Acevedocorcoran4682

ransplant recipients in our center. There was a significant association between severity of acute kidney injury and 3-month and in-hospital mortality.Ogilvie syndrome (acute colonic pseudo-obstruction) is a rare, acquired, life-threatening disorder for which treatment plans vary from simple observation to surgical intervention. Ogilvie syndrome has been reported in patients after renal or liver transplant, but its occurrence after simultaneous pancreas-kidney transplant is rare. Herein, we present the case of a 45-year-old female recipient of a deceased donor simultaneous pancreas-kidney transplant who developed Ogilvie syndrome 10 days after a previous fecal ileus that had resolved at posttransplant week 3. She demonstrated Ogilvie syndrome with obstructive colitis features (severe abdominal pain and high-grade fever), which we immediately treated with colonic decompensation by placement of a transanal ileus tube. After several screening examinations and discontinuation of unnecessary medicines, we were not able to confirm the cause of Ogilvie syndrome in our patient. After 2 weeks, the patient remained unresponsive to the conservative treatment, and so hand-assisted laparoscopic subtotal colectomy was performed to remove the dilated colon. Her symptoms gradually resolved after surgery. Histologically, we confirmed submucosal fibrotic changes, especially at the distal end of the resected colon, without evidence of amyloidosis, and the number of Auerbach plexus ganglia had decreased. Nevertheless, we observed no degenerated appearance of ganglion cells in the Auerbach plexus or the Meissner plexus. After exclusion of several collagen diseases, including systemic sclerosis, we determined that idiopathic colonic fibrosis was the likely cause of Ogilvie syndrome in our patient. When surgery is indicated in transplant patients with Ogilvie syndrome with obstructive colitis features, colectomy should be considered.Infection caused by Leishmania species has been increasingly reported in solid-organ transplant recipients since the first case report in 1979. Visceral leishmaniasis is endemic in central and eastern regions of India. Clinical features may simulate a variety of other infections, and a high index of suspicion is required for the diagnosis. Early diagnosis of this endemic infection is likely to result in improved outcome. We describe an unusual presentation of leishmaniasis in a kidney allograft recipient with organomegaly and pancytopenia sans fever detected by isolation of amastigotes in duodenal biopsy. To the best of our knowledge, this is the first case report of this kind in a kidney transplant recipient.

Graft-versus-host disease is still one of the most important complications after hematopoietic stem cell transplantation. The risk factors remain unclear, with effects of graft-versus-host disease on survival varying among different centers. We aimed to determine risk factors that may affect development of graft-versus-host disease and the corresponding patient survival rates at a single pediatric hematopoietic stem cell transplant unit.

Our study included 104 of 118 pediatric patients who underwent allogeneic hematopoietic stem cell transplant at our institute between 2005 and 2018. Patient characteristics, clinical information, pretransplant and posttransplant factors, and laboratory parameters were obtained from the database.

Acute graft-versus-host disease was seen in 19 pediatric patients. Chronic graft-versus-host disease, which was seen in 13 of our pediatric study patients, occurred more often in those with peripheral blood stem cell than in those with bone marrow transplant (odds ratio of 9.969ere are some known risk factors for graft-versus-host disease in adult patients, little is known about risk factors in children. In our comprehensive study in pediatric patients, we found that peripheral blood stem cell transplant, female-tomale transplant, and later neutrophil engraftment were associated with incidence of graft-versus-host disease. Although peripheral blood as a source of stem cells and female-to-male transplant are known risk factors, later neutrophil engraftment was a new finding as a possible risk factor for acute graft-versushost disease. This finding requires further verification in future prospective studies.Renal transplant is the treatment of choice for endstage renal failure. Since the first successful kidney transplant in 1954, advances in immunosuppression, surgical techniques, and posttransplant medical care have drastically improved the outcomes of this procedure. Despite these advances, surgical complications after renal transplant remain a challenge that can result in serious morbidity, graft loss, and recipient mortality. A significant proportion of surgical complications will have a vascular origin. Some of these vascular complications can cause irreversible damage to the transplanted kidney unless they are identified and treated urgently. In this review, common vascular complications of renal transplant are discussed, with emphasis on their mode of presentation, diagnosis, current management, and outcomes. Such knowledge can be useful for transplant clinicians, for prompt diagnosis and appropriate management of these complications.

Adiponectin has an important role in obesity, insulin resistance, and cardiovascular disease. We investigated the association between serum adiponectin levels and endothelial function in kidney transplant patients.

