• acute rejection
• death‐censored graft failure
• deceased donor kidney transplantation
• sex discordance

• Humans
• Male
• Female
• Kidney Transplantation
• Graft Rejection/etiology
• Graft Survival
• Middle Aged
• Tissue Donors
• Risk Factors
• Follow-Up Studies
• Adult
• Sex Factors
• Prognosis
• Retrospective Studies
• Postoperative Complications
• Kidney Failure, Chronic/surgery
• Transplant Recipients/statistics & numerical data
• Glomerular Filtration Rate
• Kidney Function Tests
• Survival Rate

• Graft survival
• Prune Belly Syndrome
• kidney transplantation
• renal replacement therapy

• fecal microbial transplantation
• heart transplantation
• hematopoietic stem cell transplantation
• human microbiota
• kidney transplantation
• liver transplantation
• lung transplantation
• organ transplantation

• Fecal Microbiota Transplantation
• Gastrointestinal Microbiome/physiology
• Hematopoietic Stem Cells
• Humans
• Microbiota
• Organ Transplantation/adverse effects

Inflammation within areas of interstitial fibrosis and tubular atrophy (IF/TA) is associated with kidney allograft failure. The aim of this study was to reveal new diagnostic markers of IF/TA based on bioinformatics analysis.

Raw data of IF/TA samples after kidney transplantation and control samples after kidney transplantation were extracted from the Gene Expression Omnibus (GEO) database (GSE76882 and GSE120495 datasets), and genes that were differentially expressed between the two groups (DEGs) were screened. Gene Set Enrichment Analysis (GSEA), ESTIMATE and single sample GSEA (ssGSEA), least absolute shrinkage and selection operator (LASSO) regression analysis, and competing endogenous RNA (ceRNA) network were used to analyze the data.

The results of GSEA revealed that multiple immune-related pathways were enriched in the IF/TA group, and subsequent immune landscape analysis also showed that the IF/TA group had higher immune and stromal scores and up to 15 types of immune cells occupied them, such as B cells, cytotoxic cells, and T cells. LASSO regression analysis selected 6 (including ANGPTL3, APOH, LTF, FCGR2B, HLA-DQA2, and EGF) out of 14 DE-IRGs as diagnostic genes to construct a diagnostic model. Then, receiver operating characteristic (ROC) curve analysis showed the powerful diagnostic value of the model, and the area under the curve (AUC) of a single diagnostic gene was greater than 0.75. The results of ingenuity pathway analysis (IPA) also indicated that DEGs were involved in the immune system and kidney disease-related pathways. Finally, we found multiple miRNAs that could regulate diagnostic genes from the ceRNA network.

This study identified 6 IF/TA-related genes, which might be used as a new diagnosis model in the clinical practice.

Acute kidney injury (AKI) is caused by renal ischemia/reperfusion injury (IRI) during kidney transplantation. The levels of both circular RNAs (circRNAs) and microRNAs (miRNAs/miR) appear to be critical for AKI detection. While several RNA interactions in AKI have been found, the regulatory mechanisms between the molecules remain to be fully elucidated. In the present study, miRNA expression profiling analysis was conducted using an online dataset to identify the differentially expressed miRNAs in rats with IRI. miR-328-3p was also found to be downregulated in human kidney-2 (HK-2) cells subjected to hypoxia/reperfusion (H/R), and its overexpression targeting pim-1 proto-oncogene (PIM1) resulted in an increased viability and a reduced apoptosis, as well as in the decreased expression of inflammatory factors upon H/R exposure. Putative targets and circRNAs of miR-328-3p were identified using publically available databases. The inhibition of circRNA integrin beta 1 (ITGB1; circITGB1) suppressed the inflammatory response induced by H/R by sponging miR-328-3p in HK-2 cells. Furthermore, a sequence of the functional ITGB1 promoter was studied for transcription factor GATA binding protein 1 (GATA1) binding sites. GATA1 binds to the ITGB1 promoter, leading to the expression of circITGB1. On the whole, the findings of the present study revealed a regulatory pathway modulating miR-328-3p in IRI, demonstrating that the GATA1-mediated regulation of circITGB1 enhanced the H/R-induced inflammatory response via the miR-328-3p/PIM1 axis.

