Infection with parvovirus B19 causes several clinical syndromes (fifth disease, transient aplastic crisis, pure red cell aplasia, and hydrops fetalis) and may contribute to other illnesses. B19 has been linked to renal disease in three settings: As a cause of acute glomerulopathy and as a cause of anemia in ESRD and kidney transplantation. Case reports implicate parvovirus in the pathogenesis of proliferative glomerulonephritis and collapsing glomerulopathy, but a causal relationship has not been established. A proposed role for B19 infection is based on the temporal association of renal findings with viral infection, positive serology, and identification of the viral genome in the glomerulus. Mechanisms may include cytopathic effects on glomerular epithelial cells and/or endothelial cells and glomerular deposition of immune complexes. Patients who require dialysis may have increased susceptibility to acute and chronic anemia after parvoviral infection. Factors that predispose this population to complications of B19 infection include impaired immune response, deficient erythropoietin production, and possibly decreased erythrocyte survival. The clinical burden of parvovirus B19 infection in renal transplant recipients may be underestimated; these individuals may develop persistent viremia as a result of a dysfunctional immune response. Chronic anemia and pure red blood cell aplasia are the most common complications of parvovirus infection in this population; the diagnosis should be considered in transplant recipients with unexplained anemia or pancytopenia. Allograft rejection and dysfunction have been reported in association with infection, but a cause-effect relationship has not been proved. Further investigation of the relationship between B19 and kidney disease is warranted.