The use of non–heart-beating donors could help shorten the list of patients who are waiting for a kidney transplant. Several reports describe acceptable results of transplantations from non–heart-beating donors who had in-hospital cardiac arrest, but few reports describe results of transplantations from non–heart-beating donors who had cardiac arrest that occurred outside of the hospital (Maastricht type I and type II donors). To compare graft survival rates among patients receiving kidneys from heart-beating donors versus type I or type II non–heart-beating donors. Retrospective cohort study of transplantations performed from January 1989 to December 2004. Kidney transplant program of a teaching hospital in Madrid, Spain. 320 patients who received a kidney transplant from non–heart-beating donors (273 type I donors and 47 type II donors) and 584 patients who received a kidney transplant from heart-beating donors divided into 2 groups according to donor age (age <60 years [n = 458] and age ≥60 years [n = 126]). The primary outcome measure was graft survival. The median follow-up time was 68 months (range, 9 to 198 months). One- and 5-year graft survival rates were 90.7% and 85.5%, respectively, for transplants from heart-beating donors younger than 60 years of age; 79.8% and 73.3%, respectively, for transplants from heart-beating donors 60 years of age or older (P < 0.001); and 87.4% and 82.1%, respectively, for transplants from non–heart-beating donors (P = 0.22 [vs. those from heart-beating donors < 60 years of age] and P = 0.014 [vs. those from heart-beating donors ≥ 60 years of age]). Graft survival did not differ between patients who received kidneys from heart-beating donors younger than 60 years of age and patients who received kidneys from non–heart-beating donors. This single-site, observational study was retrospective, and immunosuppressive therapy regimens given to transplant recipients varied over time. Outcomes of transplants from non–heart-beating donors and younger heart-beating donors are similar, and results for transplants from non–heart-beating donors improved compared with those from older heart-beating donors. On the basis of these results, the authors encourage other transplant units to adopt the use of type I and type II non–heart-beating donors.

Lead exposure is a known cause of hypertension. Although most studies have focused on lead-induced endothelial dysfunction and on the involvement of reactive oxygen species (ROS), it has been recently demonstrated that the vascular wall of lead-exposed rats has both an altered the endothelium-independent relaxing response and a reduced expression of soluble guanylate cyclase (sGC). The aim of the present study was to determine in in vitro incubated rat isolated aortic segments if lead downregulates sGC expression, analyzing the involvement of ROS and cyclooxygenase-2 (COX-2). The experiments were performed in isolated aortic segments from Wistar rats that were incubated with lead for 24 h. Lead significantly reduced sGC-β₁ subunit expression in a concentration-dependent manner. The maximal reduction in sGC-β₁ subunit expression was achieved with 1 ppm lead. Vitamin C (30 μmol/L) partially restored sGC-β1 subunit expression in lead (1 ppm)-exposed aortic segments. A similar protection of sGC-β₁ subunit expression was obtained with both a protein kinase A inhibitor, H89 (1 μmol/L) and with rofecoxib (1 μmol/L), an inhibitor of COX-2 activity. Moreover, lead exposure increased COX-2 expression in the arterial wall. While vitamin C reduced both COX-2 expression and superoxide anion production related to lead exposure, rofecoxib failed to modify superoxide anion generation in lead-incubated aortic segments. In conclusion, the present results suggest the involvement of ROS and COX-2 in the downexpression of sGC-β₁ subunit induced by lead in the rat vascular wall. E-mail: alopeza@fjd.es

The European Renal Association (ERA) Registry collects data on kidney replacement therapy (KRT) in patients with end-stage kidney disease (ESKD). This paper summarizes the ERA Registry Annual Report 2022, with a special focus on comparisons by sex. The supplement of this paper contains the complete ERA Registry Annual Report 2022. Data was collected from 53 national and regional KRT registries from 35 countries. Using this data, incidence, and prevalence of KRT, kidney transplantation rates, survival probabilities, and expected remaining lifetimes were calculated. In 2022, 530 million people of the European general population were covered by the ERA Registry. The incidence of KRT was 152 per million population (pmp). In incident patients, 54% were 65 years or older, 64% were male, and the most common primary renal disease (PRD) was diabetes mellitus (22%). At KRT initiation, 83% of patients received haemodialysis, 12% received peritoneal dialysis, and 5% underwent pre-emptive kidney transplantation. On 31 December 2022, the prevalence of KRT was 1074 pmp. In prevalent patients, 48% were 65 years or older, 62% were male, the most common PRD was of miscellaneous origin (18%), 56% of patients received haemodialysis, 5% received peritoneal dialysis, and 39% were living with a functioning graft. In 2022, the kidney transplantation rate was 40 pmp, with most kidneys coming from deceased donors (66%). For patients starting KRT between 2013 to 2017, 5-year survival probability was 52%. Compared with the general population, the expected remaining lifetime was 66% and 68% shorter for males and females, respectively, receiving dialysis, and 46% and 49% shorter for males and females, respectively, living with a functioning graft.

En bloc pediatric kidney transplants (EBPKT) are still a subject of controversy. The aim of this study was to determine whether acceptable long-term graft survival and function can be achieved in EBPKT compared with the transplant of single, cadaveric, adult donor kidneys. A retrospective review was conducted of 66 recipients of en bloc kidneys from cadaveric pediatric donors and 434 patients who underwent transplantation with a single kidney from an adult donor between January 1990 and May 2002 at the authors' hospital. The recipients were well-matched demographically. Both transplant groups were analyzed for short- and long-term performance in terms of transplant outcome and quality of graft function. Overall death-censored actuarial graft survival rates at 1 and 5 years were 89.2% and 84.6% in the adult kidney transplants (AKT) and 83.3% and 81.1% in EBPKT, respectively (P=0.56). In the EBPKT group, graft function was improved over that observed in AKT. Vascular thrombosis was the most common cause of graft loss in EBPKT. Acute rejection occurred more frequently in AKT and Cox's regression analysis indicated that undergoing an AKT was a predictive factor for acute vascular rejection (adjusted risk ratio, 3.8; 95% confidence interval, 1.4-10.2; P=0.001). Overall graft survival was similar in both groups, vascular complications were the main cause of graft loss in EBPKT, and the EBPKT showed excellent long-term graft function and a low incidence of acute rejection.

An animal model of post-transplant diabetes was induced in rats by treating them daily with 0.1 mg/kg body weight of tacrolimus (FK506) in two i.p. injections. Rats developed hyperglycaemia and glucose intolerance after 9 days of treatment. Pancreatic islets, isolated from treated rats on different days, showed a decreased capacity to secrete insulin in response to 20 mM glucose at days 7 and 14. This suppression of insulin secretion was preceded by a reduction of the islet insulin content on day 5 that was progressively decreasing until the end of the treatment (day 14). Islet content of insulin mRNAs, transcribed from rat insulin genes 1 and 2, was strongly suppressed, similar to the insulin content, at days 7 and 14. Islet mass was not strikingly modified by tacrolimus treatment: the DNA content was slightly decreased at the end (day 14) and the rate of islet cell apoptosis slightly increased. Tacrolimus-induced diabetes in the rat seems to be mainly provoked by a decreased insulin gene transcription with little or no alteration of islet mass. This explains that the observed suppression of all the islet and animal parameters studied was completely reversed 2 weeks after interrupting tacrolimus treatment.