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En el presente artículo, se ha estudiado el efecto del nitrógeno presente en las diferentes atmósferas de sinterización (nitrógeno-hidrógeno y amoniaco disociado) en los aceros inoxidables ferríticos (430L), fabricados mediante procedimientos pulvimetalúrgicos. Por lo cual, se ha tomado como referencia la sinterización en vacío. Se han estudiado las propiedades físicas (densidad, porosidad y variación dimensional) y las propiedades mecánicas (dureza, resistencia a la tracción y alargamiento) de los aceros inoxidables ferríticos sinterizados en las diferentes atmósferas, así como su comportamiento a la corrosión por picaduras. Del mismo modo, se ha estudiado la microestructura de los aceros dependiendo de la atmósfera utilizada en la sinterización

In this work we characterize a new material composite, formed with a polyester and crushed white marble mixture. The final purpose is double: to obtain a material for applications sufficiently competitive after an economic viability study, increasing the yield of the main commodity, using waste marble and improving the jobs in the quarries area. From the results obtained, we deduce then that this material could be used to inside and outside adornment.

Hybrid immunity, resulting from a combination of SARS-CoV-2 infection and vaccination, offers robust protection against COVID-19 in the general population. However, its impact on immunocompromised patients remains unexplored. We investigated the effect of hybrid immunity against the Omicron variant in a population of kidney transplant recipients receiving the fourth dose mRNA monovalent vaccination. By extracting data from the clinical records and performing individual interviews, participants were categorized into the hybrid cohort (previously infected and vaccinated individuals) and the vaccine cohort (vaccinated-only individuals). The study comprised 1114 participants, 442 in the hybrid and 672 in the vaccine cohorts. From April 2022 to August 2023, 286 infections, 38 hospitalizations and 9 deaths were reported. The cumulative incidence of infection was 12.1% (95% confidence interval [CI], 9.03-16.03) for the hybrid cohort and 36.54% (95% CI, 32.81-40.54) for the vaccine cohort after 300 days of follow-up. Hybrid immunity was associated to a 72% lower risk of infection (adjusted hazard ratio, 0.28; 95% CI, 0.21-0.38) and a 96% lower risk of hospitalization (adjusted hazard ratio, 0.04; 95% CI, 0.01-0.32). No deaths occurred in the hybrid cohort. Hybrid immunity was associated with a lower incidence of SARS-CoV-2 infection and severe COVID-19, underscoring its importance for risk stratification in this vulnerable patient population., Competing Interests: Declaration of competing interest The authors of this manuscript have conflicts of interest to disclose as described by the American Journal of Transplantation. J.M. Cruzado is the Associate Editor of the American Journal of Transplantation. Other authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation., (Copyright © 2024 American Society of Transplantation & American Society of Transplant Surgeons. Published by Elsevier Inc. All rights reserved.)

