Treatment of tuberculosis requires an integrated approach, due to the rapid development of resistance of Koch's bacillus to the drugs used.

Thus, the concept of diffuse changes means a fairly wide range of structural transformations that have Negative influence on the functional activity of the organ. The main goal of diagnostic manipulations is to accurately characterize these changes, which makes it possible to identify the disease with a high percentage of accuracy and develop the most effective treatment tactics.

In the classification of immunoinflammatory pathologies of the kidneys, acute diffuse glomerulonephritis occupies a special place. It is characterized by damage to the glomeruli, in which the disease spreads to all renal tissues. Glomeruli are special structures consisting of small blood vessels, the nodes of which take part in the process of filtering blood and removing excess fluid. Occurs in people of all ages, including children.

Depending on the morphological changes renal glomeruli, glomerulonephritis can be divided into the following types:

membranous type (membranous glomerulopathy);
proliferative form;
focal segmental glomerulosclerosis;
mesangio-capillary.

Membranous nephropathy is accompanied by diffuse thickening of the basement membranes of the capillaries that make up the glomeruli of the kidney. As a rule, the development of the disease is not associated with infection and it occurs most often in mature men. A third of patients complain of manifestations of hypertension and hematuria, and in half of the patients it occurs.

The proliferative type of the disease is characterized by an acute diffuse increase in cellular structures capillaries in the glomeruli of the kidney. This form is found most often in medical practice.

Focal segmental glomerulosclerosis is accompanied by sclerosis of individual loops of renal capillaries. This form usually occurs in patients with HIV infection and in people who use intravenous drugs. It is worth noting that it is considered one of the most dangerous and unfavorable options for the course of the disease.

The mesangial-capillary type of glomerulonephritis is accompanied by thickening of the capillary walls and a proliferative process in the mesangial cells, which spread to the glomeruli. The latter, in turn, acquire a peculiar lobular structure, and their basement membrane doubles.

At the same time, a collective form of the disease is identified, combining symptoms of several types at once. It is important to note that if treatment is not started in a timely manner, chronic diffuse glomerulonephritis develops, which is much more difficult to treat.

Causes

The main factor causing acute diffuse glomerulonephritis is a previous infection. This could be pneumonia, sore throat, pharyngitis and other infectious diseases. Often, the causative agent of the acute form is group A streptococci, less often pneumococci and staphylococci. Another serious risk factor is hypothermia, which inevitably impairs blood circulation in the kidneys. In medicine, cases of acute forms of pathology occurring after vaccination have been described.

Acute glomerulonephritis develops on average after 2–3 weeks due to infectious disease, when the body undergoes an immunological restructuring with a change in kidney protein under the influence of an agent. Thus, these proteins are perceived by the body as foreign, so autoantibodies begin to be produced against them. IN pathological process both kidneys are involved at once, in which general vascular lesions are observed.

A little about pathological anatomy

With any form of immunoinflammatory disease, be it proliferative, chronic, membranous glomerulonephritis or another type of disease, the glomeruli increase in size, and during examination under a microscope, signs of inflammation of the capillaries can be detected. Later, due to spasms, their ischemia and endothelial proliferation are observed. Protein exudate accumulates in the area between the glomerular capsule and capillary loops. The kidneys themselves may be slightly enlarged.

As the inflammatory process subsides, proliferation gradually decreases, and normal capillary patency is restored.

Main symptoms

Acute diffuse glomerulonephritis in adults and children occurs with characteristic symptoms. The main specific signs of the disease include:

swelling is a consequence of abnormal capillary permeability;
urination disorders with pathological changes in urine;
hypertension, which occurs due to fluid retention in the body.

Patients often complain of such general clinical manifestations as headaches, nausea, fever, weakness, and pain in the lumbar region.

Many patients acquire a characteristic appearance due to swelling of the face and pallor of the skin. Gradually, the symptom can spread to the entire body, with body weight increasing by 15 kilograms or more.

