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Internal illnesses. Diffuse glomerulonephritis (lecture notes)

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LECTURE No. 38. Diffuse glomerulonephritis

Diffuse glomerulonephritis is an immune-mediated inflammation with a predominant initial glomerular lesion and involvement of all renal structures in the pathological process, clinically manifested by renal and (or) extrarenal symptoms, leading to a secondary shrunken kidney and death from chronic renal failure.

It is divided into acute and chronic glomerulonephritis. True acute glomerulonephritis is only one that is proven by intravital morphological examination. In other cases, chronic glomerulonephritis develops, which has an acute onset.

Etiology. Exogenous factors: bacteria (β-hemolytic streptococcus group A (strains 12, 43, 49), white staphylococcus aureus, bovine corynebacterium, enterococci, typhoid salmonella, pale treponema, diplococci), viruses (cytomegalovirus, herpes simplex viruses, hepatitis B, Epstein-Barr), fungi (Candida albicans), parasites (malarial plasmodium, schistosome, toxoplasma), drugs, poisons, foreign serum.

Endogenous factors: nuclear, brush border antigen, thyroglobulin, immunoglobulins, tumor and embryonic antigens, carcinomatous antigen.

Risk factors: hypothermia

Pathogenesis. There is a passive drift of the immune complex into the glomerulus, its deposition. Antibodies circulating in the blood stream react with a structural antigen or with a triggering non-glomerular autologous or exogenous antigen. There is hyperfiltration, an increase in the transcapillary gradient - the acceleration of sclerosis in the remaining glomeruli.

Clinic. Major Syndromes acute glomerulonephritis are the following: urinary, edematous, hypertensive, nephrotic.

Flow shapes: deployed (cyclic) and monosymptomatic (latent).

Cyclic form never begins at the height of infection, not earlier than 14-25 days after the onset of infection. It is characterized by obligatory cyclicity of the course, it develops acutely, weakness, swelling (mainly of the face), headache, decreased diuresis, urine the color of meat slops, and back pain appear. Arterial hypertension develops (systolic blood pressure does not exceed 180 mm Hg, diastolic blood pressure - 120 mm Hg), tachycardia, there may be signs of acute heart (left ventricular) failure (shortness of breath, cough, attacks of cardiac asthma). There is an expansion of the boundaries of relative cardiac dullness, a systolic murmur at the apex, an accent of the II tone on the aorta, sometimes a gallop rhythm, dry and moist rales in the lungs. Urinary syndrome is characterized by proteinuria, cylindruria, macro- and microhematuria. Proteinuria is associated with gross damage to the vascular wall of the glomerular capillaries, through which albumins, globulins, and fibrinogen are released. Hematuria is a constant symptom. A small number of leukocytes. Edema persists for 10-15 days, disappears by the end of the 3rd week, blood pressure decreases, polyuria develops, urinary syndrome persists for more than 2 months, hypostenuria appears, slight proteinuria may persist for a long time (0,03-0,1 g / day), residual hematuria, leukocyturia disappears at the end of the first month.

For latent form a gradual onset is characteristic, without subjective manifestations, headaches, slight shortness of breath or swelling in the legs are possible, the duration of the condition is up to 2-6 months or more, the presence of an isolated urinary syndrome. Acute nephritis that has not resolved within a year is considered chronic glomerulonephritis.

Major Syndromes chronic glomerulonephritis: urinary, hypertensive, edematous, hyperlipidemia, hypoproteinemia, anemic, chronic renal failure.

Flow shapes: latent, hypertensive, nephrotic, mixed, malignant (subacute), terminal.

The latent form is more often detected by chance, during the clinical examination. Characterized by long-term preservation of working capacity without signs of disease (up to 10-20 years), the presence of isolated urinary syndrome, isohypostenuria, low specific gravity of urine, nocturia, possibly increased blood pressure, hypoproteinemia, hypercholesterolemia, increased ESR.

For a long time, the leading and only symptom of the hypertensive form is arterial hypertension. Initially, hypertension is intermittent in nature, in the future - permanent. On examination, there is an apex beat visible to the eye, an expansion of the relative dullness of the heart to the left, an accent of the II tone over the aorta, a gallop rhythm, with the progression of heart failure, there are manifestations of stagnation in the pulmonary circulation, hemoptysis, attacks of cardiac asthma, rarely - pulmonary edema. The fundus of the eye: neuroretinitis is moderate, only narrowing of the arteries persists for a long time.

