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English Abstract
Journal Article
[Glomerular-type proteinuria in hantavirus nephritis].
Medizinische Klinik 2004 May 16
BACKGROUND: Infection with hantavirus of the Puumala type is known to cause severe illness, fever, loin pain and impaired vision. Tubulointerstitial nephritis leads to acute renal failure.
CASE REPORTS: In four patients presenting with hantavirus infection and acute renal failure, proteinuria was analyzed by microelectrophoresis to explore possible causes of renal protein loss in hantavirus nephritis. The patients (three men, one woman) presented with a short history of fever, headache, loin pain and acute renal failure (enlarged kidneys in ultrasonography, serum creatinine 7.7/3.4/3.2/7.8 mg/dl, urinary protein excretion 1.7/0.5/1.5/9.0 g/l, IgM antibodies against hantavirus positive in all patients, subtype Puumala). Microelectrophoresis of the urine revealed a major fraction of higher molecular weight proteins such as transferrin and immunoglobulins indicating unselective glomerular-type proteinuria in all four patients. In three renal biopsy specimens obtained, morphology of glomeruli and vasculature was normal as judged by light microscopy. The tubulointerstitium exhibited interstitial hemorrhage and round-cell infiltrates. After 2 weeks, renal function had completely recovered in all patients and no persistent proteinuria developed.
CONCLUSION: Hantavirus nephritis may lead to glomerular-type proteinuria. Glomerular morphology may be normal and proteinuria may cease within 2 weeks indicating a transient lesion of the glomerular filtration barrier. Transiently increased glomerular permeability may be caused by an immunologic response to virus infection.
CASE REPORTS: In four patients presenting with hantavirus infection and acute renal failure, proteinuria was analyzed by microelectrophoresis to explore possible causes of renal protein loss in hantavirus nephritis. The patients (three men, one woman) presented with a short history of fever, headache, loin pain and acute renal failure (enlarged kidneys in ultrasonography, serum creatinine 7.7/3.4/3.2/7.8 mg/dl, urinary protein excretion 1.7/0.5/1.5/9.0 g/l, IgM antibodies against hantavirus positive in all patients, subtype Puumala). Microelectrophoresis of the urine revealed a major fraction of higher molecular weight proteins such as transferrin and immunoglobulins indicating unselective glomerular-type proteinuria in all four patients. In three renal biopsy specimens obtained, morphology of glomeruli and vasculature was normal as judged by light microscopy. The tubulointerstitium exhibited interstitial hemorrhage and round-cell infiltrates. After 2 weeks, renal function had completely recovered in all patients and no persistent proteinuria developed.
CONCLUSION: Hantavirus nephritis may lead to glomerular-type proteinuria. Glomerular morphology may be normal and proteinuria may cease within 2 weeks indicating a transient lesion of the glomerular filtration barrier. Transiently increased glomerular permeability may be caused by an immunologic response to virus infection.
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