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Membranoproliferative Glomerulonephritis

*Glomerulonephritis membranoproliferativa*

For medical students2 min readUpdated 2026-10-10

This is a group of kidney diseases characterized by thickening of the glomerular basement membrane and active proliferation of mesangial cells. The condition often presents with nephrotic syndrome and hematuria, requiring differential diagnosis based on deposit types.

Frequency5–10% of idiopathic nephrotic syndrome cases
Key feature"Tram-track" appearance (duplication of the basement membrane)
Type II markerDecreased blood levels of complement component C3
Types of depositsSubendothelial, intramembranous, and subepithelial

Morphological Features

On light microscopy, glomeruli appear large and hypercellular, acquiring a characteristic lobular appearance. The main changes include:

The hallmark of the disease is the "tram-track" phenomenon. It occurs due to mesangial interposition: cellular processes extend beneath the endothelium and synthesize a new matrix, creating a double-contour effect of the capillary wall on silver staining.

Classification by Deposit Type

Subdivision into types is based on ultrastructural data and the location of immune deposits:

  1. Type I: characterized by subendothelial deposits and classical pathway complement activation.
  2. Type II (Dense Deposit Disease): the lamina densa of the GBM is replaced by dense osmiophilic material. It is characterized by the absence of IgG and the presence of "mesangial rings" on immunohistochemistry.
  3. 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:

Clinically, patients most often present with complaints typical of nephrotic syndrome, which is frequently complicated by hematuria due to intense cellular proliferation in the glomeruli.

Mnemonic

Tram-track tracks are made of mesangial "rails" along which proliferation "runs": mesangial cells extend under the endothelium, creating a double contour of the GBM.

Frequently asked 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 renal glomeruli.

These deposits are revealed during immunohistochemical examination and are associated with the presence of immune complexes in the glomeruli. Pathogenetically, this process is accompanied by activation of the classical complement 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 levels in dense deposit disease (Type II MPGN)?

The persistent decrease in serum C3 complement levels in dense deposit disease (Type II membranoproliferative glomerulonephritis) is caused by activation of the alternative complement pathway.

In renal tissue, C3 complement distributes in a specific manner:

  • Basement membrane (lamina densa) — detected on either side of irregular segments, 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.

Why does hematuria occur in MPGN?

Hematuria is a consequence of pronounced cellular proliferation within the glomeruli, which disrupts 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 serum C3 complement levels are persistently low.

How to distinguish Type I from Type III based on deposit location?

Type I is characterized predominantly by subendothelial deposits, whereas Type III combines both subendothelial and subepithelial deposits.

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