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  • 1
    Electronic Resource
    Electronic Resource
    Ask the expert (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 138-138 
    Details
    ISSN: 1432-198X
    Keywords: Hemolytic uremic syndrome ; Immunization ; Vaccination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00862053
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Membranoproliferative glomerulonephritis type III (1998)
    Springer
    Pediatric nephrology 12 (1998), S. 512-522 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Membranoproliferative glomerulonephritis type III ; Complement components
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050497
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    In utero intervention in prune-belly syndrome (1999)
    Springer
    Pediatric nephrology 13 (1999), S. 138-138 
    Details
    ISSN: 1432-198X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050581
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Another step forward in our understanding of the hemolytic uremic syndromes: tieing up some loose ends (1995)
    Springer
    Pediatric nephrology 9 (1995), S. 30-32 
    Details
    ISSN: 1432-198X
    Keywords: Hemolytic uremic syndromes ; Thrombocytopenic purpura
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00858961
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Renal failure in the neonate associated with in utero exposure to non-steroidal anti-inflammatory agents (1994)
    Springer
    Pediatric nephrology 8 (1994), S. 700-704 
    Details
    ISSN: 1432-198X
    Keywords: Renal failure ; Fetus and neonate ; Indomethacin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In utero exposure to non-steroidal anti-inflammatory agents (NSAIAs) can produce combinations of oligohydramnios, a bleeding diathesis, ileal perforation, premature closure of the ductus, and acute or chronic renal injury. NSAIAs induce renal dysgenesis in fetal monkeys and renal structural abnormalities in the developing human fetus. We report oligohydramnios and renal failure associated with in utero exposure to early, prolonged, high-dose indomethacin in four neonates, and to ibuprofen in one neonate. Four of the affected neonates were one of twins. In each set of twins, only one of the pair was affected. One set of twins was proven to be identical, whereas the other three sets seemed to be identical. It is possible that the histopathological findings of uncertain or incomplete tubular differentiation may be the result of a direct effect of NSAIAs on developing or “immature” tubules. Therefore, the advantages of NSAIAs as tocolytics need to be weighed against the complication of severe renal injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00869093
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  • 6
    Electronic Resource
    Electronic Resource
    Management of patients with hemolytic uremic syndrome demonstrating severe azotemia but not anuria (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 671-674 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Hemolytic uremic syndrome   ;   Non-oliguric renal failure   ;   Management   ;   Dialysis   ;   Azotemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract . There are no specific indications for dialysis in a patient with typical hemolytic uremic syndrome (D+HUS) who does not have anuria, hyperkalemia, volume overload, or severe acidemia. We managed five patients with D+HUS, aged 1.5 – 14 years, without dialysis despite marked azotemia, because they were not anuric and because they had none of the acid-base, fluid, or electrolyte perturbations that may have been indications for dialysis. Each had markedly elevated blood urea nitrogen (range 137 – 234 mg/dl) and serum creatinine concentrations (range 5.4 – 15.4 mg/dl). None was anuric and one was oliguric for 4 days. There were no complications and each recovered. We have reviewed the published literature on the use of dialysis in patients with D+HUS and have not found any guidelines that relate to the management of similar cases. It is our view that management of D+HUS patients without dialysis is appropriate when the patient is passing urine and the acid-base, serum electrolyte concentrations and fluid balances can be managed without dialysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050187
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  • 7
    Electronic Resource
    Electronic Resource
    Peripheral gangrene complicating idiopathic and recessive hemolytic uremic syndromes (2000)
    Springer
    Pediatric nephrology 14 (2000), S. 985-989 
    Details
    ISSN: 1432-198X