Severe ischemia-reperfusion injury (IRI) causes acute and chronic kidney allograft damage. As therapeutic interventions to reduce damage are limited yet, research on how to promote kidney repair has gained significant interest. To address this question, we performed genome-wide transcriptome and epigenome profiling in progenitor cells isolated from the urine of deceased (severe IRI) and living (mild IRI) donor human kidney transplants and identified LIM homeobox-1 (LHX1) as an epigenetically regulated gene whose expression depends on the IRI severity. Using a mouse model of IRI, we observed a relationship between IRI severity, LHX1 promoter hypermethylation, and LHX1 gene expression. Using functional studies, we confirmed that LHX1 expression is involved in the proliferation of epithelial tubular cells and podocyte differentiation from kidney progenitor cells. Our results provide evidence that severe IRI may reduce intrinsic mechanisms of kidney repair through epigenetic signaling., Competing Interests: Declaration of competing interest The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Aims: The once-daily extended-release tacrolimus formulation (ER-Tac) has demonstrated similar efficacy and safety to the twice-daily immediate-release formulation (IR-Tac), but few population-based pharmacokinetic models have been developed in de novo kidney transplant patients to optimize doses. Therefore, this study aimed i) at developing a population pharmacokinetic model for ER-Tac in de novo adult kidney transplant patients ii) and identifying genetic factors and time-varying covariates predictive of pharmacokinetic variability to guide tacrolimus dosage during the early post-transplant period., Methods: A total of 1,067 blood tacrolimus concentrations from 138 kidney transplant patients were analyzed. A total of 29 out of 138 patients were intensively sampled for 24 h on the day 5 post-transplantation; meanwhile, for the remaining patients, concentrations were collected on days 5, 10, and 15 after transplantation. Tacrolimus daily doses and genetic and demographic characteristics were retrieved from the medical files. Biochemistry time-varying covariates were obtained on different days over the pharmacokinetic (PK) study. A simultaneous PK analysis of all concentrations was carried out using the non-linear mixed-effects approach with NONMEM 7.5., Results: A two-compartment model with linear elimination and delayed absorption best described the tacrolimus pharmacokinetics. Between-patient variability was associated with oral blood clearance (CL/F) and the central compartment distribution volume (Vc/F). Tacrolimus concentrations standardized to a hematocrit value of 45% significantly improved the model ( p < 0.001). This method outperformed the standard covariate modeling of the hematocrit-blood clearance relationship. The effect of the CYP3A5 genotype was statistically ( p < 0.001) and clinically significant on CL/F. The CL/F of patients who were CYP3A5 *1 carriers was 51% higher than that of CYP3A5 *1 non-carriers. Age also influenced CL/F variability ( p < 0.001). Specifically, CL/F declined by 0.0562 units per each increased year from the value estimated in patients who were 60 years and younger., Conclusion: The 36% between-patient variability in CL/F was explained by CYP3A5 genotype, age, and hematocrit. Hematocrit standardization to 45% explained the variability of tacrolimus whole-blood concentrations, and this was of utmost importance in order to better interpret whole-blood tacrolimus concentrations during therapeutic drug monitoring. The dose requirements of CYP3A5 */1 carriers in patients aged 60 years or younger would be highest, while CYP3A5 */1 non-carriers older than 60 years would require the lowest doses., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Fernández-Alarcón, Nolberger, Vidal-Alabró, Rigo-Bonnin, Grinyó, Melilli, Montero, Manonelles, Coloma, Favà, Codina, Cruzado, Colom and Lloberas.)

Post-transplant diabetes mellitus (PTDM) is a frequent complication after kidney transplantation (KT). This systematic review investigated the effect of different immunosuppressive regimens on the risk of PTDM. We performed a systematic literature search in MEDLINE and CENTRAL for randomized controlled trials (RCTs) that included KT recipients with any immunosuppression and reported PTDM outcomes up to 1 October 2023. The analysis included 125 RCTs. We found no differences in PTDM risk within induction therapies. In de novo KT, there was an increased risk of developing PTDM with tacrolimus versus cyclosporin (RR 1.71, 95%CI [1.38-2.11]). No differences were observed between tacrolimus+mammalian target of rapamycin inhibitor (mTORi) and tacrolimus+MMF/MPA, but there was a tendency towards a higher risk of PTDM in the cyclosporin+mTORi group (RR 1.42, 95%CI [0.99-2.04]). Conversion from cyclosporin to an mTORi increased PTDM risk (RR 1.89, 95%CI [1.18-3.03]). De novo belatacept compared with a calcineurin inhibitor resulted in 50% lower risk of PTDM (RR 0.50, 95%CI [0.32-0.79]). Steroid avoidance resulted in 31% lower PTDM risk (RR 0.69, 95%CI [0.57-0.83]), whereas steroid withdrawal resulted in no differences. Immunosuppression should be decided on an individual basis, carefully weighing the risk of future PTDM and rejection., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Parietal epithelial cells (PECs) are kidney progenitor cells with similarities to a bone marrow stem cell niche. In focal segmental glomerulosclerosis (FSGS) PECs become activated and contribute to extracellular matrix deposition. Colony stimulating factor-1 (CSF-1), a hematopoietic growth factor, acts via its specific receptor, CSF-1R, and has been implicated in several glomerular diseases, although its role on PEC activation is unknown. Here, we found that CSF-1R was upregulated in PECs and podocytes in biopsies from patients with FSGS. Through in vitro studies, PECs were found to constitutively express CSF-1R. Incubation with CSF-1 induced CSF-1R upregulation and significant transcriptional regulation of genes involved in pathways associated with PEC activation. Specifically, CSF-1/CSF-1R activated the ERK1/2 signaling pathway and upregulated CD44 in PECs, while both ERK and CSF-1R inhibitors reduced CD44 expression. Functional studies showed that CSF-1 induced PEC proliferation and migration, while reducing the differentiation of PECs into podocytes. These results were validated in the Adriamycin-induced FSGS experimental mouse model. Importantly, treatment with either the CSF-1R-specific inhibitor GW2580 or Ki20227 provided a robust therapeutic effect. Thus, we provide evidence of the role of the CSF-1/CSF-1R pathway in PEC activation in FSGS, paving the way for future clinical studies investigating the therapeutic effect of CSF-1R inhibitors on patients with FSGS., (Copyright © 2024 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Background: Studies analyzing non-antibiotic alternatives in kidney transplant UTI's are lacking. d-Mannose, a simple sugar, inhibits bacterial attachment to the urothelium, as does Proanthocyanidins; both could act as a synergic strategy preventing UTI; nonetheless their efficacy and safety have not been evaluated in kidney transplant population yet., Methods: This is a pilot prospective, double-blind randomized trial. Sixty de novo kidney transplant recipients were randomized (1:1) to receive a prophylactic strategy based on a 24-h prolonged release formulation of d-Mannose plus Proanthocyanidins vs. Proanthocyanidins (PAC) alone. The supplements were taken for the first 3 months after kidney transplant and then followed up for 3 months as well. The main objective of the study was to search if the addition of Mannose to PAC alone reduced the incidence of UTI and/or asymptomatic bacteriuria in the first 6 months post-transplantation., Results: 27% of patients experienced one UTI episode (cystitis or pyelonephritis) while asymptomatic bacteriuria was very common (57%). Incidences according UTI type or AB were: 7% vs. 4% for cystitis episode (p 0.3), 4% vs. 5% for pyelonephritis (p 0.5) and 17% vs. 14% for asymptomatic bacteriuria (p 0.4) for patients in the Mannose+PAC group vs. PAC group respectively. The most frequent bacteria isolated in both groups was Escherichia coli (28% of all episodes), UTI or AB due to E. coli was not different according to study group (30% vs. 23% for Mannose+PAC vs. PAC alone p 0.37)., Conclusions: Non-antibiotic therapy is an unmet need to prevent UTI after kidney transplantation; however, the use of d-Mannose plus PAC does not seem capable to prevent it., (Copyright © 2023 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.)

Background: There is a lack of information regarding which is the best dialysis technique after kidney transplant (KT) failure. The aim of this study is to compare the effect of kidney replacement therapy modality-peritoneal dialysis (TX-PD-TX), haemodialysis (TX-HD-TX) and preemptive deceased donor retransplantation (TX-TX) on patient survival and second KT outcomes., Methods: A retrospective observational study from the Catalan Renal Registry was carried out. We included adult patients with failing of their first KT from 2000 to 2018., Results: Among 2045 patients, 1829 started on HD (89.4%), 168 on PD (8.2%) and 48 (2.4%) received a preemptive KT. Non-inclusion on the KT waiting list and HD were associated with worse patient survival. For patients included on the waiting list, the probability of human leucocyte antigens (HLA) sensitization and to receive a second KT was similar in HD and PD. A total of 776 patients received a second KT (38%), 656 in TX-HD-TX, 72 in TX-PD-TX and 48 in TX-TX groups. Adjusted mortality after second KT was higher in TX-HD-TX patients compared with TX-TX and TX-PD-TX groups, without differences between TX-TX and TX-PD-TX groups. Death-censored second graft survival was similar in all three groups., Conclusions: Our results suggest that after first KT failure, PD is superior to HD in reducing mortality in candidates for a second KT without options for preemptive retransplantation., (© The Author(s) 2022. Published by Oxford University Press on behalf of the ERA.)