Fasting blood samples were obtained from 70 kidney transplant patients. The vascular reactivity index was measured with a digital thermal monitoring test. Serum adiponectin levels were measured with a commercially available enzyme immunoassay kit. A vascular reactivity index <1.0 was defined as poor, 1.0 or greater but less than 2.0 was intermediate, and 2.0 or greater was good.

The results showed that 10 kidney transplant patients (13.3%) were categorized with a vascular reactivity index of poor, 25 (35.7%) were intermediate, and 35 (50%) were good. Increased waist circumference (P = .037), increased serum alkaline phosphatase (P = .026), and lower serum adiponectin (P = .001) were associated with poor vascular reactivity index. Advanced age (r = -0.300; P = .012), waist circumference (r = -0.372; P = .002), serum alkaline phosphatase (r = -0.323; P = .006), and logarithmically transformed serum triglycerides (r = -0.317; P = .007) were negatively correlated with the vascular reactivity index, whereas serum adiponectin (r = 0.332; P = .005) was positively correlated with the vascular reactivity index. Multi variable forward stepwise linear regression analysis showed that waist circumference, serum alkaline phosphatase, and serum adiponectin were significantly and independently associated with the vascular reactivity index.

Fasting serum adiponectin levels were positively associated with the vascular reactivity index and negatively associated with endothelial function in kidney transplant patients.

Fasting serum adiponectin levels were positively associated with the vascular reactivity index and negatively associated with endothelial function in kidney transplant patients.

We investigated the safety of donor nephrectomy from older adult donors (age ≥60 years), as well as long-term donor, recipient, and graft outcomes.

We retrospectively analyzed data from 307 living donor kidney transplants from 1996 to 2016 and defined 2 cohorts based on donor age. Cohort A comprised donors aged 60 years and older, and cohort B comprised donors from 18 to 59 years old. We recorded donor and recipient perioperative complications, outcomes, and survival rates and used SPSS and MedCalc statistical software programs for data analyses.

The mean follow-up period for donor-recipient pairs in cohort A was 97 months (SD, 25.1 months) with median 108 months (IQR, 92-108 months) and in cohort B was 100.57 months (SD, 25.45 months) with median 120 months (IQR, 84-120 months). Mean donor age in cohort A was 64.13 years (SD, 3.78 years) with median 63 years (IQR, 61-66.5 years) and in cohort B was 41.08 years (SD, 9.15 years) with median 41 years (IQR, 34.5-48 years) (P < .001, cohort A vs B). Mean recipient age in cohort A was 47.65 years (SD, 14.26 years) with median 48.5 years (IQR, 35.5-61 years) and in cohort B was 43.55 years (SD, 13.15 years) with median 40.5 years (IQR, 33.5-54 years) (P < .001, cohort A vs B). Both cohorts showed no significant differences in perioperative donor and recipient complications. Renal function (measured as estimated glomerular filtration rate) in remaining native kidneys of cohort A showed no significant decline during median 8-year follow-up (P = .089 and P < .414, respectively). There were no significant differences in survival rates for donors, recipients, and grafts.

Living donor kidney transplant from older adult donors is safe and effective with good long-term patient and allograft survival.

Living donor kidney transplant from older adult donors is safe and effective with good long-term patient and allograft survival.Myocardial ischemia/reperfusion injury (MIRI) is the major cause of myocardial cell damage in acute myocardial infarction, and its treatment remains a clinical challenge. Ginsenoside Rb1 showed protective effects on the cardiovascular system; however, the underlying mechanism remains largely unclear. Effects of Ginsenoside Rb1 on rat MIRI-induced myocardial infarct size were evaluated through TTC staining. TUNEL assay and flow cytometry analysis were employed to estimate cell apoptosis. Apoptosis, autophagy and PI3K/Akt/mTOR pathway-related proteins were estimated via western blot. ASN007 in vitro Expression of Beclin1 in myocardial tissues were examined by immunohistochemical analysis. Expression levels of IL-1[Formula see text], TNF-[Formula see text] and IL-6 were tested by enzyme-linked immunosorbent assay (ELISA). Here, we found that Ginsenoside Rb1 treatment not only alleviated MIRI in rats but also protected H9C2 cells against hypoxia/reoxygenation induced damage. Ginsenoside Rb1 abolished the MIRI-induced activation of autophagy. