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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Proteinuria is supposedly a frequent and early manifestation of glomerulonephritis. Since albuminuria rather than proteinuria is the hallmark of glomerular disease, the present studies were designed to study the occurrence of albuminuria in normal mice (SWR/J strain) and in mice with a reproducible and predictable immune complex glomerulonephritis induced by chronic infection with lymphocytic choriomeningitis (LCM) virus. A radial immunodiffusion technique, specific for mouse albumin, was employed to quantify the albuminuria. Column chromatography of concentrated urine obtained from normal and nephritic mice demonstrated that albumin excreted in the urine had the same molecular weight as serum albumin and that identifiable fragments of albumin did not appear in the urine. Some albuminuria did occur in normal mice, 0.12 +/- SD. 0.13 mg. per 18 hours for 80 males and 0.13 +/- 0.09 mg. per 18 hours for 55 females. Increased albuminuria, defined as values greater than a normal mean + 2 S.D. (0.40 mg. per 18 hours) occurred in only 25 per cent of nephritic mice, although in more than 600 animals studied, immunofluorescent microscopy invariably demonstrated abnormal accumulation of immune complexes in the glomeruli of SWR/J mice chronically infected with LCM virus. Values of total proteinuria measured by the sulfosalicylic acid method did not correlate with radial immunodiffusion measured albuminuria. The results indicate that measurement of total proteinuria in mice is not a useful parameter of glomerular disease. Albuminuria, while increased in 25 per cent of nephritic animals, was not abnormal even in the presence of marked histologic alterations in 75 per cent of mice, suggesting that abnormal immunopathology may very commonly not be reflected in increased or pathologic albuminuria. Recent observations also suggest that this is the case in humans.
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PMID:Studies of abluminuria and proteinuria in normal mice and mice with immune complex glomerulonephritis. 81 41

Hantavirus activity in rodents and human beings in Argentina has been known since the 1980's. In this study, we retrospectively investigated hantavirus infections among Argentine Hemorrhagic Fever (AHF) cases notified between 1987 and 1994, without virological confirmation. IgG and IgM antibodies to hantavirus were tested by ELISA. Among 1028 patients included in the study, we found 13 recent infections (1.26%) and 13 remote infections (1.26%). IgG antibodies determined in 745 healthy persons living in the same localities of recent infection cases, gave only one positive result (0.13%). Nine of the 13 recent infections had the clinical presentation of Hemorrhagic Fever with Renal Syndrome (HFRS) while the other four were in the form of Hantavirus Pulmonary Syndrome (HPS). We performed a clinical and epidemiological comparison between the nine patients with FHSR and two paired control groups: one with confirmed AHF and the other with Febrile Syndrome of Undetermined Etiology (FSUE), which were negative for hantavirus, Junin and LCM. There were no differences between clinical signs or symptoms. Nevertheless, normal or high leucocyte counts, with thrombocytopenia, hemoconcentration, high creatinine levels and proteinuria in HFRS cases resulted useful for differential diagnosis. These results showed the coexistence of Junin virus and hantaviruses in the endemic area of AHF, and indicate the importance of including the infection with these viruses in the differential diagnosis of hemorrhagic fevers and respiratory distress syndromes of unknown etiology. The clinical variability found could be related to the presence of more than one hantavirus serotype in our country.
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PMID:[Retrospective detection of hantavirus clinical infections in Argentina]. 873 23

Wiskott-Aldrich syndrome (WAS) is a primary immunodeficiency caused by mutations in the gene encoding the hematopoietic-specific WAS protein (WASp). WAS is frequently associated with autoimmunity, indicating a critical role of WASp in maintenance of tolerance. The role of B cells in the induction of autoreactive immune responses in WAS has been investigated in several settings, but the mechanisms leading to the development of autoimmune manifestations have been difficult to evaluate in the mouse models of the disease that do not spontaneously develop autoimmunity. We performed an extensive characterization of Was-/- mice that provided evidence of the potential alteration in B cell selection, because of the presence of autoantibodies against double-stranded DNA, platelets, and tissue antigens. To uncover the mechanisms leading to the activation of the potentially autoreactive B cells in Was-/- mice, we performed in vivo chronic stimulations with toll-like receptors agonists (LPS and CpG) and apoptotic cells or infection with lymphocytic choriomeningitis virus. All treatments led to increased production of autoantibodies, increased proteinuria, and kidney tissue damage in Was-/- mice. These findings demonstrate that a lower clearance of pathogens and/or self-antigens and the resulting chronic inflammatory state could cause B cell tolerance breakdown leading to autoimmunity in WAS.
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PMID:In Vivo Chronic Stimulation Unveils Autoreactive Potential of Wiskott-Aldrich Syndrome Protein-Deficient B Cells. 2851 59