Glomerular Diseases
The glomeruli respond to injury primarily through inflammation, both humoral and cell-mediated. Glomerular disease can present in one of five ways:
Systemic symptoms such as edema, malaise, and hypertension.Dysmorphic RBCs or RBC casts suggests nephritic syndrome, such as can occur in a proliferative glomerular nephritis.
Four structures are prone to damage - endothelium, basement membrane, mesangium, or podocytes.
Immune-mediated glomerular injury
There are various ways immunologic agents can damage the kidneys.
Circulating immune complex nephritis is the most common mechanism. Immune complexes form outside the kidney and become trapped in the basement membrane, forming 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. The classical complement pathway becomes activated, increasing basement membrane permeability. Common antigens include:
In-situ immune complex deposition occurs when circulating antibodies bind to antigens present in the glomerulus. Anti-glomerular basement membrane (anti-GBM) disease is one example, as occurs in Goodpasture's syndrome. Antigens can also be deposited in the glomerulus and attract immunological attack. Examples include: group A or group B strep, aggregated IgG, parasites, and drugs, DNA.
Sensitized T cells, part of the cell-mediated immune response, can also contribute to progression of acute GN to chronic GN. Macrophages also appear involved.
Lastly, the alternative complement pathway can be stimulated by bacterial polysaccharides, endotoxins, and IgA aggregates, as occurs in membroproliferative GN.
focal segmental glomerulosclerosis