    Keywords: Key words Peripheral gangrene ; Thrombosis ; Idiopathic hemolytic uremic syndrome ; Recessive hemolytic uremic syndrome ; Rheumatoid arthritis ; Cortical necrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Three patients with hemolytic uremic syndrome (HUS) developed peripheral gangrene. Bilateral carotid artery thromboses occurred in one of these patients after recovery from HUS. One patient had a long history of juvenile rheumatoid arthritis. In the second patient, a flu-like illness preceded the onset of HUS. The third was one of two sisters, with the HUS appearing more than 1 year apart. None had evidence of disseminated intravascular coagulation or infection with Streptococcus pneumoniae. The patient with rheumatoid arthritis had renal cortical necrosis but recovered moderate renal function after treatment with dialysis and plasmapheresis for 6 months. The child with a genetic form of HUS died of renal failure and had massive cortical necrosis and vascular thrombosis at autopsy. This is the first report of peripheral gangrene in children with idiopathic HUS and autosomal recessive HUS.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050058
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  • 8
    Electronic Resource
    Electronic Resource
    Cytokines in childhood hemolytic uremic syndrome and thrombotic thrombocytopenic purpura (1995)
    Springer
    Pediatric nephrology 9 (1995), S. 694-699 
    Details
    ISSN: 1432-198X
    Keywords: Interleukin-6 ; Tumor necrosis factor-α ; Hemolytic uremic syndrome ; Thrombotic thrombocytopenic purpura
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Serum and urine cytokines were analyzed in children with hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Interleukin-6 (IL-6) was elevated in the serum of 33 of 35 children with HUS (94%) and in 2 of 2 children with recurrent TTP. Serum IL-6 was higher in children with HUS who developed anuria, extrarenal manifestations during the acute phase of illness and/or chronic renal sequelae. Tumor necrosis factor-α (TNF-α) was detected in the serum of 7 patients with HUS (20%) and 1 patient with TTP. IL-6 and TNF-α were elevated in the urine of 4 of 4 children with HUS and 2 of 2 children with TTP. Urinary levels were higher than serum levels, suggesting local production of cytokines in the urinary tract. Sequential serum and urine samples showed that IL-6 levels varied with disease activity. IL-6 and TNF-α were not detected in the serum (n=25) and urine (n=15) of healthy children. We conclude that IL-6 in urine may be used to monitor disease activity in HUS and TTP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00868714
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  • 9
    Electronic Resource
    Electronic Resource
    Recent advances in understanding the pathogenesis of the hemolytic uremic syndromes (1990)
    Springer
    Pediatric nephrology 4 (1990), S. 276-283 
    Details
    ISSN: 1432-198X
    Keywords: Hemolytic uremic syndrome ; Escherichia coli 0157∶H7 ; Shiga-like toxin ; Endothelial cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract One of the requirements for an agent to cause hemolytic uremic syndrome (HUS) is its ability to injure endothelial cells. Shiga-like toxin (SLT) can do this. SLT is produced byEscherichia coli andShigella dysenteriae serotype 1; both have been implicated as causes of typical HUS. Endothelial cells have receptors (GB3) for SLT and the toxin can inhibit eukaryotic protein synthesis, thereby causing cell death. Glomerular endothelial cell injury or death results in a decreased glomerular filtration rate and many of the perturbations seen in HUS. It is no longer certain that hemolysis is the result of a microangiopathy. Cell injury results in release of von Willebrand multimers; if these are ultra-large, thrombosis may ensue. There is also increasing evidence that neutrophils have a role in the pathogenesis of typical HUS.Streptococcus pneumoniae can also cause HUS and care must be taken to avoid giving plasma to patients withS. pneumoniae-associated HUS. There is compelling evidence that types of HUS are inherited by autosomal recessive and autosomal dominant modes. Patients with autosomal recessive HUS may have recurrent episodes. Mortality and morbidity rates are high for the inherited forms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00857676
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  • 10
    Electronic Resource
    Electronic Resource
    Wegener granulomatosis – an atypical case (2000)
    Springer
    Pediatric nephrology 14 (2000), S. 862-871 
    Details
    ISSN: 1432-198X
    Keywords: Key words Wegener granulomatosis ; Anti-neutrophilic cytoplasmic antibodies ; Small-vessel vasculitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  An unusual sequence of the clinical manifestations of microvascular disease is described in a 15 year-old girl. She initially presented with acute renal failure caused by a crescentic glomerulonephritis associated with positive tests for MPO-ANCA. Eighteen months later she had pulmonary hemorrhage and respiratory failure. An open lung biopsy showed granulomas that were diagnostic for Wegener granulomatosis. We discuss the diagnostic dilemmas faced in attempts to distinguish infective causes of pulmonary granulomas, such as tuberculosis or fungi, from granulomas associated with vasculitis, in a patient previously treated with immunosuppressive therapy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00013445
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