Introduction: Transplant renal artery stenosis (TRAS) is the most common vascular complication following kidney transplantation. Deceased donor kidneys exhibiting severe atherosclerosis involving the renal artery, if untreated, represent one cause of TRAS.

Methods: We report herein two cases of TRAS that occurred following back bench ex vivo eversion endarterectomy (EE) prior to deceased donor kidney transplantation (DDKT).

Results: Both patients presented in the first year following DDKT with worsening hypertension and one patient experienced acute kidney injury. Duplex ultrasonography was suspicious for markedly elevated renal artery velocities in the proximal to mid-renal artery segment with evidence for distal turbulence. Subsequent arteriography through an ipsilateral femoral approach confirmed severe TRAS that was successfully treated with balloon angioplasty and stenting. Both patients experienced improvements in blood pressure control, and one patient had resolution of acute kidney injury.

Conclusion: Ex vivo EE may be performed successfully as a rescue procedure to prevent nonuse of donor kidneys with severe intrinsic atherosclerosis. However, these patients may still be at risk for developing TRAS, possibly from a localized dissection occurring secondary to an intimal flap.

Historically, the presence of stones in a donor kidney has been a contraindication to kidney use for transplantation. However, favorable experiences transplanting living donor kidneys with isolated stones as well as successful management of de novo stone formation following living or deceased donor kidney transplantation have provided insights regarding the benefits and risks of this strategy. The limited supply of available donor kidneys has led to a reexamination of donor selection criteria to meet demand. This reevaluation is also influenced by medical advancements that have allowed for the safe management of allograft kidney stones without compromising outcomes. Herein we report the accidental transplantation of a kidney with a large pre-existing calculus from an otherwise acceptable deceased donor. Based on literature review and given the benefits of kidney transplantation versus dialysis in the setting of prolonged waiting times, expansion of the donor pool to include kidneys with large or multiple stones may be a feasible option to improve utilization and access without necessarily compromising subsequent outcomes.

Background: Proteinuria occurs commonly in transplant recipients treated with mechanistic target of rapamycin inhibitor (mTORi); although cause is unclear. Different mechanisms have been proposed such as podocyte injury due to the inhibitory effects of sirolimus on glomerular VEGF protein synthesis. Here, we describe a case of new-onset nephrotic range proteinuria and subsequent development of collapsing focal segmental glomerulosclerosis that occurred after conversion from tacrolimus to mTORi in a kidney transplant recipient in the setting of treating resistant CMV viremia.

Presentation: A 64-year-old woman with autosomal dominant polycystic liver and kidney disease underwent a second deceased-donor kidney transplant (November 2023). She was CMV high-risk (D+/R–) and initially demonstrated excellent allograft function. Six-months post-transplant, she developed severe CMV-viremia refractory to valganciclovir, requiring sequential therapy with ganciclovir, foscarnet, maribavir, letermovir, and adjunctive CMV immune globulin. Immunosuppression was reduced, including discontinuation of mycophenolate and conversion from tacrolimus to sirolimus. reduction in proteinuria. Two months after initiating sirolimus, she abruptly developed nephrotic-range proteinuria (19 g/day) and a rapid increase in serum creatinine from baseline of 1.2 to 2.9 mg/dL. Renal transplant biopsy showed changes consistent with focal segmental glomerulosclerosis with features of collapsing glomerulopathy, and CMV immunostaining was negative. Sirolimus was discontinued and tacrolimus reintroduced, resulting in partial recovery of renal function and significant

Discussion: This case highlights sirolimus-associated collapsing FSGS as an important and potentially reversible cause of severe proteinuria in kidney transplant recipients. The clinical course underscores the need for careful monitoring of proteinuria following mTORi initiation.

Organ transplantation remains the definitive therapy for end-stage organ failure, yet long-term graft survival depends on precise and timely detection of injury. Conventional markers such as serum creatinine and histology identify damage only after functional decline. In contrast, emerging molecular and functional biomarkers—spanning mRNA and microRNA signatures, exosomal vesicles, donor-derived cell-free DNA (dd-cfDNA), HLA and non-HLA antibody repertoires, proteomic, and metabolic profiles—are reshaping transplant surveillance through earlier and more specific insights into graft health. This review integrates data from over 200 recent studies on diagnostic biomarkers across kidney, liver, heart, and lung transplantation. A list of 30 important references is listed in Table 1. The analysis emphasizes cross-organ trends in multi-omics integration, spatial and single-cell profiling, and AI-enabled analytics that collectively predict graft dysfunction with increasing accuracy and reproducibility. Transplant diagnostics is transitioning from single analyte testing to integrated, predictive, and personalized biomarker ecosystems. The convergence of multi-omics assays, machine-learning algorithms, and regulatory standardization is driving this evolution toward pre-informed long-term graft survival strategies. While broad clinical adoption requires further multicenter validation, the next decade will likely see these molecular diagnostics redefine how transplant injury is detected, interpreted, and prevented.

The limited supply of available donor kidneys has led to a reexamination of donor selection criteria to meet demand. This reevaluation is also influenced by medical advancements that have allowed for the prompt identification and safe management of donor-transmitted infections without compromising outcomes. Historically, the presence of aspergillosis in a deceased donor has been a contraindication to kidney use in transplantation. However, isolated favorable reports, coupled with successful management of de novo aspergillosis following kidney transplantation, have provided insights regarding the benefits and risks of this strategy. Herein, we report the successful transplantation of a kidney donated after circulatory death from a donor with chronic cavitary pulmonary aspergillosis. Based on literature review and given the benefits of kidney transplantation versus dialysis in the setting of prolonged waiting times, expansion of the donor pool to include kidneys from donors being actively treated for opportunistic infections may be an alternative option to increase utilization and access.

