RESUMO
Glomerulonephritis with proteinuria of sufficient degree to manifest the nephrotic syndrome followed aplastic crises induced by human parvovirus (B19) in seven patients with homozygous sickle-cell disease, within 7 days in five patients and 6-7 weeks in two. Segmental proliferative glomerulonephritis was found in all four patients who underwent acute renal biopsies and focal segmental glomerulosclerosis was found in the fifth patient who had a biopsy 4 months later. One patient recovered completely, one died in chronic renal failure after 3 months, and the others had impaired creatinine clearance, four with continuing proteinuria (AU)
Assuntos
Adulto , Relatos de Casos , Feminino , Humanos , Masculino , Adolescente , Anemia Falciforme/genética , Eritema Infeccioso/complicações , Glomerulosclerose Segmentar e Focal/etiologia , Anemia Falciforme/complicações , Anticorpos Antivirais/análise , Biópsia , DNA Viral/análise , Glomerulosclerose Segmentar e Focal/patologia , Homozigoto , Rim/patologia , Síndrome Nefrótica/etiologia , Parvovirus B19 Humano/genética , Parvovirus B19 Humano/imunologia , Proteinúria/etiologia , JamaicaRESUMO
Proteinuria of sufficient severity to manifest the nephrotic syndrome and renal impairment has been associated with human parvovirus (B19) infection in 7 patients with homozygous sickle-cell (SS) disease. In most patients, the proteinuria resolved but renal impairment remained. The glomerular histology showed evidence of segmental proliferative glomerulonephritis in 4 out of 5 biopsies. Most events occurred within 2 weeks of B19 associated aplastic crisis, and the mechanism is at present unknown. This association may add to the pathogenic significance of B19 infection in SS disease (AU)