Chronic kidney disease (CKD) will become the fifth global cause of death by 2040, thus emphasizing the need to better understand the molecular mechanisms of damage and regeneration in the kidney. CKD predisposes to acute kidney injury (AKI) which, in turn, promotes CKD progression. This implies that CKD or the AKI-to-CKD transition are associated with dysfunctional kidney repair mechanisms. Current therapeutic options slow CKD progression but fail to treat or accelerate recovery from AKI and are unable to promote kidney regeneration. Unraveling the cellular and molecular mechanisms involved in kidney injury and repair, including the failure of this process, may provide novel biomarkers and therapeutic tools. We now review the contribution of different molecular and cellular events to the AKI-to-CKD transition, focusing on the role of macrophages in kidney injury, the different forms of regulated cell death and necroinflammation, cellular senescence and the senescence-associated secretory phenotype (SAPS), polyploidization, and podocyte injury and activation of parietal epithelial cells. Next, we discuss key contributors to repair of kidney injury and opportunities for their therapeutic manipulation, with a focus on resident renal progenitor cells, stem cells and their reparative secretome, certain macrophage subphenotypes within the M2 phenotype and senescent cell clearance.

Outcomes of kidney transplantation (KT) after controlled circulatory death (cDCD) with highly expanded criteria donors (ECD) and recipients have not been thoroughly evaluated. We analyzed in a multicenter cohort of 1161 consecutive KT, granular baseline donor and recipient factors predicting transplant outcomes, selected by bootstrapping and Cox proportional hazards, and were validated in a contemporaneous European KT cohort (n = 1585). 74.3% were DBD and 25.7% cDCD-KT. ECD-KT showed the poorest graft survival rates, irrespective of cDCD or DBD (log-rank < 0.001). Besides standard ECD classification, dialysis vintage, older age, and previous cardiovascular recipient events together with low class-II-HLA match, long cold ischemia time and combining a diabetic donor with a cDCD predicted graft loss (C-Index 0.715, 95% CI 0.675-0.755). External validation showed good prediction accuracy (C-Index 0.697, 95%CI 0.643-0.741). Recipient older age, male gender, dialysis vintage, previous cardiovascular events, and receiving a cDCD independently predicted patient death. Benefit/risk assessment of undergoing KT was compared with concurrent waitlisted candidates, and despite the fact that undergoing KT outperformed remaining waitlisted, remarkably high mortality rates were predicted if KT was undertaken under the worst risk-prediction model. Strategies to increase the donor pool, including cDCD transplants with highly expanded donor and recipient candidates, should be performed with caution., (© 2021 Steunstichting ESOT. Published by John Wiley & Sons Ltd.)

Chronic kidney disease (CKD) is increasing in most countries and kidney transplantation is the best option for those patients requiring renal replacement therapy. Therefore, there is a significant number of patients living with a functioning kidney allograft. However, progressive kidney allograft functional deterioration remains unchanged despite of major advances in the field. After the first post-transplant year, it has been estimated that this chronic allograft damage may cause a 5% graft loss per year. Most studies focused on mechanisms of kidney graft damage, especially on ischemia-reperfusion injury, alloimmunity, nephrotoxicity, infection and disease recurrence. Thus, therapeutic interventions focus on those modifiable factors associated with chronic kidney allograft disease (CKaD). There are strategies to reduce ischemia-reperfusion injury, to improve the immunologic risk stratification and monitoring, to reduce calcineurin-inhibitor exposure and to identify recurrence of primary renal disease early. On the other hand, control of risk factors for chronic disease progression are particularly relevant as kidney transplantation is inherently associated with renal mass reduction. However, despite progress in pathophysiology and interventions, clinical advances in terms of long-term kidney allograft survival have been subtle. New approaches are needed and probably a holistic view can help. Chronic kidney allograft deterioration is probably the consequence of damage from various etiologies but can be attenuated by kidney repair mechanisms. Thus, besides immunological and other mechanisms of damage, the intrinsic repair kidney graft capacity should be considered to generate new hypothesis and potential therapeutic targets. In this review, the critical risk factors that define CKaD will be discussed but also how the renal mechanisms of regeneration could contribute to a change chronic kidney allograft disease paradigm., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Codina, Manonelles, Tormo, Sola and Cruzado.)

