Glomerulonephritis - a disease that damages the structure of the kidneys, primarily affects glomeruli - renal glomeruli responsible for the filtration of blood. The acute form of pathology provokes the loss of this ability for a while, the result of inadequate purification of blood from toxins - a violation of kidney function.
Acute form of pathology is formed as a result of infections and allergies. The disease is more typical for patients aged 12-40 years, male representatives are more exposed. Acute glomerulonephritis has a seasonal factor, favorable conditions for it - a cold climate with high humidity.
According to the International Classification of Diseases ICD-10 revision - "acute nephritic syndrome", code N00.
The formation of acute glomerulonephritis is a consequence of the presence of inflammation in glomeruli. Often the disease occurs after angina, tonsillitis, pharyngitis of streptococcal nature, glomerulonephritis provokes hemolytic group A streptococcus. Migration of bacteria from the ENT organs to the kidneys is explained by a decrease in the function of the body's defenses.
Other causes of acute glomerulonephritis:
|pneumonia, endocarditis;||allergic purpura;Scarlet fever|
|;||is lupus erythematosus;|
|typhoid fever;||blood transfusion;|
|hepatitis B;||effects of radiation therapy;|
|chicken pox;||intoxication with alcoholic beverages;|
|disease caused by Coxsackie viruses.||ingestion of lead, mercury;|
|ingestion of organic poisons.|
Another major cause of the disease is hypothermia. With prolonged exposure to cold, reflex disorders of blood supply arise, this affects the course of immunological reactions.
Urology defines acute glomerulonephritis as an immunocomplex disease, preceded by an autoimmune process. Due to inflammatory processes, most often against the background of streptococcal activity, antigens( proteins of viruses, bacteria) appear in the patient's blood. Streptococcal antigen affects the endothelium of the capillaries, the basal membrane, the epithelium of nephrons.
Antigens to human immunity responds to the production of antibodies - these are blood plasma proteins that neutralize and prevent the reproduction of antigens. Interacting in the blood, the antigen-antibody pair is deposited on the walls of the vessels, so the immune complexes are formed. They injure the walls of the capillaries, provoke the formation of microthrombi, and also clog the lumen of the vessels, triggering a chain reaction, the result of which is damage to the glomerulus and the kidney itself.
Vascular tissue begins to be replaced by a connective tissue. The death of healthy cells and replacement of their connective scar tissue provokes the development of renal failure. In this case, glomeruli can not perform their basic function qualitatively, because of the lack of complete purification, toxins accumulate in the blood.
The process of activation of acute diffuse glomerulonephritis takes 2-3 weeks, during this time there is an accumulation of antigens and antibodies.
Syndromes of acute pathology:
- With nephrotic syndrome - renal edema is typical, changes in urine are observed - protein concentration increases whereas blood protein content decreases;
- hypertensive - the most vivid symptom - blood pressure;
- nephritic - the most severe form, features - pronounced changes in the composition of urine and blood, hypertension, anemia, severe swelling.
Classification of diffuse acute glomerulonephritis according to the histological type:
- mesangioproliferative - scar tissue grows between the glomerulus vessels, resulting in narrowing of the capillaries;
- intracapillary - connective tissue replaces the inner layer of the vascular wall, as a result of narrowing the capillaries;
- mesangiocapillary - mixed form, actively progressing;
- membranous nephropathy - connective tissue replaced capillary walls, their thickening occurs against the background of subsidence of antigen-antibody pairs in large quantities;
- fast-progressive is the most severe kind of disease.
Separately isolated poststreptococcal form - the development of this disease is preceded by infectious diseases caused by the activity of streptococcus.
On video, causes, pathogenesis and classification of acute glomerulonephritis:
Main manifestations of pathology:
- marked swelling;
- arterial hypertension;
- change in the composition of urine.
Edemas appear at an early stage of the acute form of the disease, it is a common sign, its presence is noted in 70-90% of cases. Puffiness mostly affects the face, by the evening passes into the legs. In protracted cases of the disease, the symptom can grow to ascites, hydropericardium. The moisture loss in tissues is evidenced by the causeless increase in the weight of the patient.
Swelling of the brain of the head provokes the development of cerebral syndrome, which includes headaches, nausea and vomiting, sensations of "shroud" before the eyes, deterioration of hearing and vision, psychomotor excitability. In severe cases, convulsions occur, the patient may lose consciousness.
Increased blood pressure in acute glomerulonephritis persistent, but moderate, millimeters of mercury does not exceed 160/100.Rapid heart rate is a frequent companion of hypertension. The syndrome provokes an acute disruption of the cardiac function, hypertrophy of the left ventricle of the heart and an increase in the myocardium.
The change in the urine composition is based on an increased concentration of protein( proteinuria) and erythrocytes( in the form of microhematuria or macrohematuria).These conditions explain the change in the color of urine, which has a pink or red hue, the color of meat waste. Against the background of constant thirst, oliguria develops( a decrease in the volume of urine output), in rare cases - anuria( absence of urine).
Patients may be worried about low back pain, they are symmetrical, appear against a background of stretching of renal capsules and disorders of urinary excretion.
External manifestations and some results of diffuse acute glomerulonephritis are similar to exacerbation of the chronic form of the disease. To differentiate the doctor's condition, the time interval from infection to the lesion of the renal glomeruli is of primary interest. In acute condition, it takes 1-3 weeks, the chronic form is aggravated in a couple of days.
The main analysis is a general urine sample, the presence of proteins and erythrocytes indicates a pathology. Proteinuria occurs only in the first week of the disease, early development in the urine contains 10-20 or more grams of protein per liter, then the condition stabilizes. Detect pathology of hematuria, the microhematuria account for 75% of cases, while the hematuria occupies no more than 15%.In some cases, leucocyturia is found.
Erythrocytes are always larger than leukocytes in pathology, it can be proved by Nechiporenko's test with calculation of urinary sediment elements. When Zimnitsky's trial shows an increased volume of urine, increased density.
Blood analysis( biochemical) - protein reduction, detection of reactive protein, increased cholesterol, the presence of sialic acids, an increase in the amount of nitrogenous compounds. In many cases, an increased rate of erythrocyte sedimentation can be observed. The concentration in the blood of leukocytes is determined by the primary or concomitant infection, it depends on the pathogen whether the patient's temperature rises.
If the signs of pathology are not characteristic of the post-streptococcal form, the physician prescribes a biopsy.
When still undergoing biopsy:
- when the glomerular filtration rate decreases, if the indices do not reach half the normal values;
- when the amount of the C3 component in a complex of complex proteins decreases and is at a reduced level for more than three months;
- in the presence of a stable macrohematuria, if it does not pass for three months;
- when the nephrotic syndrome developed.
Since the disease develops as a result of the settling of immune complexes on the walls of blood vessels, it is advisable to conduct immunological tests. Such diagnostic measures allow detecting the presence of antibodies IgG, IgM, IgA.
To determine the hypertensive form prescribed ECG and examination of the fundus.
Patients are assigned bed rest. Patient rest is required in order to prevent the accelerated formation of toxic nitrogen compounds, which quickly occurs with physical stress.
Violation of the body provokes changes in the electrolyte balance of blood, as well as the loss of body nutrients and the accumulation of toxins. A special diet helps to reduce the negative impact of the pathological process. In the treatment of acute glomerulonephritis, patients are assigned a seventh table.
Basic principles of the diet:
- reduced salt intake;
- limit the amount of liquid consumed;
- inclusion in the menu of products with a high content of potassium and calcium;
- the exclusion of products that contain sodium in large quantities;
- restriction of protein intake;
- inclusion in the diet of fresh vegetables and fruits and other complex carbohydrates, vegetable oils.
|Antiaggregants and anticoagulants( Heparin, Ticlopidine, Dipiridamole)|| increase in blood fluidity; |
prevention of blood clots in the vessels glomerul
| Heparin - 20-40 IU per day for three to ten weeks; |
Ticlopidine - twice a day for 0.25 grams;
Dipyridamole - a day of 400-600 milligrams.
|Immunosuppressors( Azathioprine, Cyclosporine, Cyclophosphamide, Chlorambucil), including steroid agents( Prednisolone)|| suppression of immunity activity; |
cessation of destructive processes
| Azathioprine - 1.5-3 milligrams per kilogram of body weight per day; |
Cyclosporine is 2.5-3.5 milligrams per kilogram of body weight per day;
Cyclophosphamide - 2-3 milligrams per 1 kg per day;
Chlorambucil is 0.1-0.2 milligrams per kilogram per day;
Prednisolone - in the first 2-3 months of 1 mg per kilogram per day, then 30 milligrams per day.
|Drugs for lowering blood pressure( Enalapril, Captopril, Ramipril)||lowering of blood pressure|| Enalapril - 10-20 mg per day; |
Captopril - 50-100 milligrams per day;
Ramipril - at a dosage of 2.5-10 mg per day.
|Diuretics( Uregit, Aldactone, Hypothiazide, Furosemide)|| removing excess fluid from the body; |
decrease in blood pressure
| Ureit and Hypotazide - 50-100 milligrams; |
Aldactone - up to 300 milligrams per day;
Furosemide - 40-80 mg per day.
|Antibacterial drugs||are prescribed to eliminate infection, they are selected individually for each case, depending on the pathogen of infection, individual characteristics of the patient.|
The disease requires immediate medical attention and targeted treatment. Serious complications of acute glomerulonephritis develop quite rapidly.
The main consequence is the transition of the disease to the chronic stage and the violation of renal function. Blockage of blood vessels and thrombi provokes acute cardiac dysfunction. Complications also include hemorrhagic stroke, eclampsia, temporary blindness.
The prognosis of the disease can not be called completely favorable. Only in 50% of cases there is a complete recovery, the forecast is affected by the speed of seeking medical help. In half the cases, the chronic form of the disease develops. If the patient starts treatment on time, he will be able to recover in two to three months of therapy.
On the video about the treatment, consequences and complications of acute glomerulonephritis: