Introduction

Glomerulonephritis (GN) Glomerulonephritis is a kidney disease with inflammatory changes, especially on the glomeruli, as a result of an immunologically conditioned process. From a clinical point of view, it can be divided into acute, rapid and chronic. Acute glomerulonephritis is a sterile inflammatory inflammation of all glomeruli, which arises from the activation of immunological events immediately after some infections of the body. Chronic glomerulonephritis usually occurs from the beginning, inconspicuously, is progressive in nature and gradually causes chronic renal insufficiency with renal wrinkling over several years. We refer to glomerulonephritis as a rapidly occurring one in which chronic renal insufficiency develops rapidly within a few months after an acute illness.

I. Acute glomerulonephritis

Acute glomerulonephritis is a bilateral, sudden kidney disease in which all glomeruli are affected by severe sterile inflammation. They mainly affect school-age children and adolescents, more often men. From an etiological, clinical and prognostic point of view, acute post-streptococcal glomerulonephritis should be distinguished from other acute post-infectious glomerulonephritis. Acute glomerulonephritis is characterized by a rapid onset. Hematuria and proteinuria occur, accompanied by azotemia due to decreased glomerular filtration. Salt and water retention is also present. If the reduction in glomerular filtration is significant, oliguria occurs. Salt and water retention causes circulatory congestion, hypertension and edema. Fluid retention is caused by decreased glomerular filtration and increased reabsorption of water and salt, especially in the distal renal tubules. Edema is localized in areas with low tissue pressure. Congestion is manifested by an increase in systemic and pulmonary pressure. Plasma renin activity, aldosterone and sympathetic nervous system activity are relatively attenuated. The most common and very significant symptom of acute glomerulonephritis is hematuria. Hematuria is often accompanied by the presence of erythrocyte cylinders in the urine. Macroscopically, there are leukocytes and leukocyte cylinders in the urine. The course of glomerulonephritis depends on the nature of the glomerular damage. In some cases, fluid retention and hypertension may resolve spontaneously. In other cases, renal failure develops rapidly.

1. Acute post-streptococcal glomerulonephritis

It is caused by hemolytic group A streptococci (nephritogenic). The disease begins one to three weeks after the streptococcal infection (tonsillitis, pharyngitis, sinusitis, otitis media, scarlet fever, streptococcal pyoderma, bacterial endocarditis). Nephritogenic streptococci produce antigens of glycoprotein character, of which the most important is the plasma membrane antigen, the so-called endostreptosin. This antigen has a positive electric charge and therefore passes easily through the negatively charged glomerular basement membrane. Specific antibodies pass with this antigen, which upon binding to the antigen form deposits of immunocomplexes on the outside of the basement membranes, the capillaries of the glomerulus. 80-85 % of glomerulonephritis is a typical disease from immunocomplexes. Immune amplification systems, genetic factors, cellular immunity and others are also involved in its pathogenesis. Acute post-streptococcal glomerulonephritis also exerts the effect of the streptococcal enzyme neuraminidase, which cleaves sialic acid in the glomerular basement membrane and alters the host IgG structure. The altered IgGs become an autoantigen, autoantibodies are formed, and upon binding to the altered IgG, immunocomplexes are formed. The disease begins after a period of latency after the onset of an acute streptococcal infection with general symptoms such as upset, loss of appetite, headache, and sometimes indeterminate lumbar pain. Swelling on the lashes and ankles are typical. At the same time, there is a paleness of the face that resembles a doll. Arterial hypertension with systolic blood pressure of about 160-200 mmHg and diastolic blood pressure of about 110-130 mmHg is a regular symptom. Diagnosis: based on anamnestic data and evidence of initial streptococcal infection (increased ASLO titer, antideoxyribonucleases B, antihyaluronidases), swelling and arterial hypertension. Hematuria, proteinuria and pathological urinary sediment are found in the urine. Glomerular filtration tends to be markedly reduced, serum creatinine may be increased, but in most cases is adjusted quickly. In 90 % of the disease, the serum C3 complement concentration is temporarily reduced. Examination of the ocular background reveals signs of spasms of small aa. Erythrocyte sedimentation rate tends to be accelerated. Differential diagnosis: with a fully developed image of acute post-streptococcal glomerulonephritis does not cause diagnostic difficulties.