Glomerulonephritis

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Introduction

The Case of...

a simple case introducing clincial presentation and calling for a differential diagnosis to get students thinking.

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Causes and Risk Factors

Idiopathic glomerulonephritis

minimal change disease

Membranoproliferative glomerulonephritis

associated with heptatitis C and autoimmune
immune complex deposition in glomerular mesangium and BM
complement activation
glomeruli damage
GBM is rebuilt on deposits

Cytokine-related glomerular epithelial cell injury

T lymphocytes release inflammatory mediators, increasing albumin permeability. This can occur in nephrotic syndrome.

Podocytes anchored to the GBM via dystroglycans are reduced in this condition.

Immune complex-mediated injury

immunie complexes can be deposited directly from circulation or are formed in situ .

This type III hypersensitivity also involves complement.

Different glomerular injury patterns vary with site of complex deposits. Factors influencing immune complex deposition include antigen charge, immune complex size, and antibody affinity.

Antibody mediated

circulating antibodies bind to

accumulation of proteins, lipids in the glomerulus

Circulating Immune Complex Nephritis

Glomerular injury can be caused by circulating immune complexes that have formed between antibody and antigen in the blood.

Antibodies may be endogenous in origin, as in SLE, or they can be against certain organisms, incuding streptococcus, HBV, HCV, Treponema pallidum, Plasmodium falciparum, and other viruses.

Immune complexes become trapped in the basement membrane between endothelial cells and podocytes in granular deposits. Normally immune complexes are removed by phagocytic cells and proteases, resulting in a resolution of inflammation. However, in cases of constant or repeated immune complex formation, chronic inflammation may result.

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