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Volume 2 Issue 1, January 2006

Editorial

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Viewpoint

  • Transcriptome-based assessment of blood, urine or biopsy tissue could have a powerful impact on the management of renal transplants, with the potential to detect injurious mechanisms before graft injury is established. This Viewpoint article explores the promise held by transcriptomics and high-density microarrays, and examines the challenges of applying these new technologies in renal transplant recipients.

    • Philip F Halloran
    • Gunilla Einecke
    Viewpoint
  • The plasma concentration of sodium ions normally exceeds the sum of the plasma concentrations of chloride and bicarbonate ions. Calculation of the resulting 'anion gap' can aid the diagnosis of various acid–base and electrolyte disorders. Michael Emmett discusses the utility of this approach, and highlights the potential disrupting factors which should be taken into account when interpreting anion gap calculations.

    • Michael Emmett
    Viewpoint
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Research Highlight

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Practice Point

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Review Article

  • There is no specific treatment for kidney damage secondary to deposition of polymeric IgA. Nephrologists' opinions on the optimal management strategy for IgA nephropathy therefore vary widely, encompassing perturbation of the renin–angiotensin system, tonsillectomy, fish oil, steroids and cytotoxic agents. The data supporting these and other therapeutic options are presented in this critical analysis.

    • Francesco Locatelli
    • Lucia Del Vecchio
    • Claudio Pozzi
    Review Article
  • Maintaining cardiovascular stability while eliminating toxins is the challenge that confronts intensivists managing critically ill patients whose kidneys have failed. Generally treated with continuous venovenous hemofiltration or intermittent hemodialysis, evidence is emerging that prolonged dialysis at low flow rates has equivalent safety and efficacy in acute renal failure, plus the advantages of flexible treatment timing and reduced costs.

    • Danilo Fliser
    • Jan T Kielstein
    Review Article
  • The mutations ofPKD1 and PKD2, and PKHD1, which cause autosomal dominant and autosomal recessive polycystic kidney disease, respectively, disrupt the function of polycystins and fibrocystin in tubular epithelial cells. The cellular consequences of these perturbations are reviewed here by Torres and Harris, with emphasis on the affected signaling pathways.

    • Vicente E Torres
    • Peter C Harris
    Review Article
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