RџSЂRё nephrotic form trophic changes appear: dryness of the skin, a decrease in its elasticity, muscle hypotrophy, edema develops due to a decrease in oncotic pressure, at first insignificant in the morning under the eyes, on the ankles, then permanent with a transition to the trunk; hydrothorax, ascites, hydropericardium. There is a dissociation of protein-lipid ratios (hypoproteinemia, hypercholesterolemia), urinary syndrome may appear: hematuria, decreased filtration function, blood pressure does not increase.

For mixed form the severity of edema, urinary syndrome, arterial hypertension, as well as the progressive course and development of renal failure (within 2-5 years) are characteristic.

For malignant (subacute form) characterized by a rapid and persistent decrease in kidney function, increasing changes in the fundus.

terminal form refers to the stage of renal decompensation, associated with insufficiency of nitrogen excretion function. Pronounced nephrotic and hypertensive syndromes, increased levels of urea, creatinine, indican, reduced glomerular filtration, increased filtration fraction.

Additional diagnostic study. A complete blood count (neurophilic leukocytosis, increased ESR, anemia), a biochemical blood test (increased fibrinogen, C-reactive protein, LDH4-5 alkaline phosphatase), and a general urine test are performed.

In acute glomerulonephritis, a decrease in the amount of urine to 400-700 ml / day is characteristic, anuria rarely occurs, protein - from 1 to 10 g / day, albuminuria decreases after 7-10 days, the amount of protein becomes less than 1 g / day, erythrocytes, single hyaline and granular casts, a slight increase in the number of leukocytes, an increase in the specific gravity of urine.

In chronic glomerulonephritis in the stage of renal compensation, there is an increase in the amount of urine, a persistent decrease in specific gravity (isohyposthenuria), nocturia. Insignificant amounts of protein, an increase in erythrocytes, their predominance over leukocytes are noted.

In chronic glomerulonephritis in the stage of renal decompensation, there is a decrease in the amount of urine, an increase in protein, specific gravity, urea, creatinine, and indican in the blood.

The Nechiporenko test is performed (determination of the number of erythrocytes, leukocytes and cylinders in 1 ml of urine: normally, erythrocytes - up to 1000, leukocytes - up to 2000, cylinders - up to 50, with glomerulonephritis, erythrocytes prevail over leukocytes), Kakovsky-Addis test (determination of the number of erythrocytes, leukocytes, cylinders in the daily volume of urine: normal erythrocytes - up to 1, leukocytes - up to 000, cylinders - up to 000, with glomerulonephritis, erythrocytes predominate over leukocytes), urine culture with a quantitative assessment of bacteriuria (if detected in 2 ml urine more than 000 bacteria). They also determine enzymes in the urine: transaminases, redox and their isoforms (LDG000-100), cholinesterases (with glomerulonephritis increase), determination of β2-microglobulin in urine (β2-MG) (assessment of the functional state of the kidneys). If the tubules are damaged, protein readsorption is impaired, excretion of β2-MG increases, no other proteins are detected, the glomeruli are not affected, with an isolated lesion of the glomeruli, the content of β2-MG is within the normal range, medium molecular weight proteins (albumins) increase, with a mixed process, a simultaneous increase in β is noted2-MG and albumin.

A Zimnitsky test is carried out to assess the ability of the kidneys to concentrate and dilute urine: under the conditions of normal water and food regimens, 8 portions of urine are collected separately, its quantity and relative density are determined; evaluate daytime (from 8 am to 8 pm) and night (from 8 pm to 8 am) diuresis, dynamics of quantity, relative density of individual portions, nocturia.

In the Folgard concentration test (with dry diet), daily diuresis decreases to 300-500 ml, the specific gravity of urine increases, reaching 4-8 in 1028-1035 hours, not lower than 1025.

Reberg-Tareev test: glomerular filtration rate for creatinine - 80-160 ml / min, tubular reabsorption - 98-99%, with glomerulonephritis, the indicators decrease; in acute glomerulonephritis, the changes are transient; in chronic glomerulonephritis, they are persistent.

An ultrasound examination of the kidneys is mandatory: determining the size of the kidneys, their position, the thickness of the parenchyma to characterize sclerotic processes, deformation of the cavity systems.

