HIV-associated nephropathy
| HIV-associated nephropathy | |
|---|---|
| Classification and external resources | |
| Specialty | Lua error in Module:Wikidata at line 446: attempt to index field 'wikibase' (a nil value). |
| eMedicine | med/3203 |
| Patient UK | HIV-associated nephropathy |
| MeSH | D016263 |
HIV-associated nephropathy (HIVAN) refers to kidney disease developing in association with HIV infection. The most common, or "classical", type of HIV-associated nephropathy is a collapsing focal segmental glomerulosclerosis (FSGS), though other forms of kidney disease may also occur with HIV.[1] Regardless of the underlying histology, renal disease in HIV-positive patients is associated with an increased risk of death.[2]
HIVAN may be caused by direct infection of the renal cells with the HIV-1 virus, with resulting 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 kidney failure. Despite being a cause of chronic kidney failure, kidney sizes are usually normal or large.
Contents
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 microcystic tubular dilatation.
The characteristic feature of collapsing glomerulopathy is collapse of glomerular tuft and proliferation and hyperplasia of glomerular visceral epithelial cells. Its prognosis is always poor.
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 kidney failure are adjunctive.
Corticosteroid treatment can be useful in patients who do not respond to the above treatment. There is some evidence that cyclosporine might be helpful in selective cases, however further trials are required on both steroids and cyclosporine before these drugs can become standardised treatment if at all.
