ABSTRACT
Viral infections can be causative in many glomerular disease, and human immunodeficiency virus (HIV) infection is closely related to a collapsing focal segmental glomerulosclerosis (FSGS). This is known as HIV associated nephropathy (HIVAN) and is characterized clinically by proteinuria, often of sudden onset, with rapidly progressive renal dysfunction resulting in end stage renal disease (ESRD) over several months. Increasingly, other primary renal diseases are being described in HIV infected patients, including IgA nephropathy, an immune complex lupus-like neprhopathy, and tubulonephritis. We observed rare HIVAN case presenting membranous glomerulonephritis with nephrotic syndrome in a woman who was positive for HIV without hepatitis B viral infection. She was treated with Methylprednisolone 60 mg/day, zidovudine 600 mg/day, efavirenz 60 mg/day, and lamivudine 300 mg/day for 5 months. After treatment, proteinuria decreased from 4,092 mg/day to 419 mg/day and CD4 T cell count rose from 594/mL to 1,176/mL. The effectiveness and safety of corticosteroids in the treatment of HIVAN remained controversial but this case showed good response for steroid with triple antiviral therapy about HIVAN especially membranous glomerulonephritis.
Subject(s)
Female , Humans , Adrenal Cortex Hormones , AIDS-Associated Nephropathy , Antigen-Antibody Complex , Cell Count , Glomerulonephritis, IGA , Glomerulonephritis, Membranous , Glomerulosclerosis, Focal Segmental , Hepatitis B , HIV Infections , HIV , Kidney Failure, Chronic , Lamivudine , Methylprednisolone , Nephrotic Syndrome , Proteinuria , ZidovudineABSTRACT
A depressed level of natural killer (NK) activity is one of the various immunologic abnormalities in human immunodeficiency virus (HIV) infection. Interleukin-15 (IL-15), an immunotherapeutic candidate in HIV infection, increases NK activity and induces the excretion of CC-chemokines from divergent immune cells, but the mechanisms of NK activity enhancement by IL-15 stimulation is not clearly established in HIV infection. This study examined whether CC-chemokines, which are known to increase NK activity, are secreted adequately in HIV-infected individuals, and also investigated whether P-glycoprotein is involved in NK activity enhancement after IL-15 administration. NK activity increased with IL-15 stimulation in NK cells of HIV-infected individuals, as it does in normal NK cells. IL-15 stimulates NK cells to secrete CC-chemokines, such as, macrophage inflammatory protein-1alpha (MIP-1alpha), macrophage chemotactic protein-1alpha (MCP-1alpha) and regulated upon activation, normal T cells expressed and secreted (RANTES) in both HIV-infected individuals and controls with no significant difference. P-glycoprotein expression and function is decreased in HIV-infected individuals and restored only in NK cells of HIV-infected individuals after IL-15 stimulation. P-glycoprotein may play a role in the mechanism of increased NK cell activity in HIV-infected individuals after IL-15 stimulation.