Acute and rapidly progressive forms
These variants of the disease are characterized by an acute onset and a rapid course, often threatening the function of the organ.
- Acute diffuse proliferative glomerulonephritis. Manifests with classic acute nephritic syndrome (triad: hematuria, arterial hypertension, edema). Additionally, proteinuria and oliguria are noted. The main complication is the risk of developing acute kidney injury. Microscopic examination reveals a diffuse nature of the lesion (most renal corpuscles are affected). Glomerular hypercellularity is typical, caused by leukocyte infiltration (neutrophils, monocytes) and proliferation of resident cells (endothelium, mesangiocytes).
- Crescentic (extracapillary) glomerulonephritis. Differs by an extremely unfavorable course in the form of rapidly progressive glomerulonephritis syndrome. Patients suffer from edema, proteinuria, and malignant hypertension, leading to rapid progression of renal failure. The pathomorphological basis is fibrinoid necrosis in the capillary loops and the formation of "crescents" in Bowman's space. These crescents consist of proliferating epithelium of the parietal layer, macrophages, and fibrin strands.
Variants with mesangial involvement
In these forms of inflammation, the mesangial tissue becomes the primary target or one of the main participants in the pathological process.
- Mesangioproliferative glomerulonephritis. Has a chronic course. Clinically, hematuria, proteinuria, hypertension, and a decrease in the glomerular filtration rate (GFR) are detected. Proliferation of mesangial cells and noticeable expansion of the mesangial matrix occur.
- Mesangioprogressive (membranoproliferative) glomerulonephritis. A severe form combining nephrotic and nephritic syndromes, with a very rapid decline in GFR. The damage is combined in nature. Diffuse cell proliferation and an increase in matrix are noted in the mesangium, and the glomerulus itself is infiltrated by macrophages. The basement membrane is heavily thickened and doubles, forming the specific "tram-track" phenomenon.
Nephrotic forms and glomerulosclerosis
For this group of diseases, the leading clinical manifestation is nephrotic syndrome of varying severity.
- Minimal change disease. Diagnostic dissociation is typical for this form: light microscopy shows no deviations from the norm, but electron microscopy reveals fusion ("effacement") of the small foot processes (pedicels) of podocytes.
- Focal segmental glomerulosclerosis (FSGS). Accompanied by a drop in GFR to 10–30%. The distribution of the process is specific: focal means involvement of less than 50% of all glomeruli, and segmental means damage to only a portion of the capillary loops within an individual glomerulus. Collapse of the capillaries and deposition of amorphous hyaline (sclerosis) occur. Electron microscopy also shows podocyte foot process "effacement".
- Membranous glomerulonephritis. Clinically similar to FSGS. The localization of the process is concentrated on the basement membrane, which thickens diffusely. A characteristic feature is the formation of subepithelial projections ("spikes") of membrane material around immune complexes, giving it a "spiked" appearance.
- Fibroplastic nephritis. Represents the terminal stage of inflammatory kidney diseases with an irreversible outcome resulting in sclerosis and renal shrinkage.
Briefly: answers to topical questions
What are the main etiological factors in the development of acute diffuse proliferative glomerulonephritis?
The main etiological factor in the development of the classical form of acute glomerulonephritis is infection caused by nephritogenic strains of group A β-hemolytic streptococcus. This pathology usually occurs after preceding upper respiratory tract infections (pharyngitis, tonsillitis) or skin infections (impetigo).
Non-streptococcal acute glomerulonephritis is also distinguished, which is associated with the following groups of infections:
- Bacterial — staphylococcal endocarditis, pneumococcal pneumonia, meningococcemia.
- Viral — viral hepatitis B, mumps, chickenpox, infectious mononucleosis.
- Parasitic — malaria, toxoplasmosis.
Visual microscopy markers for memorization: "Tram tracks" — membranoproliferative, "Spiked projections" — membranous, "Crescents" — extracapillary, "Effaced foot processes" — minimal change disease.
Class and exam questions
What is the essence of the historical term "Bright's disease"?
Richard Bright first correlated the clinical triad (massive edema and albuminuria) with morphological kidney changes at autopsy. Later, this condition came to be called glomerulonephritis.
What is the "tram-track" phenomenon and where is it found?
This is the microscopic picture of thickening and duplication of the glomerular capillary basement membrane. This sign is specific for mesangioproliferative (membranoproliferative) glomerulonephritis.
Why is minimal change disease difficult to diagnose under a standard microscope?
Under light microscopy, the glomeruli appear completely normal. Specific damage (fusion of podocyte small foot processes) can only be detected using electron microscopy.
What do the terms "focal" and "segmental" mean in the name of FSGS?
"Focal" means that less than 50% of all renal corpuscles have undergone sclerosis, and "segmental" means that the pathology affects not the entire glomerulus, but only a portion of its capillary loops.
What else to study on this topic
- Pathogenesis of acute nephritic syndrome
- Mechanisms of massive proteinuria and edema formation
- Acute kidney injury as a complication of glomerular inflammation
- Structure and functions of the basement membrane and podocytes
- Malignant arterial hypertension in glomerulonephritis
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