Acute esophageal necrosis (AEN) is defined as a diffused black discoloration of the esophageal mucosa involving mainly the distal part of the esophagus. It is considered a rare clinical entity with a high mortality rate. The etiology of AEN is unknown, but it has been correlated to many causes such as malignancies, infections, and hemodynamics instability. Here, we report a case of a patient developing AEN a few days after kidney transplantation. Case Presentation. A 57-year-old male was admitted electively for kidney transplantation that he received from his son. The surgery was complicated with a significant drop in blood pressure but otherwise was uneventful. The patient was showing good signs of recovery but then suffered from significant hematemesis. An urgent upper esophagogastroduodenoscopy revealed black discoloration of the esophageal mucosa in keeping with AEN. The patient was treated with proton pump inhibitors infusion and started empirically on antivirals and antifungals. The patient's condition improved in regards to the AEN; nonetheless, the complications resulted in graft loss, and the patient returned to hemodialysis.

AEN is a critical condition that mandates early intervention. Identifying high-risk populations may aid in early anticipation and diagnosis. Patients with chronic kidney disease are at risk of atherosclerosis leading to a low flow state which is exacerbated during renal transplantation surgery, especially if the procedure was complicated with a drop in blood pressure.

• renal insufficiency, chronic
• kidney transplantation
• patient care team
• health services research
• graft survival.
• insuficiência renal, crônica
• transplante renal
• equipe de assistência ao paciente
• pesquisa de serviços de saúde
• sobrevivência de enxerto.

• Follow-Up Studies
• Glomerular Filtration Rate
• Humans
• Kidney
• Kidney Transplantation
• Renal Insufficiency, Chronic/complications
• Renal Insufficiency, Chronic/therapy

Post-transplant erythrocytosis (PTE) is defined as persistently elevated hemoglobin > 17 g/dL or hematocrit levels > 51% following kidney transplantation, independent of duration. It is a relatively common complication within 8 months to 24 months post-transplantation, occurring in 8%-15% of kidney transplant recipients. Established PTE risk factors include male gender, normal hemoglobin/hematocrit pre-transplant (suggestive of robust native kidney erythropoietin production), renal artery stenosis, patients with a well-functioning graft, and dialysis before transplantation. Many factors play a role in the development of PTE, however, underlying endogenous erythropoietin secretion pre-and post-transplant is significant. Other contributory factors include the renin-angiotensin- aldosterone system, insulin-like growth factors, endogenous androgens, and local renal hypoxia. Most patients with PTE experience mild symptoms like malaise, headache, fatigue, and dizziness. While prior investigations showed an increased risk of thromboembolic events, more recent evidence tells a different story-that PTE perhaps has lessened risk of thromboembolic events or negative graft outcomes than previously thought. In the evaluation of PTE, it is important to exclude other causes of erythrocytosis including malignancy before treatment. Angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs) are the mainstays of treatment. Increased ACE-I/ARB use has likely contributed to the falling incidence of erythrocytosis. In this review article, we summarize the current literature in the field of post-transplant erythrocytosis after kidney transplantation.

• Post-transplant erythrocytosis
• Kidney transplantation
• Epidemiology
• Treatment
• Guidelines
• Outcomes

