Renal pathologies following viral infections have become an emerging public health problem in both developed and developing countries. Diagnostic criteria are complex. In most cases, they involve correlation between clinical, biological and histological data, with occasional recourse to molecular biology techniques. Several mechanisms are involved in the pathogenesis of virus-related nephropathy, including virus tropism in the kidney, formation of immune complexes in situ or in the bloodstream, direct cytopathogenic effects, and multiple organ failure. The hepatitis C virus is responsible for three main types of kidney disease: membranoproliferative glomerulnephritis, cryoglobulinemia and membranous nephropathy. Hepatitis B virus is associated with membranous nephropathy, membranoproliferative glomerulnethritis, and IgA nephropathy. HIV (human immunodeficiency virus) infection is associated with several glomerular and tubular kidney damage. HIVAN (HIV-associated nephropathy), a specific entity mainly affecting Africans and African-Americans, presents as a rapidly progressive glomerulonephritis rapidly progressing to the terminal stage. Infections secondary to adenovirus, cytomegalovirus, epstein-barr virus, poliomavirus and coronavirus are often responsible for acute or chronic tubulointerstitial nephritis. Treatment is mainly symptomatic, based on nephroprotection measures, rarely combined with antiviral therapy. Prophylaxis with vacci-nation, when available, remains the best means of preventing viral nephropathy.