Nephropathology
   
Case 15
Diagnosis and discussion
 
     
Versión en Español

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Diagnosis: Membranous Glomerulonephritis, Stage I

Membranous glomerulonephritis (MGN) is one of the more common forms of nephrotic syndrome in the adult population. The frequency of MGN in our center is 9.7% of the total primary glomerulopathies, a percentage that is lower than in USA and Europe.

The characteristic changes in MGN are in the glomerular capillary walls. The initial phase of the glomerulopathy is marked by subepithelial granular deposits: in the external part of the glomerular basement membrane (GBM), between this one and podocyte cytoplasm. Initially these deposits do not generate reaction of the GBM and therefore there are not "spikes". In few cases the deposits are as large as to be seen with light microscopy with a good section and a good trichrome stain; they appear fuchsinophilic (red). This phase of the MGN evolution is called: STAGE I, the diagnosis can be missed if we do not have immunofluorescence (IF) or electron microscopy (EM); these deposits are immune and will be positive for IgG and, in most of cases, for C3, in addition, they are electron-dense. Without IF or EM it is very probable that we can not diagnose this stage, and possibly we will think in minimal change disease.

In STAGE II the histologic findings with light microscopy allow an easier diagnosis. The glomerular architecture is preserved and the capillary walls appear thickened. The cellularity usually is not increased and the capillary lumina are ample. There is formation of material with similar aspect to the GBM (although with different composition) that projects perpendicularly to this one: “spikes”. These spikes are originated in reaction to the deposits and go progressively surrounding them.

In the present case there are not spikes, but the IF was positive for IgG and C3 in capillary walls. Glomeruli show mild mesangial hipercellularity, without other changes.

In follow-up the patient does not present systemic alterations or other features suggesting a secondary form of MGN.

See the chapter Membranous glomerulonephritis (English version).

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Bibliography

  • Ronco P, Debiec H. New insights into the pathogenesis of membranous glomerulonephritis. Curr Opin Nephrol Hypertens. 2006;15:258-63. [PubMed link]
  • Lai KN. Membranous nephropathy: when and how to treat. Kidney Int. 2007;71:841-3. [PubMed link]
  • Couser WG, Nangaku M. Cellular and molecular biology of membranous nephropathy. J Nephrol. 2006 Nov-Dec;19(6):699-705. [PubMed link] [Free full text]
  • Mansur A. Membranous glomerulonephritis, In eMedicine. Link: http://www.emedicine.com/med/topic885.htm Consulted May 19th 2007.
  • Azad NS, Muzaffar S, Pervez S, Ahmed A, Rabbani A, Ali A. Demographic and Clinicopathologic features of membranous glomerulonephritis. J Coll Physicians Surg Pak. 2004;14:35-8. [PubMed link]

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