A complex case of congenital cystic renal disease.

This case outlines the potential complexity of autosomal recessive polycystic kidney disease (ARPKD). It highlights the challenges involved in managing this condition, some of the complications faced and areas of uncertainty in the decision making process. With a paucity of published paediatric cases on this subject, this should add to the pool of information currently available.

Five-year outcomes after a change from a cyclosporin-based to a 'low-dose' tacrolimus-based primary immunosuppression regimen for incident kidney transplants--the Glasgow experience.

In January 2007, our centre changed from a cyclosporin (CyA)/azathioprine (Aza)/ prednisolone (Pred) primary immunosuppression regimen (with basiliximab induction and mycophenolate mofetil [MMF] for those at immunologically high risk) to a tacrolimus (Tac) (low dose)/MMF/Pred regimen with basiliximab induction, following presentation of Symphony trial results. This analysis assesses the impact of this change on 5-year outcomes. Three hundred consecutive renal-only transplants were identified: 140 from the 2005-06 era and 160 from the 2007-08 era. The proportions of living donor (37.5 vs. 22.9%; p = 0.04) and donors after circulatory death (11.9 vs. 5.0%; p = 0.03) were higher in the 2007-08 cohort. Five-year actuarial patient survival was higher in the 2007-08 cohort (96.8 vs. 87.1%; p = 0.003), with a trend toward higher 5-year transplant survival (84.7 vs. 76.3%; p = 0.08). Estimated glomerular filtration rate (eGFR) was higher than in the 2005-06 era at 1 (53.5 vs. 44.5 ml/min/1.73m2; p = 0.0006) and 3 years (50.9 vs. 43.4 ml/min/1.73m2; p = 0.02), with a trend toward higher eGFR at 5 years (41.8 vs. 49.6 ml/min/1.73m2; p = 0.09). Differences were consistent when living donor and deceased donor transplants were analysed separately. In a "real world" population, a change from a CyA-based to a Tac (low-dose)/MMF/Pred primary immunosuppression regimen has been associated with better 5-year outcomes.

Xanthine oxidoreductase and preservation injury in human liver transplantation.

BACKGROUND: Preservation injury is a major cause of primary graft dysfunction in liver transplantation (LT). Oxidative damage is considered to be the first event leading to graft damage. Xanthine oxidoreductase (XOR) and neutrophil activation, two sources of reactive oxygen species, could play a role in the development of graft dysfunction. METHODS: We determined activities of XOR forms, polymorphonuclear elastase (PMN-E), aminotransferases, and hyaluronic acid in plasma of 20 patients undergoing LT. Samples were taken from the radial artery (RA) before the anhepatic phase; from the portal vein (PV) before reperfusion; from graft caval effluent (CE) at reperfusion; and from RA, PV, and the hepatic vein (HV) 10 and 90 min postreperfusion. RESULTS: The graft, but not recipient bowel, released XOR into blood (XOR in CE, median, 61.2 mU/g protein [range, 1.9-160.4 vs. undetectable in PV before reperfusion). Circulating XOR was transformed from dehydrogenase to reversible oxidase (XOrev) (XOrev-to-XOR ratio, 48.1% in CE and 65.1% in HV 90 min postreperfusion). Neutrophil activation was detected in the recipients before reperfusion, and in liver at early post-reperfusion (median PMN-E was 0.85 microg/g protein [range, 0.01-1.58] in RA before the anhepatic phase; 2.22 microg/g protein [range, 0.20-5.88] in PV prereperfu-sion; and 3.60 microg/g protein [range, 0.48-6.78] in HV 10 min postreperfusion). XOR, but none of the other markers, was higher in the CE of patients with moderate primary graft dysfunction than in those with slight primary graft dysfunction. CONCLUSIONS: XOR release and neutrophil activation are produced during LT, and they are potentially injurious mechanisms associated with this therapy.