Patients with chronic kidney disease (CKD) are at a high risk for cardiovascular disease (CVD), and approximately half of all deaths among patients with CKD are a direct result of CVD. The premature cardiovascular disease extends from mild to moderate CKD stages, and the severity of CVD and the risk of death increase with a decline in kidney function. Successful kidney transplantation significantly decreases the risk of death relative to long-term dialysis treatment; nevertheless, the prevalence of CVD remains high and is responsible for approximately 20-35% of mortality in renal transplant recipients. The prevalence of traditional and nontraditional risk factors for CVD is higher in patients with CKD and transplant recipients compared with the general population; however, it can only partly explain the highly increased cardiovascular burden in CKD patients. Nontraditional risk factors, unique to CKD patients, include proteinuria, disturbed calcium, and phosphate metabolism, anemia, fluid overload, and accumulation of uremic toxins. This accumulation of uremic toxins is associated with systemic alterations including inflammation and oxidative stress which are considered crucial in CKD progression and CKD-related CVD. Kidney transplantation can mitigate the impact of some of these nontraditional factors, but they typically persist to some degree following transplantation. Taking into consideration the scarcity of data on uremic waste products, oxidative stress, and their relation to atherosclerosis in renal transplantation, in the review, we discussed the impact of uremic toxins on vascular dysfunction in CKD patients and kidney transplant recipients. Special attention was paid to the role of native and transplanted kidney function.

Clinical application of biomarkers is an integral component of transplant care. Clinicians and scientists alike are in search of better biomarkers than the current serologic (serum creatinine, donor-specific antibodies), urine-derived (urinalysis, urine protein), and histologic ones we now use. The science behind recent biomarker discovery spans across multiple molecular biologic disciplines, including transcriptomics, proteomics, and metabolomics. Innovative methodology and integration of basic and clinical approaches have allowed researchers to unearth molecular phenomena preceding clinical disease. Biomarkers can be classified in several ways. In this review, we have classified them via their origin and outcome: Primarily immunologic, i.e., representative of immune regulation and dysfunction and non-immunologic, pertaining to delayed graft function, cardiovascular events/mortality, infection, malignancy, post-transplant diabetes, graft, and patient survival. Novel biomarker uses to guide the diagnosis and management of transplant-related outcomes is a promising area of research. However, the use of biomarkers to predict outcomes after kidney transplantation is not well studied. In this review, we summarize the recent studies illustrating biomarker use and transplant outcomes.

• Biomarkers
• Kidney Transplantation
• Rejection
• Infection
• Mortality
• Graft survival

Organ transplantation is undergoing profound changes. Contraindications for donation have been revised in order to better meet the organ demand. The use of lower-quality organs and organs with greater preoperative damage, including those from donation after cardiac death (DCD), has become an established routine but increases the risk of graft malfunction. This risk is further aggravated by ischemia and reperfusion injury (IRI) in the process of transplantation. These circumstances demand a preservation technology that ameliorates IRI and allows for assessment of viability and function prior to transplantation. Oxygenated hypothermic and normothermic machine perfusion (MP) have emerged as valid novel modalities for advanced organ preservation and conditioning. Ex vivo prolonged lung preservation has resulted in successful transplantation of high-risk donor lungs. Normothermic MP of hearts and livers has displayed safe (heart) and superior (liver) preservation in randomized controlled trials (RCT). Normothermic kidney preservation for 24 h was recently established. Early clinical outcomes beyond the market entry trials indicate bioenergetics reconditioning, improved preservation of structures subject to IRI, and significant prolongation of the preservation time. The monitoring of perfusion parameters, the biochemical investigation of preservation fluids, and the assessment of tissue viability and bioenergetics function now offer a comprehensive assessment of organ quality and function ex situ. Gene and protein expression profiling, investigation of passenger leukocytes, and advanced imaging may further enhance the understanding of the condition of an organ during MP. In addition, MP offers a platform for organ reconditioning and regeneration and hence catalyzes the clinical realization of tissue engineering. Organ modification may include immunological modification and the generation of chimeric organs. While these ideas are not conceptually new, MP now offers a platform for clinical realization. Defatting of steatotic livers, modulation of inflammation during preservation in lungs, vasodilatation of livers, and hepatitis C elimination have been successfully demonstrated in experimental and clinical trials. Targeted treatment of lesions and surgical treatment or graft modification have been attempted. In this review, we address the current state of MP and advanced organ monitoring and speculate about logical future steps and how this evolution of a novel technology can result in a medial revolution.

