Evgenia Gurevich1,2, Eytan Israel1,2, Yael Segev3, Daniel Landau3,4. 1. Soroka University Medical Center, Ben-Gurion University of the Negev, Beersheba, Israel. 2. Division of Pediatrics, Ben-Gurion University of the Negev, Beersheba, Israel. 3. Department of Microbiology and Immunology, Ben-Gurion University of the Negev, Beersheba, Israel. 4. Department of Pediatrics B, Schneider Children's Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
Abstract
Background: Transient proteinuria during febrile illness is a common phenomenon. Recent studies have re-examined the pathophysiology of proteinuria and new urinary markers to characterize it, including B7-1 (CD80), which is expressed also in glomerular podocytes and influences the glomerular barrier. Aim: To investigate the pattern of proteinuria in febrile non-renal diseases, including B7-1. Methods: We prospectively analyzed urine samples of 44 febrile children and 28 afebrile controls for different protein components: albumin (glomerular marker), β2-microglobulin (tubular marker), uromodulin (Tamm Horsfall protein-THP, a renal endogenous protein) and B7-1. Febrile illness was characterized as focal bacterial vs. viral. Exclusion criteria were underlying renal disease, steroid treatment or urinary tract infection. Results: Elevated urine albumin (64.5 ± 10.3 vs. 17.8 ± 4 mg/g, mean ± S.E.M., p = 0.0009) and β2-microglobulin (1.44 ± 0.34 vs. 0.182 ± 0.03 mg/g, mean ± S.E.M., p = 0.005] and decreased uromodulin (10.5 ± 1 vs. 26.7 ± 2.2 Arbitrary units, mean ± S.E.M., p = 0.0001) excretion were found during febrile illness vs. controls. Urine B7-1 was also increased in the febrile group (0.27 ± 0.05 vs. 0.07 ± 0.01 ng/ml, mean ± S.E.M., p = 0.001), and was the only marker which was significantly higher in bacterial vs. viral disease. Conclusions: Febrile proteinuria is not generalized: while proteins of both glomerular and tubular origin increase, uromodulin decreases. Urine B7-1 is increased during fever, more significantly in bacterial infections. Thus, urinary B7-1 may be used as an additional marker to differentiate between febrile states of bacterial vs. viral origin.
Background: Transient proteinuria during febrile illness is a common phenomenon. Recent studies have re-examined the pathophysiology of proteinuria and new urinary markers to characterize it, including B7-1 (CD80), which is expressed also in glomerular podocytes and influences the glomerular barrier. Aim: To investigate the pattern of proteinuria in febrile non-renal diseases, including B7-1. Methods: We prospectively analyzed urine samples of 44 febrile children and 28 afebrile controls for different protein components: albumin (glomerular marker), β2-microglobulin (tubular marker), uromodulin (Tamm Horsfall protein-THP, a renal endogenous protein) and B7-1. Febrile illness was characterized as focal bacterial vs. viral. Exclusion criteria were underlying renal disease, steroid treatment or urinary tract infection. Results: Elevated urine albumin (64.5 ± 10.3 vs. 17.8 ± 4 mg/g, mean ± S.E.M., p = 0.0009) and β2-microglobulin (1.44 ± 0.34 vs. 0.182 ± 0.03 mg/g, mean ± S.E.M., p = 0.005] and decreased uromodulin (10.5 ± 1 vs. 26.7 ± 2.2 Arbitrary units, mean ± S.E.M., p = 0.0001) excretion were found during febrile illness vs. controls. Urine B7-1 was also increased in the febrile group (0.27 ± 0.05 vs. 0.07 ± 0.01 ng/ml, mean ± S.E.M., p = 0.001), and was the only marker which was significantly higher in bacterial vs. viral disease. Conclusions: Febrile proteinuria is not generalized: while proteins of both glomerular and tubular origin increase, uromodulin decreases. Urine B7-1 is increased during fever, more significantly in bacterial infections. Thus, urinary B7-1 may be used as an additional marker to differentiate between febrile states of bacterial vs. viral origin.
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