Abstract
Human Immunodeficiency Virus (HIV)-Associated Nephropathy (HIVAN) is one of the most important renal complications found in HIV-infected individua ls. Morbidity and mortality in this group of patien ts increases due to End-Stage Renal Disease (ESRD). Classic histological characteristics of HIVAN are collapsing Focal Segmental Glomerulosclerosis (FSGS), microcystic tubular dilation and interstitial inflammation and fibrosis. High prevalence of HIVAN among people of African descent can be explained by host genetic susceptibility, which is associated with several genes on human chromosome 22. HIV can infect renal epithelial cells via uncon ventional mechanisms and cause changes in multiple host cellular pathways, especially in renal tubular cells and podocytes. Accurate diagnosis of HIVAN relies mainly on renal biopsy. Antiretroviral thera py is the mainstay treatment for HIVAN and current standard guidelines recommend the initiation of Hig hly Active Antiretroviral Therapy (HAART) in all HIV-infected individuals with HIVAN, regardless of CD4 level. Other possible treatments for HIVAN including steroids, Angiotensin Converting Enzyme ( ACE) inhibitors, renal replacement therapy and renal transplantation are reviewed in this chapter.
Highlights
Human Immunodeficiency Virus (HIV)-associated nephropathy or HIV-Associated Nephropathy (HIVAN) was first described in patients with Acquired Immunodeficiency Syndrome (AIDS) in (Pardo et al, 1984; Rao et al, 1984)
High prevalence of HIVAN among people of African descent can be explained by host genetic susceptibility, which is associated with several genes on human chromosome 22
Antiretroviral therapy is the mainstay treatment for HIVAN and current standard guidelines recommend the initiation of Highly Active Antiretroviral Therapy (HAART) in all HIV-infected individuals with HIVAN, regardless of CD4 level
Summary
Human Immunodeficiency Virus (HIV)-associated nephropathy or HIVAN was first described in patients with Acquired Immunodeficiency Syndrome (AIDS) in (Pardo et al, 1984; Rao et al, 1984). It was named AIDS-nephropathy; because descent (Lucas et al, 2004; Lescure et al, 2012; Schwartz et al, 2005). Renal histopathologic defective findings were demonstrated in asymptomatic patients, the name was changed to HIVAN. Collapsing Focal Segmental Glomerulosclerosis (FSGS) with tubulointerstitial lesions, the classical histopathologic pattern in HIVAN is more prevalent in patients of African
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