• expanded criteria donor
• graft
• immunogenecity
• immunomodulation
• machine perfusion
• marginal
• reconditioning
• transplantation

Hydrogen sulfide (H₂S), produced from metabolism of dietary sulfur‐containing amino acids, is allegedly a renoprotective compound. Twenty‐four‐hour urinary sulfate excretion (USE) may reflect H₂S bioavailability. We aimed to investigate the association of USE with graft failure in a large prospective cohort of renal transplant recipients (RTR). We included 704 stable RTR, recruited at least 1 year after transplantation. We applied log‐rank testing and Cox regression analyses to study association of USE, measured from baseline 24 h urine samples, with graft failure. Median age was 55 [45–63] years (57% male, eGFR was 45 ± 19 ml/min/1.73 m²). Median USE was 17.1 [13.1–21.1] mmol/24 h. Over median follow‐up of 5.3 [4.5–6.0] years, 84 RTR experienced graft failure. RTR in the lowest sex‐specific tertile of USE experienced a higher rate of graft failure during follow‐up than RTR in the middle and highest sex‐specific tertiles (18%, 13%, and 5%, respectively, log‐rank P < 0.001). In Cox regression analyses, USE was inversely associated with graft failure [HR per 10 mmol/24 h: 0.37 (0.24–0.55), P < 0.001]. The association remained independent of adjustment for potential confounders, including age, sex, eGFR, proteinuria, time between transplantation and baseline, BMI, smoking, and high sensitivity C‐reactive protein [HR per 10 mmol/24 h: 0.51 (0.31–0.82), P = 0.01]. In conclusion, this study demonstrates a significant inverse association of USE with graft failure in RTR, suggesting high H₂S bioavailability as a novel, potentially modifiable factor for prevention of graft failure in RTR.

• chronic graft failure
• hydrogen sulfide
• protein intake
• renal transplantation

• clinical research/practice
• immunosuppressant -fusion proteins and monoclonal antibodies
• immunosuppressant-antiproliferative agent: mycophenolate mofetil
• immunosuppressant-calcineurin inhibitor: tacrolimus
• immunosuppression/immune modulation
• kidney transplantation/nephrology
• kidney transplantation: living donor
• translational research/science

• Acute rejection
• Graft failure
• Interstitial fibrosis and tubular atrophy
• Kidney biopsy
• Transplant glomerulopathy

• K23 DK122136 NIDDK NIH HHS

• chronic kidney disease
• kidney transplant
• multidisciplinary
• progression
• risk factors

• Bariatric surgery
• Graft survival
• Kidney transplantation
• Morbid obesity

• Cardiovascular disease
• Complications
• Infections
• Kidney transplant
• Malignancy
• Survival

• Adult
• Aged
• Donor Selection/methods
• Donor Selection/standards
• Female
• Glomerular Filtration Rate
• Graft Survival
• Humans
• Kidney
• Kidney Transplantation/methods
• Kidney Transplantation/mortality
• Male
• Middle Aged
• Retrospective Studies
• Survival Rate
• Tissue Donors/supply & distribution
• Treatment Outcome

• RNA-Seq
• high-fat diet
• obesity-related kidney disease
• sex differences

• Balance control
• Dual task
• Kidney
• Postural control
• Transplantation

• CKD
• CKD-T
• ESRD
• Kidney transplant

• stress, psychological
• adaptation, psychological
• medication adherence
• patient compliance
• kidney transplantation
• estresse psicológico
• adaptação psicológica
• adesão à medicação
• cooperação do paciente
• transplante de rim

• Adaptation, Psychological
• Adult
• Behavior Rating Scale
• Cross-Sectional Studies
• Educational Status
• Female
• Humans
• Immunosuppressive Agents/therapeutic use
• Kidney Transplantation/psychology
• Logistic Models
• Male
• Medication Adherence/psychology
• Medication Adherence/statistics & numerical data
• Middle Aged
• Palliative Care/psychology
• Self Report
• Statistics, Nonparametric
• Stress, Psychological
• Treatment Refusal/psychology