Hospital therapy. Kidney diseases. Acute glomerulonephritis (lecture notes)

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Hospital therapy. Kidney diseases. Acute glomerulonephritis (lecture notes)

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LECTURE No. 15. Diseases of the kidneys. Acute glomerulonephritis

Acute glomerulonephritis (AGN) is an acute diffuse kidney disease of an infectious-allergic nature, localized in the glomeruli. AGN can be an independent disease (primary) or be secondary as part of another disease, complicating the clinical picture and diagnosis of the latter. AGN usually affects young and middle-aged men.

Etiology. AGN occurs most often after a coccal infection (influenza, acute tonsillitis, pharyngitis caused by so-called nephritogenic strains of microorganisms).

In 60-80% of patients, group A β-hemolytic streptococcus is detected; in 1/3 of cases, the etiology of AGN cannot be established. Prolonged hypothermia, especially in conditions of high humidity, contributes to the development of AGN. Vaccination is also a factor in the onset of the disease, and in 75% of cases the kidneys are affected after the second or third injection.

Pathogenesis. The pathogenesis of the disease has an immune mechanism: when antigens (streptococcal, medicinal, foreign proteins) enter the body, antibodies are formed in response, binding these antigens and, together with the 3rd fraction of complement, forming immune complexes circulating in the vascular bed. The complexes are capable of depositing on the outer side of the basement membrane of the glomerular capillaries, causing their damage through the release of complement breakdown products, which increase the permeability of the capillaries and cause local changes in the latter. Neutrophils rush to the sites of deposition of immune complexes, whose lysosomal enzymes aggravate damage to the endothelium and basement membrane, separating them from each other. Platelet degranulation causes the release of serotonin, leading to hemocoagulation and fibrin deposition on the basement membrane.

The elimination of immune complexes from the body is facilitated by a macrophage reaction in the form of proliferation of mesangial and endothelial cells, with the effectiveness of this process, recovery occurs.

clinical picture. The clinical picture of the disease consists of the following syndromes.

urinary syndrome.

1. Proteinuria due to the passage of protein molecules through the spaces of the capillary wall of the glomerulus, formed during the deposition of immune complexes on them. Proteinuria is selective in nature, in which predominantly albumins pass through the glomerular "filter".

2. Hematuria due to involvement in the pathological process of capillary mesangium and interstitial tissue. Erythrocytes penetrate through the smallest breaks in the basement membrane, changing their shape.

3. Cylindruria - urinary excretion of cylindrical cells of the tubules. During dystrophic processes in the tubules of the disintegrated cells of the renal epithelium, granular cylinders are formed, consisting of a dense granular mass; waxy cylinders have sharp contours and a homogeneous structure; hyaline casts are proteinaceous formations.

Hypertensive syndrome is observed due to:

1) sodium and water retention;

2) activation of the renin-angiotensin-aldosterone and sympathoadrenal systems;

3) decrease in the function of the depressor system of the kidneys.

Edema syndrome is associated with the following factors:

1) a decrease in glomerular filtration due to their defeat;

2) a decrease in the filtration charge of sodium and an increase in its reabsorption;

3) water retention due to sodium retention in the body;

4) an increase in BCC;

5) secondary hyperaldosteronism;

6) an increase in the secretion of ADH and an increase in the sensitivity of the distal nephron to it, leading to fluid retention;

7) an increase in the permeability of the capillary walls and the release of plasma into the tissues;

8) a decrease in plasma oncotic pressure with massive proteinuria.

Complaints presented in AGN are not specific and occur in various diseases. It is very important to indicate in the anamnesis a recent sore throat, exacerbation of chronic tonsillitis, hypothermia, etc. Some patients note a decrease in urine output, combined with some swelling (pasto) of the face in the morning. In 1/3-3/4 patients in the first days of the disease, there are not very strong, aching pains in the lumbar region associated with an increase in the size of the kidneys. There are also increased fatigue, headache, shortness of breath during physical exertion, a short-term increase in body temperature to subfebrile.

Arterial hypertension, detected only in half of the patients, is characterized by an increase in numbers to 140-160 / 85-90 mm Hg. Art. (rarely - up to 180/100 mm Hg. Art.).

Diagnostics. In 100% of cases, urine examination reveals proteinuria of varying severity, cylindruria and, what is most important for diagnosis, hematuria of varying severity - from microhematuria (up to 10 red blood cells in the field of view) to macrohematuria (albeit quite rare). However, if AGN is suspected, it is necessary to conduct a series of repeated urine tests or perform a Nechiporenko test (determining the number of formed elements in 1 μl), since red blood cells may not be detected in a single portion of urine.

When examining the blood, acute phase indicators are detected (increase in the content of fibrinogen and α₂-globulin, C-reactive protein, ESR acceleration), the number of leukocytes changes little, moderate anemia. In an uncomplicated course of AGN, the content of nitrogenous substances (creatinine, indican, urea) in the blood does not change.

In the initial phase of the disease, a change in the Reberg test is observed - a decrease in glomerular filtration and an increase in tubular reabsorption, which normalizes as it recovers.