A characteristic sign of diffuse glomerulonephritis is urination disturbance, which can be frequent and sometimes even painful. People diagnosed with acute or chronic diffuse glomerulonephritis experience oliguria (usually on the first day of the disease), characterized by a small amount of urine excreted and anuria (lack of urination). It is worth noting that episodes of anuria are replaced by polyuria. A third of patients experience pain in the lumbar region, which may be caused by stretching of the kidney capsule.

Urine tests in adults and children with glomerulonephritis reveal various pathological impurities in the form of protein (proteinuria), epithelium, blood, and less commonly, leukocytes. The urine becomes cloudy and dark red or reddish-brown. Bacteriuria will indicate the addition of an infection.

Another characteristic symptom that accompanies proliferative and other types of glomerulonephritis is hypertension with an increase in systolic pressure to 150–200 mm Hg. Art., diastolic – up to 105 mm. Due to the increased mass of circulating blood, indicators venous pressure are increasing. In most patients, episodes of hypertension are short-lived.

The basis for increased blood pressure in adults and children is a condition such as renal ischemia and the formation of renin in them, which is converted into an active pressor substance called angiotensin. It is with this phenomenon that headaches that occur in many patients can be associated.

When acute glomerulonephritis worsens due to cerebral edema, encephalopathy and eclampsia may occur. Sometimes in the preeclamptic period intense headaches occur, and the arterial pressure. During an attack of eclampsia, loss of consciousness occurs, the pulse slows, skin turn pale, muscle cramps, involuntary urination or loss of feces occur.

Clinical signs in children

Diffuse glomerulonephritis in childhood has similar symptoms. Some time after suffering an infectious disease, the child develops lethargy, nausea and vomiting, headache. Against the background of reduced diuresis, thirst and swelling are noted. If the swelling extends to the heart muscle, children experience bradycardia. Severe circulatory failure occurs rarely, but renal eclampsia occurs in approximately 7-10% of patients.

Most often, in children, proliferative glomerulonephritis occurs cyclically with an increase and stabilization of symptoms. Remission occurs on average after 2 months, but we can talk about complete recovery much later - after 1.5-2 years. The duration of symptoms for more than 12 months indicates that the child has chronic diffuse glomerulonephritis.

Differential diagnosis

Competent treatment can only be prescribed if it is of high quality differential examination. There are a number of kidney pathologies that may be accompanied by similar symptoms. Thus, the appearance of symptoms in a period of less than twenty days after the infectious process rather indicates an exacerbation of chronic renal pathology.

It is important to differentiate the disease from pyelonephritis (based on the results of kidney function tests), focal forms of nephritis, and heart pathologies characterized by swelling.

Therapeutic measures

Treatment of adults and children with acute glomerulonephritis should be carried out in a hospital setting. All patients are required to remain in bed until the underlying causes are eliminated. clinical signs. In the first week, a salt-free diet and a reduced amount of protein are prescribed, after which patients are recommended a diet with a complete protein composition, but with low salt consumption.

Therapy for adult patients and children is prescribed according to the same principle and includes:

Etiological treatment is antibiotic therapy aimed at suppressing the infectious pathogen (if one is identified). Most often, the development of acute diffuse glomerulonephritis is associated with streptococcal infection, which can be treated with penicillin.
Pathogenetic therapy - performed using non-hormonal and hormonal immunosuppressants, steroids, heparin, antiplatelet agents and anticoagulants to improve blood microcirculation.
Symptomatic treatment – elimination of hematuria, edema, arterial hypertension with the help of appropriate medications.

Patients with diffuse glomerulonephritis are usually prescribed diuretics, antiallergic drugs, and glucocorticoids. Intensive care requires a complicated course of the disease. For anuria in children and adults, hemodialysis can be prescribed - artificial purification of the blood from toxins. Eclampsia and pulmonary edema require bloodletting.