Introduction: The study purpose was to analyze in consecutive periods our nearly 19-year experience in simultaneous pancreas-kidney transplantation (SPKT) with an emphasis on changes in practice that improved outcomes in the most recent era.

Methods: Single center retrospective cohort study of all SPKTs performed in two sequential eras: Era 1 (E1): 11/1/2001 – 12/31/2010; Era 2 (E2) 1/1/2011 - 8/12/20). Immunosuppression and management protocols were standardized in both eras.

Results: 255 consecutive SPKTs were analyzed (E1, n=126; E2, n=129). By design, E2 patients received organs from younger donors (mean E1 28.1 vs. E2 23.7 years) with shorter pancreas cold ischemia times (CITs, mean E1 16.8 vs. E2 13.4 hours, both p<0.05). In addition, donors with either hypertension or cerebrovascular cause of death were more common in E1 compared to E2 (both p<0.05). More E2 patients received alemtuzumab induction (52.4% E1 vs 97.7% E2, p<0.0001). One-year pancreas graft survival rates (PGSRs, 84.9% Era 1 versus 94.6% Era 2, p=0.02) and four-year PGSRs (70.6% E1 versus 85.5% E2, p=0.002) were significantly higher in E2 and by Kaplan-Meier analysis. In univariate analysis, alemtuzumab induction and E2 were associated with superior and longer pancreas CIT with inferior death-censored PGSRs. Only alemtuzumab induction had a significant (protective) effect on censored PGSR in the multivariate model.

Conclusions: In our experience, optimizing donor quality (younger donors without hypertension or cerebrovascular cause of death), minimizing pancreas CIT, and use of alemtuzumab induction are associated with improved outcomes following SPKT.

Abbreviations

BMI: Body Mass Index; CIT: Cold Ischemia Time; CMV: Cytomegalovirus; DWFG: Death with a Functioning Graft; GSR: Graft Survival Rate; HR: Hazard Ratio; P-E: Portal-Enteric; PTx: Pancreas Transplant; RATG: Rabbit Anti-Thymocyte Globulin; S-E: Systemic-Enteric; SPKT: Simultaneous Pancreas-Kidney Transplant; US: United States

Radiation nephropathy is the damage to the renal parenchyma and blood vessels caused by ionizing radiation, and its mechanism of injury involves oxidative stress, DNA damage, cellular senescence, and other processes, among which oxidative stress plays an obvious role. In the case of excessive accumulation of oxidative stress products, it can lead to lipid peroxidation and iron distribution abnormalities caused by ferroptosis; the latter is involved in a variety of pathophysiological processes, while currently there is no role in radiation nephropathy. The present study sought to investigate the role of ferroptosis in radiation nephropathy, and the mechanism of FG-4592 in relieviating radiation nephropathy, C57BL/6 mice and TCMK-1 cell are separately irradiated with 12GY, 10GY X-ray to construct radiation nephropathy models in vivo and in vitro. Compared with the control group, X-rays promoted the occurrence of lipid peroxidation and ferroptosis, and oxidative stress and lipid peroxidation products were increased and antioxidant products were decreased in the X-rays-induced radionephropathy model; intervention in ferroptosis could alleviate radiation nephropathy, and FG-4592 could regulate lipid metabolism and oxidative reactions to ameliorate feroptosis and attenuate kidney injury through the modulation of HIF activity. In conclusion, in this study, transcriptome analysis was utilized to screen out the pathways involved in the regulation of radiation nephropathy, which provided the basis for the subsequent study of drug intervention in radioactive kidney injury. And FG-4592 had a certain anti-radiation effect in this experiment, which had a protective effect in radiation nephropathy. This study provides new ideas for the development of novel low toxicity, effective radiation-resistant agents.

Introduction : This study aimed to explore the changes in ferroptosis markers and their relationship with fundus lesion severity in chronic kidney disease (CKD).

Methods : We enrolled 118 CKD patients and collected clinical, renal function, fundus imaging data, and ferroptosis markers. We performed correlation and regression analyses between renal dysfunction and fundus lesions, and assessed the changes and mediating roles of serum iron (Fe), malondialdehyde (MDA), and reduced glutathione (GSH) in CKD deterioration and retinal damage.

Results : Levels of Fe, MDA, and GSH showed significant differences across CKD stages (P<0.001). Logistic regression identified sex, mean arterial pressure, total cholesterol, hemoglobin, ferritin, Fe, MDA, and GSH as significant factors in CKD-related fundus lesions (P<0.05). MDA (β=0.15, 95%CI: 0.03–0.26) and GSH (β=0.33, 95%CI: 0.16–0.54) significantly mediated the link between renal decline and retinal damage (P≤0.001).

Conclusions : Early fundus screening is clinically valuable for managing CKD progression. Fundus damage severity in CKD closely tracks renal decline, with ferroptosis likely playing a key role. MDA and GSH are promising biomarkers for early detection and intervention in CKD-related retinal pathology.

Diuretics are established fall-risk increasing drugs. However, not all diuretics users experience fall incidents. Due to interindividual
heterogeneity in older populations, it is difficult to identify which older adults are at highest risk of medication-related falls. Therefore, we assessed if diuretic plasma concentrations are associated with fall risk in users. We analyzed plasma samples of 307 hydrochlorothiazide and 110 furosemide users from a cohort of older community-dwelling adults. Cox proportional hazard and logistic regression models were used to analyze associations between diuretic concentration at baseline, changes over time and fall risk. There was no significant association between fall risk and plasma concentration of either hydrochlorothiazide or furosemide at baseline. Nor was a change in concentration over time associated with fall risk. Thus, diuretic plasma concentration is not associated with fall risk in older communitydwelling adults.