No abstract

Renal transplantation, first performed successfully in the 1950s, is the treatment of choice for most patients with end-stage renal failure. It confers longer term survival and a better quality of life than do both haemodialysis and peritoneal dialysis. The success of renal transplantation is dependent on the preservation of renal graft function and despite the many advances in surgical techniques, immunosuppressive regimens and supportive therapies, many challenges remain including post-operative ureteral obstruction. This complication can pose a risk to graft, and, occasionally, to patient survival. In this pictorial review, we describe the causes of ureteral obstruction following renal transplantation and illustrate the pivotal role of radiology in both diagnosing and managing these complications.

Coagulation proteases are involved in generating fibrin after vascular injury (hemostasis) but they also have multiple other effects, many of which are mediated independently of fibrin generation, via interactions with specific cell membrane-expressed 'protease activated receptors'. In inflammation, this family of proteins has a complex influence, the facets of which are still incompletely understood, though a common feature in different models appears to be amplification of innate signals that are initially generated by pathogenic elements or, in the context of transplantation, ischemia or anti-graft antibodies, for instance. There is increasing evidence that these proteases may also have specific effects on cells involved in adaptive immunity and on cells that mediate chronic inflammation and fibrosis. Understanding whether these effects are relevant in the responses generated against transplanted organs is important, as it could lead ultimately to the development of novel ways to promote long-term graft survival.

Organs expressing cytoprotective HO-1 have a direct influence on the recipient immune response. Given the important role of CD8 T cells and IFN-gamma in chronic rejection, these data suggest that donor HO-1 expression may be useful to augment other immunosuppressive therapies to prolong graft survival and inhibit intimal hyperplasia.