Causes of HIVAN
What is the etiology of HIVAN?
HIVAN is a direct result of active HIV infection in kidney tissue. Current research shows that the HIV virus gains entry into kidney tissue including the podocytes, mesangial cells, and tubular epithelial cells.
Once inside the cells, the viral genome is translated and the gene products lead to alterations of cellular function and development. Some of the candidate genes whose products are responsible for HIVAN include negative factor for viral replication (NEF), transactivating factor, and virus protein R. Research studies are still investigating what types of receptors the virus uses to enter kidney tissue.
The viral gene proteins lead to an interruption of normal cell maturation, and the infected cells de-differentiate into an immature cell phenotype.
The delicate balance between cell growth and apoptosis is offset and, being unable to control their own proliferation, the podocytes—as well as the infected parietal epithelial cells—increase in number and cause collapsing FSGS followed by tubular dilation from proliferating epithelial cells, forming the large microcysts.
