Acute post-streptococcal glomerulonephritis - Information Review

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 transient renal dysfunction. Acute glomerulonephritis is often associated with infectious diseases. One of such post-infectious nephritis is acute post-streptococcal glomerulonephritis diffuse proliferative (APSGN), which differs from other acute glomerulonephritides by typical serological and histological signs.

Acute poststreptococcal glomerulonephritis occurs sporadically or in epidemics. Acute diffuse proliferative poststreptococcal glomerulonephritis is much more common in children than in adults; the peak incidence is between 2 and 6 years of age; about 5% in children under 2 years of age and 5 to 10% in adults over 40 years of age. Subclinical forms are detected 4-10 times more often than forms with clinical symptoms, with a pronounced clinical picture usually observed in men. Acute poststreptococcal glomerulonephritis often develops in the winter months and mainly after pharyngitis.

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Epidemiology of acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis is caused by group A streptococci, particularly certain types. Group A streptococci are typed using specific antisera directed to the microbial cell wall proteins (M and T proteins). The most well-known nephritogenic strains include M types 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60. However, many cases of acute diffuse proliferative poststreptococcal glomerulonephritis are associated with streptococcal serotypes that lack M or T proteins.

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

A decrease in the incidence of post-streptococcal glomerulonephritis has been noted in the United States, Great Britain, and Central Europe, where it has virtually disappeared in some regions. The reason for this is not entirely clear, but it is thought to be related to improved living conditions and increased natural resistance in the population. However, post-streptococcal glomerulonephritis remains a widespread disease in other countries: in Venezuela and Singapore, more than 70% of children hospitalized with acute glomerulonephritis have streptococcal etiology.

In sporadic and epidemic cases, poststreptococcal glomerulonephritis develops after an upper respiratory tract or skin infection. The risk of developing glomerulonephritis after a streptococcal infection is on average about 15%, but during epidemics this figure ranges from 5 to 25%.

Sporadic cases occur as clusters in poor urban and rural areas. Epidemic outbreaks develop in closed communities or in densely populated areas. In certain areas with poor socioeconomic and hygienic conditions, these epidemics become cyclical; the most famous are the recurrent epidemics in the Red Lake Indian Reservation in Minnesota, Trinidad, and Maracaibo. Limited outbreaks have been reported in rugby team members with infected skin lesions, when the disease was called "fighter's kidney".

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What causes acute poststreptococcal glomerulonephritis?

Acute poststreptococcal glomerulonephritis was first described by Shick in 1907, when he noted 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 the streptococcal cause of scarlet fever was identified, the nephritis that followed it was considered an "allergic" reaction to the introduction of bacteria. Although nephritogenic streptococci 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. The attention of many researchers has been focused on the characterization of these nephritogenic 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

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

In some patients, the only symptom of acute glomerulonephritis may be microhematuria, while others develop macrohematuria, proteinuria, sometimes reaching nephrotic levels (>3.5 g/day/1.73 m2 ⁾, 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 casts.

Freshly collected urine samples often contain red blood cell casts, and phase-contrast microscopy can reveal dysmorphic ("altered") red blood cells, indicating a glomerular origin of hematuria. Also often present are tubular epithelial cells, granular and pigment casts, and leukocytes. Leukocyte casts are sometimes found in patients with severe exudative glomerulonephritis. Proteinuria is a characteristic clinical symptom of acute poststreptococcal glomerulonephritis; however, nephrotic syndrome is present at the onset of the disease in only 5% of patients.

Diagnosis of acute poststreptococcal glomerulonephritis

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Treatment of acute poststreptococcal glomerulonephritis

Given the connection between acute nephritis and streptococcal infection, treatment of acute post-streptococcal glomerulonephritis consists of prescribing an antibiotic from the penicillin group (phenoxymethylpenicillin - 125 mg every 6 hours for 7-10 days) in the first days of the disease and, in case of allergy to them, erythromycin (250 mg every 6 hours for 7-10 days). Such treatment of acute post-streptococcal glomerulonephritis is primarily indicated if acute post-streptococcal glomerulonephritis occurs after pharyngitis, tonsillitis, skin lesions, especially with positive results of skin and throat cultures, as well as with high titers of antistreptococcal antibodies in the blood. Long-term antibacterial treatment of acute post-streptococcal glomerulonephritis is necessary in the development of acute nephritis in the context of sepsis, including septic endocarditis.

Treatment and prevention of acute poststreptococcal glomerulonephritis

Prognosis for acute poststreptococcal glomerulonephritis

In general, the prognosis for acute poststreptococcal glomerulonephritis is quite favorable. In children, it is very good, progression to terminal chronic renal 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 crescents in the renal biopsy;
• uncontrolled arterial hypertension.

Death in the acute period or terminal renal failure are observed in less than 2% of patients. This is due to the favorable natural course of the disease and modern treatment options for complications of acute diffuse proliferative poststreptococcal glomerulonephritis. The prognosis is better in children than in adults.

The prognosis is worse in patients over 40 years of age with rapidly progressing renal failure and extracapillary glomerulonephritis. There do not appear to be any significant differences in outcome between sporadic and epidemic forms. Persistent changes in urine and morphological patterns are quite common and may persist for several years. Acute poststreptococcal glomerulonephritis usually ends favorably and the incidence of chronic renal failure is extremely low. However, in one study (Baldwin et al.), a significant percentage of patients developed persistent hypertension and/or end-stage renal failure many years after an episode of acute glomerulonephritis. This study failed to establish whether the progressive renal failure was associated with the development of nephrosclerosis due to poor blood pressure control or with a hidden sclerotic process in the renal glomeruli.