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A 68-year old Caucasian male with a past medical history of human immunodeficiency virus (HIV) infection presented with acute oliguric renal failure and maculopapular rash. Renal biopsy demonstrated extensive foot process effacement as well as confluent small subepithelial electron-dense deposits, which is diagnostic of membranous glomerulonephritis. Subsequent serological tests showed venereal disease research laboratory test was positive in both serum and cerebral spinal fluid. Following penicillin treatment, the patient's creatinine returned to baseline 4 weeks later. Secondary membranous glomerulonephritis caused by syphilis in patients with HIV is discussed.

Aberrant immune responses underwrite lupus glomerulonephritis and may contribute to glomerular cell proliferation and inflammation. Recent studies provide evidence that apoptotic immune cells may initiate immune events leading to tissue damage. Nucleosomes within apoptotic particles are recognized by B cells and other antigen presenting cells and represent the most likely inciting antigen for autoantibody production. Some of these antibodies are nephritogenic depending on fine structural composition and antigen recognition in the circulation or on renal cells. Deficient complement components contribute to reduced clearance of circulating and native kidney apoptotic cells. This review summarizes current concepts in lupus immune pathogenesis and attempts to bridge immunology to pathology of lupus glomerulonephritis.