Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
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.
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.
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.
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.
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.