Forms of glomerulonephritis

Today, the classification of glomerulonephritis, as before, is based on the features of the morphological picture. There are several forms (variants) of histological damage, which are observed during the examination of the renal biopsy using light, immunofluorescence and electron microscopy. This classification of glomerulonephritis does not seem ideal, since it does not have an unambiguous connection between the morphological picture, clinical picture, etiology and pathogenesis of glomerulonephritis: the same histological variant can have different etiology and different clinical picture. Moreover, the same etiology can cause a number of histological variants of glomerulonephritis (for example, a number of histological forms observed in viral hepatitis or systemic lupus erythematosus). It is therefore appropriate to view each of these renal biopsy variants not as a “disease” but as an “image” (“picture”) that often has multiple clinical manifestations, multiple potential etiologic factors, and often multiple immune mechanisms.

The first group of inflammatory lesions of the glomerulus consists of proliferative glomerulonephritis:

• mesangioproliferative (if mesangial cells predominantly proliferate);
• diffuse proliferative;
• extracapillary glomerulonephritis.

These diseases are characterized primarily by nephritic syndrome: “active” urinary sediment (erythrocytes, erythrocyte casts, leukocytes);

• proteinuria (usually no more than 3 g/day);
• renal failure, the severity of which depends on the extent of proliferation and necrosis, i.e. the active (acute) process.

Classification of primary glomerulonephritis

Proliferative forms	Non-proliferative forms
Acute diffuse proliferative glomerulonephritis Extracapillary (glomerulonephritis with "crescents") - with immune deposits (anti-GBM, immune complex) and "low-immune" Mesangioproliferative glomerulonephritis (MPGN) IgA nephropathy Mesangiocapillary glomerulonephritis	Minimal changes Focal segmental glomerulosclerosis Membranous glomerulonephritis

The next group consists of non-proliferative glomerulonephritis - diseases in which the layers of the glomerular filter that form the main barrier primarily for proteins are affected, namely podocytes and the basement membrane:

• membranous nephropathy;
• minimal change disease;
• focal segmental glomerulosclerosis.

These diseases are manifested mainly by the development of nephrotic syndrome - high (over 3 g/day) proteinuria, leading to hypoalbuminemia, edema and hyperlipidemia.

Mesangiocapillary glomerulonephritis combines the features of the two groups described above. Morphologically, it is characterized by damage to the basement membranes in combination with proliferation of glomerular cells (hence another name for the disease - membranoproliferative glomerulonephritis), and clinically - by a combination of nephritic and nephrotic syndromes.

In Europe and the USA, glomerulonephritis ranks third after diabetes mellitus and arterial hypertension among the causes of end-stage renal failure requiring replacement therapy.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ], [ 9 ], [ 10 ]