Acute post-streptococcal glomerulonephritis: a review of information

Acute glomerulonephritis is one of the forms of glomerulonephritis, characterized by the sudden development of hematuria, proteinuria, arterial hypertension and edema, which in some cases is combined with a transient impairment of kidney function. Acute glomerulonephritis is often associated with infectious diseases. One such postinfection nephritis is acute poststreptococcal diffuse proliferative glomerulonephritis (OPSGN), which differs from other acute glomerulonephritis by typical serological and histological signs.

Acute poststreptococcal glomerulonephritis occurs in the form of sporadic cases or epidemics. Acute diffuse proliferative post-streptococcal glomerulonephritis is much more common in children than in adults; The peak incidence falls on the age of 2 to 6 years; about 5% - for children under 2 years and from 5 to 10% - for adults over 40 years. Subclinical forms are detected 4-10 times more often than forms with clinical symptoms, while a bright clinical picture is usually observed in men. Acute poststreptococcal glomerulonephritis often develops during the winter months and mainly after pharyngitis.

[1], [2], [3], [4]

Epidemiology of acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis is caused by Group A streptococci, especially some of their types. Streptococcus group A is typified by specific antisera directed towards the proteins of the cell wall of microbes (M- and T-proteins). M-types 1, 2, 4, 12, 18, 25, 49, 55, 57 and 60 are among the most known nephritogenic strains. However, many cases of acute diffuse proliferative post-streptococcal glomerulonephritis are associated with streptococcus serotypes that do not have M- or T-proteins .

The risk of developing acute poststreptococcal glomerulonephritis after infection with a nephritogenic strain of streptococcus depends on the localization of the focus of the infection. For example, if you are infected with streptococcus serotype 49, the risk of developing glomerulonephritis with skin infection is 5 times higher than with pharyngitis.

The decrease in the frequency of post-streptococcal glomerulonephritis has been noted in the United States, Great Britain and Central Europe, where it has practically disappeared in a number of regions. The reason for this is not clear enough, but it suggests a connection with an improvement in living conditions and an increase in the natural resistance of the population. Nevertheless, post-streptococcal glomerulonephritis remains a widespread disease in other countries of the world: in Venezuela and Singapore more than 70% of children hospitalized with acute glomerulonephritis are diagnosed with streptococcal etiology.

In sporadic and epidemic cases, post-streptococcal glomerulonephritis develops after infection of the upper respiratory tract or skin. The risk of developing glomerulonephritis after a streptococcal infection is about 15% on average, but in the epidemic period this figure is from 5 to 25%.

Sporadic cases are observed in the form of group diseases in poor urban and rural areas. Epidemic outbreaks develop in closed communities or in densely populated areas. In certain areas with poor socio-economic and hygienic conditions, these epidemics become cyclical; the most famous are the repeated epidemics in the Indian reservation on the Red Lake in Minnesota, Trinidad and Maracaibo. Reports of limited outbreaks of rugby team members with infected skin injuries were reported when the disease became known as the "kidney of the fighters".

[5], [6], [7]

What causes acute poststreptococcal glomerulonephritis?

First described the acute poststreptococcal glomerulonephritis Shick in 1907, when the scientist noted the presence of a latent period between scarlet fever and the development of glomerulonephritis and suggested a common pathogenesis of nephritis after scarlet fever and experimental serum sickness. After revealing the streptococcal cause of scarlet fever, the developing nephrite began to be considered an "allergic" response to the introduction of bacteria. Although nephritogenic species of streptococcus have been identified and characterized, the sequence of reactions leading to the formation of immune deposits and inflammation in the renal glomeruli has not yet been fully studied. Attention of many researchers was focused on the characteristics of these nephritogenic species of streptococci and their products, resulting in three main theories of the pathogenesis of acute poststreptococcal glomerulonephritis.

Causes and pathogenesis of acute poststreptococcal glomerulonephritis

Symptoms of acute poststreptococcal glomerulonephritis

Symptoms of acute poststreptococcal glomerulonephritis caused by group A hemolytic streptococcus are well known. The development of jade is preceded by a latent period, which after pharyngitis averages 1-2 weeks, and after skin infection is usually 3-6 weeks. During this latent period, some patients may have a microhematuria that precedes the unfolded clinical picture of nephritis.

In some patients, the only symptom of acute glomerulonephritis may be a microhematuria, others develop macrogematuria, proteinuria, sometimes reaching a nephrotic level (> 3.5 g / day / 1.73 m ² ), arterial hypertension and edema.

Symptoms of acute poststreptococcal glomerulonephritis

Diagnosis of acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis is always accompanied by pathological changes in the urine. Diagnosis of acute poststreptococcal glomerulonephritis shows the presence of hematuria and proteinuria, usually there are cylinders.

In freshly collected urine samples, erythrocyte cylinders are often detected, and phase-contrast microscopy can reveal dysmorphic ("altered") erythrocytes, indicating the glomerular origin of hematuria. Also often present are tubular epithelial cells, granular and pigmented cylinders, and leukocytes. In patients with severe exudative glomerulonephritis, leukocyte cylinders are sometimes found. Proteinuria is a characteristic clinical symptom of acute poststreptococcal glomerulonephritis; nephrotic syndrome at the onset of the disease is present in only 5% of patients.

Diagnosis of acute poststreptococcal glomerulonephritis

[8], [9], [10], [11], [12]

Treatment of acute poststreptococcal glomerulonephritis

Given the association of acute acute nephritis with streptococcal infection, treatment of acute poststreptococcal glomerulonephritis consists in the appointment in the early days of the disease of an antibiotic from the penicillin group (125 mg phenoxymethylpenicillin every 6 hours for 7-10 days) and with allergy to erythromycin (250 mg every 6 hours for 7-10 days). Such treatment of acute poststreptococcal glomerulonephritis is primarily indicated if acute poststreptococcal glomerulonephritis occurs after the transferred pharyngitis, tonsillitis, skin lesions, especially with positive results of crops from the skin, throat, as well as with high titres of anti-streptococcal antibodies in the blood. Prolonged antibacterial treatment of acute post-streptococcal glomerulonephritis is necessary in the development of acute nephritis within the framework of sepsis, including septic endocarditis.

Treatment and prevention of acute poststreptococcal glomerulonephritis

Prognosis for acute poststreptococcal glomerulonephritis

In general, the prognosis of acute poststreptococcal glomerulonephritis is quite favorable. In children, it is very good, progression to terminal chronic kidney failure occurs in less than 2% of cases. In adults, the prognosis is good, but some may have signs of an unfavorable course of the disease:

• rapidly progressive renal failure;
• a large number of half-moons in the kidney biopsy;
• uncontrolled arterial hypertension.

Death in the acute period or terminal renal failure is observed in less than 2% of patients. This is associated with a favorable natural course of the disease and with modern possibilities for treating complications of acute diffuse proliferative post-streptococcal glomerulonephritis. Children have a better prognosis than adults.

The prognosis is worse in patients older than 40 with rapidly progressive renal failure and extracapillary glomerulonephritis. There are apparently no significant differences in outcomes between sporadic and epidemic forms. Persistent changes in urine and morphological pattern are observed quite often and can persist for several years. Acute poststreptococcal glomerulonephritis in most cases ends favorably and the incidence of chronic renal failure is extremely low. Yet in one study (Baldwin et al.), A significant percentage of patients developed persistent arterial hypertension and / or terminal renal failure many years after the episode of acute glomerulonephritis. In this work, it was not possible to establish whether progressive renal failure was associated with the development of nephrosclerosis due to poor control of arterial pressure, or because of a latently growing sclerotic process in the renal glomeruli.