As glomerulonephritis (Greek nephros, kidney ,- itis, inflammation, pl glomerulonephritis, abbreviated. GN) is a bilateral inflammation of the kidneys called, in which the renal corpuscles ( glomeruli ) are affected first. We distinguish between different forms that belong in their entirety to the most common causes of chronic renal failure. The glomerular diseases are a subset of glomerular disease ( glomerulopathy ).
The classification of glomerulonephritis is not uniform, since they can be classified according to their origin, the histological appearance and clinical form and thus can be classified from different perspectives. One can distinguish on the basis of the pathogenesis of primary and secondary glomerulonephritis
This is understood to various forms of autoimmune- related glomerulonephritis preceded by no other disease or has not yet been determined, for example, the mesangial proliferative glomerulonephritis IgA type ( IgA nephropathy, Maladie de Berger), the membranous GN, the Membranoproliferative GN, the focal segmental glomerulosclerosis and minimal-change GN having visible only under the electron microscope changes in the glomeruli and therefore, no "true" is inflammation.
The secondary glomerular diseases are due to a disease outside the kidney or generalized disease, such as infection in the endocapillary proliferative GN ( = post infectious GN or post- streptococcal GN ), autoimmune diseases such as Goodpasture 's syndrome, granulomatosis with polyangiitis, the lupus erythematosus, drugs such as gold or penicillamine, or genetic defects Alport syndrome.
Necrotizing intra-/extrakapillär-proliferative GN with diffuse crescent formation ( = rapid- progressive GN RPGN ) has a special role, as it can occur in various forms of GN and the clinical course describes.
Also not to the glomerulonephritis associated with renal disease, and degenerative changes in the glomeruli in systemic diseases such as diabetes mellitus, lupus erythematosus, or amyloidosis, such as glomerulonephritis can eventually lead to sclerosis of the glomeruli ( glomerulosclerosis ).
Glomerular minimal lesions ( minimal change glomerulopathy ) and primary forms of focal and segmental glomerulosclerosis, can not formally be regarded as glomerulonephritis, since they lack the characteristic features of inflammation ( -itis ), while the minimal change glomerulopathy as minimal change glomerulonephritis ( MCGN ) referred to.
List of glomerulonephritis
- Fibrillary glomerulonephritis ( = immunotaktoide glomerulonephritis )
- Membranoproliferative glomerulonephritis type I, type II and type III
- Membranous ( epimembranöse ) glomerulonephritis
- Mesangial proliferative glomerulonephritis, with the most common special form of IgA nephropathy
- Necrotizing glomerulonephritis, rapidly progressive glomerulonephritis clinically referred to as
- Postinfectious or better infection -associated glomerulonephritis, usually as a post- streptococcal glomerulonephritis
- Alport syndrome is a hereditary with the synonym glomerulonephritis usually designated X - linked dominant inherited defect of collagen which is found among others in the kidneys.
Glomerulonephritis manifest themselves mostly as nephritic syndrome ( hematuria, proteinuria less than 3 g / day, salt and water retention, arterial hypertension ) or nephrotic syndrome ( urinary protein excretion > 3.0 to 3.5 g / day in adults, hypoalbuminemia, Hyperlidpidämie, thrombosis, edema ). It is not true that always express chronic glomerulonephritis with nephrotic syndrome and acute nephritic syndrome always with a. The nephrotic syndrome usually occurs in a membranous glomerulonephritis and membranoproliferative glomerulonephritis in on (the latter often with hematuria). Mesangial proliferative glomerulonephritis manifest themselves mostly as nephritic syndrome. Proliferative glomerulonephritis Extrakapillär mostly as rapidly progressive glomerulonephritis with hematuria, proteinuria, and rapidly deteriorating renal function.
By serum tests can narrow down the exact diagnosis, the definitive diagnosis is possible only by renal biopsy.
The suspected glomerulonephritis results based on the laboratory diagnosis of blood and urine. In most cases a renal biopsy for definitive diagnosis should be sought. Exceptions are self-limiting forms, such as a post - streptococcal glomerulonephritis. From the histological examination in conjunction with an electron microscopic examination and immunohistochemical staining of the biopsy specimen conclusions can be drawn for the therapy and the prognosis can be drawn.
Vary depending on the form of the disease and the treatment methods. It usually come Immunosuppressive therapies used. However, it should be known to treat the type of disease.