A kidney biopsy is performed to clarify the diagnosis of a parenchymal disease; There are 3 types: open (during surgery), semi-open (through a surgical incision of the skin and subcutaneous tissue) and closed, or percutaneous (using a puncture needle). Contraindications: hemorrhagic diathesis, single kidney, polycystic, hydro- and pyelonephritis, severe hypertension, nephrocalcinosis, kidney tumor, negative attitude of the patient.

An immunological blood test is carried out: determining the number of the main immunocompetent forms of lymphocytes, immunoglobulins of classes A, M and J, total complement and the 3rd complement fraction, the number of circulating immune complexes to assess the state of all parts of the immune response, with acute glomerulonephritis and with exacerbation of chronic glomerulonephritis decreases the level of total complement and the 3rd fraction, the number of circulating immune complexes, immunoglobulins of all classes increases, the titer of antistreptolysin O increases.

They also conduct an ECG study (signs of left ventricular hypertrophy), an examination of the fundus (exudation, retinal edema, changes in the papillae of the optic nerve that appear with the development of chronic renal failure).

Complications. Complications in acute glomerulonephritis are acute renal failure, acute heart failure, renal eclampsia. In chronic glomerulonephritis, complications are left ventricular heart failure, chronic renal failure, anemia, uremic stomatitis, gastritis, colitis, bronchitis, polyserositis.

Differential diagnostics. When acute glomerulonephritis differential diagnosis is carried out with chronic glomerulonephritis, collagenosis, bacterial endocarditis, focal nephritis, urological diseases.

RџSЂRё chronic glomerulonephritis differential diagnosis is carried out with hypertension, left ventricular type heart failure, diabetic glomerulosclerosis, liver cirrhosis, amyloidosis, congestive kidney.

Treatment. Patients are shown a diet and regimen: with sufficient kidney function, protein restriction (within 1 g / kg of body weight), with the development of arterial hypertension, salt restriction, with edema - salt and water, restrictions during a pronounced inflammatory process. Glucocorticoids are prescribed (immunosuppressive, anti-inflammatory and desensitizing effect) - an initial dose of 60 mg / day for 3 weeks, then a decrease by 5 mg for 4 days to 40 mg, then by 2,5 mg for 2-3 days, maintenance therapy with persistent urinary syndrome. Cytostatics are administered (with a long process, the presence of a hypertensive syndrome, initial signs of renal failure, with the ineffectiveness of hormone therapy): azathioprine (daily dose of 150 mg), cyclophosphamide (daily dose of 200 mg) to suppress final immune responses; delagin, rezoquin, chloroquine. Also shown are anticoagulants and antiaggregants - heparin 20 thousand units per day for 5 days, then 5 thousand units daily for up to 3-4 weeks, chimes up to 300 mg per day orally on an empty stomach for 6-8 months; in severe renal bleeding aprotinin (antifibrinolytic drug), non-steroidal anti-inflammatory drugs (methindol) 100-150 mg per day for 1-2 months or more in acute glomerulonephritis with nephrotic syndrome. Calcium channel blockers, angiotensin-converting enzyme inhibitors (as pathogenetic therapy), reduction of proteinuria are prescribed.

Symptomatic therapy is carried out: antihypertensive, diuretic drugs, calcium salts, cardiac glycosides, desensitizing agents, large doses of vitamin C are prescribed. In case of uncomplicated AGN, in the first days, complete exclusion of salt, fluid restriction, ascorbic acid, calcium gluconate, if necessary, correction electrolyte disorders. With a persistent course of arterial hypertension, it is necessary to connect pathogenetic, antihypertensive, diuretic therapy. Programmed hemodialysis is carried out (in the absence of the effect of treatment, with an increase in renal failure), plasmapheresis.

Flow. In acute glomerulonephritis, there is usually a complete recovery or recovery with persistent proteinuria. In chronic glomerulonephritis, depending on the form, the course is progressive, with the development of chronic renal failure.

Forecast. In acute glomerulonephritis, the prognosis is favorable (mortality rate is 2%), in chronic glomerulonephritis, it is favorable in the latent form and unfavorable in other forms.

Prevention. Primary prevention measures include sanitation of foci of infection, their adequate treatment, and only appropriate vaccination.

Measures of secondary prevention: dispensary observation, treatment of complications and exacerbations, rational employment.

Author: Myshkina A.A.

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