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==Overview==
'''HIV-Associated Nephropathy''' (HIVAN) is a type of collapsing [[FSGS]].  Serious renal complication of advanced [[HIV]] infection and [[AIDS]] leading to chronic and eventually [[end stage renal failure]](ESRF).  HIVAN is caused by direct infection of the renal cells with the HIV-1 virus and leads to renal damage through the viral gene products.  It could also be caused by changes in the release of [[cytokines]] during HIV infection.
'''HIV-Associated Nephropathy''' (HIVAN) is a type of collapsing [[FSGS]].  Serious renal complication of advanced [[HIV]] infection and [[AIDS]] leading to chronic and eventually [[end stage renal failure]](ESRF).  HIVAN is caused by direct infection of the renal cells with the HIV-1 virus and leads to renal damage through the viral gene products.  It could also be caused by changes in the release of [[cytokines]] during HIV infection.



Revision as of 20:47, 17 February 2012

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Overview

HIV-Associated Nephropathy (HIVAN) is a type of collapsing FSGS. Serious renal complication of advanced HIV infection and AIDS leading to chronic and eventually end stage renal failure(ESRF). HIVAN is caused by direct infection of the renal cells with the HIV-1 virus and leads to renal damage through the viral gene products. It could also be caused by changes in the release of cytokines during HIV infection.

Usually occurs only in advanced disease and approximately 80% of patients with HIVAN have a CD4 count of less than 200. HIVAN presents with nephrotic syndrome and progressive renal failure. Despite being a cause of chronic renal failure kidney sizes are usually normal or large.

Incidence

Much more common in Black and African American patients with HIV. In the USA 12% of patients dying with AIDS have histologically proven HIVAN, the worldwide incidence amongst AIDS patients appears to be similar. A South African study at Tygerberg Hospital, Stellenbosch University, has shown HIVAN histology in 33/61(54%) biopsies performed in HIV positive patients.

Among black adults in the USA it is the third most common cause of ESRF.

Pathology

Involves all components of the nephron. Typical findings are that of collapsing FSGS (Focal segmental glomerulosclerosis)and mycrocystic tubular dilatation.

Treatment

There is as yet inadeqaute data from randomised controlled trials.

Treatment with HAART and ACE inhibitors/Angiotensin receptor blockers has been shown to be beneficial and should be given to all patients unless otherwise contra-indicated. General renoprotective measures and the treatment of the complications of nephrotic syndrome and renal failure are adjunctive.

Corticosteroid treatment can be useful in patients who do not respond to the above treatment. There is some evidence that cyclophosphamide might be helpful in selective cases, however further trials are required on both steroids and cyclophosphamide before these drugs can become standardised treatmen if at all.

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