BACKGROUND: This study is designed to test the toxicity and pharmacokinetics of different doses of BAY 43-9006 (Sorafenib) in patients with Kaposi s sarcoma (KS). It will also assess, in a preliminary manner, the activity of BAY 43-9006 in this disease and its effect on biological markers. BAY 43-9006 is a potent inhibitor of wild-type and mutant c-Raf kinase isoforms. In addition, this agent also inhibits p38, c-kit, vascular endothelial growth factor receptor 2(VEGFR2), VEGF-R3, and platelet derived growth factor receptor beta (PDGFR-B). There is evidence that several of these receptors, and especially VEGF-R2, VEGF-R3, and PDGF-RB, are important in KS pathogenesis. The principle tumor cells of KS lesions are spindle cells, which are derived from endothelial cells. Spindle cells proliferate in response to VEGF, VEGF-C (a ligand for VEGF-R3), and PDGF, and the stimulation of spindle cells by these factors appears to be an important component in the pathogenesis of KS. There is also evidence that c-kit is important in KS. Because BAY 43-9006 can inhibit the function of these receptors and c-kit, it may have specific activity against this tumor. BAY 43-9006 is metabolized at least in part by CYP 3A4, and ritonavir, an HIV protease inhibitor commonly used in AIDS patients, is an inhibitor of CYP 3A4. Also, AIDS patients are often quite sensitive to drug toxicities. Thus, patients with AIDS-KS on ritonavir may be particularly sensitive to BAY 43-9006.