Morphological Features
On light microscopy, the glomeruli appear enlarged and hypercellular, acquiring a characteristic lobular appearance. The main changes include:
- Pronounced proliferation of mesangial cells.
- Increased volume of the mesangial matrix.
- Diffuse thickening of the glomerular basement membrane (GBM).
A hallmark of the disease is the «tram-track» phenomenon. It occurs due to mesangial interposition: cellular processes penetrate beneath the endothelium and synthesize new matrix, which, upon silver staining, creates the effect of double contouring of the capillary wall.
Classification by deposit type
Subdivision into types is based on ultrastructural data and the localization of immune deposits:
- Type I: characterized by subendothelial deposits and classical pathway complement activation.
- Type II (dense deposit disease): the lamina densa of the GBM is replaced by a dense substance. It is characterized by the absence of IgG and the presence of «mesangial rings» on immunohistochemistry.
- Type III: combines features of both subendothelial and subepithelial deposits.
Etiology and clinical presentation
The disease can be either primary or secondary. Secondary forms are often associated with systemic pathologies:
- Systemic lupus erythematosus (SLE).
- Viral hepatitis B and C.
- Cryoglobulinemia and malignancies.
- Infectious processes (e.g., infected shunts).
Clinically, patients most commonly present with symptoms characteristic of nephrotic syndrome, which is frequently complicated by hematuria due to intense cellular proliferation within the glomeruli.
Briefly: answers to topical questions
Which classes of immunoglobulins and complement fractions are detected in the glomeruli in type I membranoproliferative glomerulonephritis by immunofluorescence?
In type I membranoproliferative glomerulonephritis, granular deposits of immunoglobulin G (IgG) and the C3 complement fraction are detected in the renal glomeruli.
These deposits are identified during immunohistochemical examination and are associated with the presence of immune complexes in the glomeruli. Pathogenetically, this process is accompanied by activation of the complement system via the classical pathway. On electron microscopy, these deposits are localized predominantly subendothelially (in two-thirds of cases) as well as in the mesangium.
What is the pathogenesis of the persistent decrease in blood C3 complement component levels in dense deposit disease (type II MPGN)?
The persistent decrease in serum C3 complement component levels in dense deposit disease (type II membranoproliferative glomerulonephritis) is caused by activation of the complement system via the alternative pathway.
In renal tissue, the C3 complement is distributed in a specific manner:
- Basement membrane (lamina densa) — detected on either side of irregular areas, but absent within the dense deposits themselves.
- Mesangium (mesangium) — identified as characteristic rounded inclusions, forming «mesangial rings».
At the same time, immunoglobulin G (IgG) deposits in the glomeruli are typically absent.
Tram-tracks are «rails» made of mesangium along which proliferation «rides»: the mesangium penetrates under the endothelium, creating a double contour of the GBM.
Class and exam questions
Why does hematuria occur in MPGN?
Hematuria is a consequence of pronounced cellular proliferation in the glomeruli, which damages the structure of the capillary wall.
What is «dense deposit disease»?
This is type II MPGN, in which the lamina densa of the basement membrane transforms into a ribbon-like electron-dense structure, and blood levels of the C3 component are persistently decreased.
How to distinguish type I from type III based on deposit localization?
Type I is characterized predominantly by subendothelial deposits, whereas type III combines subendothelial and subepithelial deposits.
What else to study on this topic
- Mechanisms of complement system activation in different types of MPGN.
- Differential diagnosis of MPGN and membranous nephropathy.
- The role of alpha-1 antitrypsin deficiency in the development of secondary MPGN.
- Features of the immunohistochemical profile in various types of deposits.
- Prognosis and treatment approaches depending on the type of the disease.
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