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Träfflista för sökning "L773:1432 198X srt2:(2005-2009)"

Sökning: L773:1432 198X > (2005-2009)

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1.
  • Andersson, Lena, 1980, et al. (författare)
  • Urinary proteins in children with urinary tract infection
  • 2009
  • Ingår i: Pediatric Nephrology. - : Springer Science and Business Media LLC. - 0931-041X .- 1432-198X. ; 24:8, s. 1533-1538
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract The aim of this study was to test our hypothesis that the urinary excretion of C-reactive protein (CRP), alpha 1-microglobulin (A1M), retinol-binding protein (RBP) and Clara cell protein (CC16) is increased in children with urinary tract infection (UTI) and relates to renal damage as measured by acute dimercaptosuccinic acid (DMSA) scintigraphy. Fifty-two children <2 years of age with UTI were enrolled in the study, 44 of whom were febrile. The control group consisted of 23 patients with non-UTI infection and elevated serum CRP (s-CRP) levels. Thirty-six patients had abnormal DMSA uptake, classified as mild, moderate or severe damage (DMSA class 1, 2, 3, respectively). There was a significant association between DMSA class and the excretion of urinary RBP (u-RBP) and u-CC16. There was also a significant difference in u-CRP levels between children with UTI and control children with non-UTI infections, although u-CRP excretion was not significantly correlated to DMSA class. In conclusion, the urinary excretion of the low-molecular-weight proteins RBP and CC16 showed a strong association with uptake defects on renal DMSA scans. The urinary level of CRP seems to distinguish between children with UTI and other febrile conditions. A combination of these biomarkers may be useful in the clinical assessment of children with UTI.
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  • Ariceta, Gema, et al. (författare)
  • Guideline for the investigation and initial therapy of diarrhea-negative hemolytic uremic syndrome
  • 2009
  • Ingår i: Pediatric Nephrology. - : Springer Science and Business Media LLC. - 1432-198X .- 0931-041X. ; 24:4, s. 687-696
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • This guideline for the investigation and initial treatment of atypical hemolytic uremic syndrome (HUS) is intended to offer an approach based on opinion, as evidence is lacking. It builds on the current ability to identify the etiology of specific diagnostic sub-groups of HUS. HUS in children is mostly due to infection, enterohemorrhagic Escherichia coli (EHEC), Shigella dysenteriae type 1 in some geographic regions, and invasive Streptococcus pneumoniae. These sub-groups are relatively straightforward to diagnose. Their management, which is outside the remit of this guideline, is related to control of infection where that is necessary and supportive measures for the anemia and acute renal failure. A thorough investigation of the remainder of childhood HUS cases, commonly referred to as "atypical" HUS, will reveal a risk factor for the syndrome in approximately 60% of cases. Disorders of complement regulation are, numerically, the most important. The outcome for children with atypical HUS is poor, and, because of the rarity of these disorders, clinical experience is scanty. Some cases of complement dysfunction appear to respond to plasma therapy. The therapeutic part of this guideline is the consensus of the contributing authors and is based on limited information from uncontrolled studies. The guideline proposes urgent and empirical plasmapheresis replacement with whole plasma fraction for the first month after diagnosis. This should only be undertaken in specialized pediatric nephrology centers where appropriate medical and nursing skills are available. The guideline includes defined terminology and audit points so that the early clinical effectiveness of the strategy can be evaluated.
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  • Dietrich, Andreas, et al. (författare)
  • Analysis of genes encoding laminin beta 2 and related proteins in patients with Galloway-Mowat syndrome
  • 2008
  • Ingår i: Pediatric Nephrology. - : Springer Science and Business Media LLC. - 1432-198X .- 0931-041X. ; 23:10, s. 1779-1786
  • Tidskriftsartikel (refereegranskat)abstract
    • Galloway-Mowat syndrome (GMS) is a rare autosomal recessive disorder characterized by early onset nephrotic syndrome and microcephaly with various anomalies of the central nervous system. GMS likely represents a heterogeneous group of disorders with hitherto unknown genetic etiology. The clinical phenotype to some extent overlaps that of Pierson syndrome (PS), which comprises congenital nephrotic syndrome and distinct ocular abnormalities but which may also include neurodevelopmental deficits and microcephaly. PS is caused by mutations of LAMB2, the gene encoding laminin beta 2. We hypothesized that GMS might be allelic to PS or be caused by defects in proteins that interact with laminin beta 2. In a cohort of 18 patients with GMS or a GMS-like phenotype we therefore analyzed the genes encoding laminin beta 2 (LAMB2), laminin alpha 5 (LAMA5), alpha 3-integrin (ITGA3), beta 1-integrin (ITGB1) and alpha-actinin-4 (ACTN4), but we failed to find causative mutations in these genes. We inferred that LAMA5, ITGA3, ITGB1, and ACTN4 are not directly involved in the pathogenesis of GMS. We excluded LAMB2 as a candidate gene for GMS. Further studies are required, including linkage analysis in families with GMS to identify genes underlying this disease.
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  • Hansson, Sverker, 1946, et al. (författare)
  • Urinary tract infection caused by Haemophilus influenzae and Haemophilus parainfluenzae in children.
  • 2007
  • Ingår i: Pediatric nephrology (Berlin, Germany). - : Springer Science and Business Media LLC. - 0931-041X .- 1432-198X. ; 22:9, s. 1321-5
  • Tidskriftsartikel (refereegranskat)abstract
    • There are few reports on urinary tract infections caused by Haemophilus influenzae or Haemophilus parainfluenzae in children. The true incidence is not known, since bacteria of Haemophilus species do not grow in standard urine culture media. With the objective of investigating the occurrence and character of urinary tract infections (UTIs) caused by Haemophilus bacteria in children, we searched the files of our UTI clinic. Over a 24-year period 36 children with Haemophilus spp. bacteriuria were identified out of a total of more than 5,000 UTI episodes. There was a significant gender difference in that Haemophilus influenzae dominated in girls and Haemophilus parainfluenzae in boys. With one exception, all children had important urinary tract abnormalities, such as malformation, gross reflux or bladder dysfunction. Permanent renal damage was seen in 25. We conclude that growth of Haemophilus bacteria in urine is associated with serious urinary tract abnormalities. The inability of bacteria of the Haemophilus species to grow in standard media commonly used for culture of uropathogens suggests that the true frequency of these strains as a cause of urinary tract infections is underestimated.
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