An x-ray examination in patients with severe arterial hypertension may show a moderate increase in the left ventricle, which takes on the same size as the patient recovers.

There are 3 clinical variants of AGN.

1) Monosymptomatic variant: minor complaints, absence of edema and arterial hypertension, there is only urinary syndrome; the most common variant of the course of the disease (86% of cases).

2) Nephrotic variant: edema, oliguria are pronounced, it is possible to increase blood pressure to relatively low numbers, it is detected in 8% of patients.

3) Extended version: arterial hypertension, reaching high numbers (180/100 mm Hg. Art.), moderately pronounced edema, circulatory failure, occurs in 6% of cases.

Differential diagnostics. AGN must be distinguished from chronic glomerulonephritis, which is not difficult with the acute onset of AGN and subsequent complete reversal of symptoms. However, in the absence of an acute onset, as well as in the long-term persistence of certain signs of the disease, diagnosis becomes significantly more complicated. If differentiation is difficult, a puncture biopsy of the kidney is resorted to.

It is difficult to differentiate AGN from pyelonephritis due to the presence of leukocyturia in both diseases. However, AGN is accompanied by more massive proteinuria and, in some cases, edema. Differential diagnosis is also helped by the clinical symptoms of pyelonephritis in the form of more pronounced pain in the lower back, accompanied by fever and dysuric disorders. Also of diagnostic value is the definition of bacteriuria in pyelonephritis, the identification of "active" leukocytes, as well as x-ray (deformation of the cups) and isotope-renographic (asymmetry of kidney function) studies.

AGN as an independent disease must be differentiated from chronic diffuse connective tissue diseases, in which AGN is one of the manifestations of the disease. This situation usually occurs with the severity of urinary, hypertensive and edematous syndromes and insufficient clarity of other symptoms of the disease, more often with SLE (systemic lupus erythematosus). The correct diagnosis in SLE can be made by taking into account the articular syndrome, damage to the skin and other organs (heart), pronounced immunological changes (detection of anti-organ antibodies in high titer, lupus erythematosus cells, antibodies to DNA and RNA), as well as monitoring the dynamics of the clinical picture.

Treatment. Treatment for AGN is complex and includes the following measures.

1. Mode. If AGN is suspected or immediately after the diagnosis is established, the patient should be immediately hospitalized. Strict bed rest must be observed for about 2-4 weeks until the elimination of edema and normalization of blood pressure. Staying in bed provides uniform warming of the body, which leads to a decrease in vasospasm (hence, to a decrease in blood pressure) and to an increase in glomerular filtration and diuresis. After discharge from the hospital, home treatment is indicated for up to 4 months from the date of onset of the disease, which is the best prevention of the transition of AGN to the chronic stage.

2. Diet. Depending on the severity of clinical symptoms, it is very important to restrict fluid and sodium chloride. With an expanded and nephrotic form, a complete fast is recommended for 1-2 days with fluid intake in an amount equal to diuresis. On the 2-3rd day, the consumption of food rich in potassium salts (rice porridge, potatoes) is shown. The total amount of water drunk per day should be equal to the volume of urine allocated for the previous day plus 300-500 ml. After 3-4 days, the patient is transferred to a diet with protein restriction (up to 60 g per day), and the total amount of salt is not more than 3-5 g / day. Such a diet is recommended until the disappearance of all extrarenal symptoms and a sharp improvement in urinary sediment.

3. Drug therapy includes, first of all, antibacterial therapy, which, however, should be carried out only if the infectious nature of AGN is reliably established (the pathogen has been isolated and no more than 3 weeks have passed since the onset of the disease). Usually prescribed penicillin or its semi-synthetic analogues in conventional dosages. The presence of obvious foci of chronic infection (tonsillitis, sinusitis, etc.) is also a direct indication for antibiotic therapy. Diuretics in the treatment of AGN are indicated only with fluid retention, increased blood pressure and the appearance of heart failure. The most effective furosemide (40-80 mg), used until the elimination of edema and hypertension. There is no need for a long-term prescription of these drugs, 3-4 doses are enough.

In the absence of edema, but persistent hypertension or with an insufficient antihypertensive effect of saluretics, antihypertensive drugs (clophelin, dopegyt) are prescribed with a duration of administration that depends on the persistence of arterial hypertension.

In the nephrotic form of AGN, immunosuppressive therapy is prescribed (corticosteroids - prednisone 60-120 mg per day, followed by a gradual decrease in dose, duration of use for 4-8 weeks).

In case of AGN with severe edema and a significant decrease in diuresis, heparin is administered at 20-000 IU per day for 30-000 weeks, achieving an increase in blood clotting time by 4-6 times.

With prolonged proteinuria, indomethacin or voltaren is prescribed at 75-150 mg per day (in the absence of hypertension and oliguria). The prognosis is favorable, however, with prolonged forms, there is a possibility that the process will become chronic.

Prevention of AGN comes down to effective treatment of focal infection, rational hardening. In order to timely detect the onset of the disease after vaccination, transferred ARVI in all patients, it is necessary to examine the urine.

Author: Mostovaya O.S.

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