Background: Data from the WHO show an increasing rate of overweight and obesity in general population in the last decades. This increase in obesity also affects population with end-stage renal disease (ESRD) and kidney transplant (KT) candidates., Summary: In this review, we focused on how obesity impacts on KT stages: access to KT and outcomes of KT candidates; how to reduce weight and its consequences; short and long-term outcomes in obese recipients and the impact of weight variations; and the implications of obesity in living donor KT. We searched MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials until November 30, 2020. We selected systematic reviews and meta-analyses and randomized clinical trials. When no such reports were found for a topic, observational studies were included in the assessment. Key Messages: Although obesity is a risk factor to present worst outcomes after KT, several studies have demonstrated a survival benefit compared to patients who continue on dialysis. There is a need for a public health campaign to raise awareness in KT candidates and to highlight the importance of self-care, increasing exercise, healthy diet, and weight loss., (© 2021 S. Karger AG, Basel.)

Tertiary hyperparathyroidism is a common cause of hypercalcemia after kidney transplantation (KT) and has been associated with renal dysfunction, bone mineral density loss, and increased risk of fracture and cardiovascular events. In a previous 12-month clinical trial, we demonstrated that subtotal parathyroidectomy was more effective than cinacalcet for controlling hypercalcemia. In the current study, we retrospectively evaluate whether this effect is maintained after 5 years of follow-up. In total, 24 patients had data available at 5 years, 13 in the cinacalcet group and 11 in the parathyroidectomy group. At 5 years, 7 of 11 patients (64%) in the parathyroidectomy group and 6 of 13 patients (46%) in the cinacalcet group (P = .44) showed normocalcemia. However, recurrence of hypercalcemia was only observed in the cinacalcet group (P = .016). Subtotal parathyroidectomy retained a greater reduction in intact parathyroid hormone (iPTH) compared with cinacalcet group. No differences were observed in kidney function and incidence of fragility fractures between both groups. Cinacalcet was discontinued in 5 out of 13 patients. In conclusion, in kidney transplant patients with tertiary hyperparathyroidism recurrence of hypercalcemia after 5-year follow-up is more frequent in cinacalcet than after subtotal parathyroidectomy., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Complications arising from vascular access are major causes of morbidity in patients on renal replacement therapy. They contribute to frustration of health care providers and to high medical cost. To prevent failures in the future it will be helpful to identify the factors that are related to vascular access, malfunction. In a retrospective analysis we analysed the types, duration and primary patency rate of 1,033 permanent vascular access in 544 consecutive patients established during a 13-year period in a tertiary care hospital. Patient characteristics, incidence and risk factors related to vascular access failure were registered. In addition vascular access outcomes in patients who started haemodialysis with a catheter and in whom initial vascular access failure occurred were analysed separately. Forty-five per cent of patients required a central catheter at the start of HD, but 92% of them were being dialysed with an a-v fistula at the last observation. The total number of complications was 0.24 episodes per patient per year at risk, and the rate of thrombosis 0.1. A total of 52% of patients were dialysed throughout the observation period with their initial a-v fistula; 9.3% had more than three episodes of vascular access failure. The radiocephalic a-v fistula was the access with the best median duration, exceeding 7 years, but also the type that had the highest initial failure rate, i.e. 25% of patients and 13% of events. The brachiocephalic a-v fistula was the second most frequent type of vascular access, with a median duration of function of 3.6 years, in contrast the humerobasilar a-v fistula, lasted on average over 5 years. Average patency of the different types of grafts did not exceed 1 year, with the exception of the autologous saphenous graft with a median duration of function of 1.4 years. Patients with glomerulonephritis had the best function rates for their access, the median duration exceeding the duration of the study, whereas in half of diabetic patients it was less than 1 year. The duration of patency of the vascular access was twice as long in patients below age 65 years and in elderly males compared to elderly females. Patients who start HD with a catheter, as well as those with initial vascular access failure, have a higher rate of access failure in the subsequent course on renal replacement therapy. In conclusion, the radiocephalic and the brachiocephalic a-v fistula are the two types of vascular access with the longest duration of function, although a high rate of initial failure is seen with the radiocephalic a-v fistula. Age, female gender, presence of diabetic nephropathy, start of dialysis with a catheter, and failure to wait for initial maturation of vascular access are risk factors, and account for the majority of vascular access failure during renal replacement therapy.

