Transplant glomerulopathy (TG) is a histologic entity described more than four decades ago. In the last few years, our understanding of TG has improved significantly. Current evidence supports the postulate that TG is a unique pathologic and pathogenic entity distinct from other forms of chronic allograft injury. Detailed electron microscopic studies have shown basement membrane abnormalities in glomerular and peritubular capillaries, indicating that this is a disease of the entire renal capillary network. Staining biopsies for the complement fragment, C4d, showed positivity in subgroups of TG, suggesting the participation of antidonor antibodies. Consistent with this postulate, the incidence of TG is increased in patients with antidonor HLA antibodies prior to the transplant. The use of surveillance biopsies has demonstrated that TG can develop during the first few months after transplantation, although it may remain clinically quiescent for several years. However, TG is progressive, leading to reduced graft survival. Recent studies demonstrated a close association between TG and anti-HLA class II antibodies. Current therapies for TG are likely of limited value. However, it is also likely that an improved understanding of TG pathogenesis will result in the development of effective therapies for this form of progressive kidney allograft damage.