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Glomerulonephritis - Information Overview
Medical expert of the article
Last reviewed: 05.07.2025
Glomerulonephritis is a group of diseases characterized by inflammatory changes, mainly in the glomeruli of the kidneys, and the associated symptoms of glomerulonephritis - proteinuria, hematuria, often sodium and water retention, edema, arterial hypertension, decreased renal function.
Glomerular damage is combined with varying degrees of tubulointerstitial changes, especially with prolonged massive proteinuria. This aggravates clinical manifestations (primarily arterial hypertension) and accelerates the progression of renal failure.
Glomerulonephritis can be primary (idiopathic), the clinical manifestations of which are limited only to the kidneys, or secondary - part of a systemic disease (usually systemic lupus erythematosus or vasculitis).
It should be noted that, although glomerulonephritis can be suspected based on clinical and laboratory data, a definitive diagnosis is only possible after a histological examination of the renal tissue.
[ What causes glomerulonephritis?
The causes of glomerulonephritis are unknown. The role of infection has been established in the development of some forms of glomerulonephritis - bacterial, especially nephritogenic strains of group A beta-hemolytic streptococcus (epidemics of acute post-streptococcal glomerulonephritis are still a reality today), viral, in particular hepatitis B and C viruses, HIV infection; drugs (gold, D-penicillamine); tumors and other factors of exogenous and endogenous origin.
Infectious and other stimuli induce glomerulonephritis by triggering an immune response with the formation and deposition of antibodies and immune complexes in the glomeruli of the kidneys and/or by enhancing the cell-mediated immune response. After the initial injury, activation of complement, recruitment of circulating leukocytes, synthesis of various chemokines, cytokines, and growth factors, release of proteolytic enzymes, activation of the coagulation cascade, and formation of lipid mediator substances occur.
Histopathology of glomerulonephritis
A complete diagnostic examination of a renal biopsy includes light microscopy, electron microscopy, and examination of immune deposits stained with immunofluorescence or immunoperoxidase.
Glomerulonephritis: Light Microscopy
In glomerulonephritis, the dominant, but not the only, histologic lesion is localized to the glomeruli. Glomerulonephritis is characterized as focal (if only some glomeruli are affected) or diffuse. In any given glomerulus, the lesion may be segmental (affecting only part of the glomerulus) or total.
When examining a kidney biopsy, errors may occur:
- associated with the size of the tissue sample: in small-sized biopsies, the extent of the process may be misdetermined;
- In sections passing across the glomerulus, segmental lesions may be missed.
Lesions may be hypercellular due to proliferation of endogenous endothelial or mesangial cells (called "proliferative") and/or infiltration by inflammatory leukocytes (called "exudative"). Severe acute inflammation causes necrosis in the glomeruli, often focal.
Thickening of the glomerular capillary wall occurs due to increased production of the material constituting the glomerular basement membrane (GBM) and accumulation of immune deposits. Silver staining of the biopsy specimen is useful for its detection, since silver stains the basement membranes and other matrix black. Staining reveals, for example, the double contour of the glomerular basement membrane due to cell interposition or an increase in the mesangial matrix, which is not detected by other methods.
Segmental sclerosis is characterized by segmental collapse of capillaries with accumulation of hyaline material and mesangial matrix, often with attachment of the capillary wall to the Shumlyansky-Bowman capsule (formation of adhesion or "synechiae").
Crescents (accumulations of inflammatory cells within the cavity of the Bowman capsule) occur when severe glomerular injury results in ruptures of the capillary wall or Bowman's capsule, allowing plasma proteins and inflammatory cells to enter the space of the Bowman capsule and accumulate. Crescents consist of proliferating parietal epithelial cells, infiltrating monocytes/macrophages, fibroblasts, lymphocytes, often with focal fibrin deposition.
The crescents got their name from the appearance they have on sections of the renal glomerulus. The crescents cause destruction of the glomeruli, rapidly increasing in size and compressing the capillary bundle until it is completely occluded. After the acute injury has ceased, the crescents become fibrotic, causing irreversible loss of renal function. The crescents are a pathological marker of rapidly progressive glomerulonephritis, which most often develops with necrotizing vasculitis, Goodpasture's disease, cryoglobulinemia, and systemic lupus erythematosus due to infections.
The damage in glomerulonephritis is not limited to the glomeruli. Tubulointerstitial inflammation often develops, more pronounced in active and severe glomerulonephritis. As glomerulonephritis progresses and the glomeruli die, the associated tubules atrophy, and interstitial fibrosis develops - a picture characteristic of all chronic progressive kidney diseases.
Glomerulonephritis: Immunofluorescence Microscopy
Immunofluorescence and immunoperoxidase staining are used to detect immune reactants in renal tissue. This is a routine method for searching for immunoglobulins (IgG, IgM, IgA), components of the classical and alternative pathways of complement activation (usually C3, C4, and Clq), and fibrin, which is deposited in the crescents and capillaries in thrombotic disorders (hemolytic uremic and antiphospholipid syndromes). Immune deposits are located along capillary loops or in the mesangial area. They can be continuous (linear) or discontinuous (granular).
Granular deposits in the glomeruli are often called "immune complexes", which implies the deposition or local formation of antigen-antibody complexes in the glomeruli. The term "immune complexes" derives from studies in experimental models of glomerulonephritis, where there is strong evidence of the induction of glomerular damage by antigen-antibody complexes of known composition. However, in human nephritis, it is only very rare that a potential antigen can be detected, and even rarer is it possible to demonstrate the deposition of an antigen together with the corresponding antibodies. Therefore, the broader term "immune deposits" is preferred.
Glomerulonephritis: Electron Microscopy
Electron microscopy is essential for assessing the anatomical structure of the basement membranes (in some inherited nephropathies, such as Alport syndrome and thin basement membrane nephropathy) and for localizing the location of immune deposits, which usually appear homogeneous and electron-dense. Electron-dense deposits are seen in the mesangium or along the capillary wall on the subendothelial or subepithelial side of the glomerular basement membrane. Rarely, electron-dense material is located linearly within the glomerular basement membrane. The location of immune deposits within the glomeruli is one of the main features in classifying the different types of glomerulonephritis.
Glomerulonephritis, in which the number of cells in the glomerulus increases (hypercellularity), is called proliferative: it can be endocapillary (along with inflammatory cells that have migrated from the circulation, the number of endothelial and mesangial cells is increased) and extracapillary (the number of parietal epithelial cells is increased, which, together with macrophages, form characteristic arcuate thickenings of the glomerular capsule - crescents).
Glomerulonephritis that is no more than a few weeks old is called acute. If the disease lasts for a year or more, it is called chronic glomerulonephritis. Glomerulonephritis with crescents leads to renal failure within a few weeks or months, i.e. it is a rapidly progressing glomerulonephritis.
Where does it hurt?
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 cause can cause a number of histological variants of glomerulonephritis (for example, a number of histological forms observed in viral hepatitis or systemic lupus erythematosus).
What do need to examine?
What tests are needed?
Who to contact?
Treatment of glomerulonephritis
Treatment of glomerulonephritis has the following objectives:
- to assess how great the activity and probability of progression of nephritis are and whether they justify the risk of using certain therapeutic interventions;
- achieve reversal of kidney damage (ideally, complete recovery);
- stop the progression of nephritis or at least slow down the rate of increase in renal failure.
Drugs