Background: Complications arising from vascular access (VA) are major causes of morbidity in patients on renal replacement therapy (RRT). They contribute to frustration of health care providers and to high medical cost. To prevent failures in the future it will be helpful to identify the factors that are related to VA malfunction., Methods: In a retrospective analysis we analysed the types, duration and primary rate of patency of 1033 permanent vascular accesses in 544 consecutive patients established during a 13-year period in a tertiary care hospital. Patient characteristics, incidence, and risk factors related to VA failure were registered. In addition, VA outcomes in patients who started haemodialysis with a catheter and in whom initial VA failure occurred were analysed separately., Results: Forty-five per cent of patients required a central catheter at the start of HD, but 92% of them were being dialysed with an a-v fistula at the last observation. The total number of complications was 0.24 episodes per patient per year at risk and the rate of thrombosis 0.1. A total of 52% of patients were dialysed throughout the observation period with their initial a-v fistula; 9.3% had more than three episodes of VA failure. The radiocephalic a-v fistula was the VA with the best median duration, exceeding 7 years, but also the type that had the highest initial failure rate, i.e. 25% of patients and 13% of the events. The brachiocephalic a-v fistula was the second most frequent type of VA, with a median duration of function of 3.6 years, in contrast to the humerobasilic a-v fistula, which exceeded 5 years. Average patency of the different types of grafts did not exceed 1 year, with the exception of the autologous saphenous graft with a median duration of function of 1.4 years. Patients with glomerulonephritis had the best function rates for their VA, the median exceeding the duration of the study, whereas in half of the diabetic patients it was less than 1 year. The duration of patency of the VA was twice in patients below age 65 years and in elderly males compared to elderly females. Patients who started HD with a catheter, as well as those with initial VA failure, had a higher rate of VA failure in the subsequent course on RRT., Conclusion: The radiocephalic and the humerobasilic a-v fistulae are the two types of VA with the longest duration of function, although a high rate of initial failure is seen with the radiocephalic a-v fistula. Age, female gender, presence of diabetic nephropathy, start of dialysis with a catheter, and failure to wait for initial maturation of the VA are risk factors, and account for the majority of VA failures during RRT.

We present here the first described case of Nail-patella syndrome (NPS) and pregnancy. Complications occurred during the pregnancy with the onset of preeclampsia at 22 weeks, leading to intrauterine fetal death at 24 weeks. The nephropathy of the NPS began clinically during the course of gestation. Postpartum, it persisted as isolated proteinuria, which became a nephrotic syndrome 18 months later.

The arteriovenous fistula is the vascular access of choice for hemodialysis treatment in patients with chronic renal failure. Clinical occurrence of local circulatory troubles caused by the fistula in addition to arterial robbery or venous hypertension are infrequent but may provoke serious consequences. Two patients with arteriovenous fistula with cutaneous trophic disorders secondary to the venous hypertension syndrome (case 1) and to the arterial robbery syndrome (case 2) are present. Prevalence, pathogenic factors, physiopathology, clinical aspects, and diagnosis and treatment of both syndromes are reviewed. Finally, the difficulty and morbidity of the creation of an efficient arteriovenous fistula in the diabetic patient is underlined.

A review is made of the deaths which occurred in a hemodialysis unit between 1969 and 1977. Sixty-two patients were treated during this period, 18 of whom died. The actuarial percentages of survival are also established. The mortality rate was 15.5 percent during the initial period and 31.5 percent after the fourth year. Deaths in the first monts were caused by cardiac and infectious complications. Those occurring at a later period resulted from the lack of good vascular access which is necessary to maintain a good quality of dialysis.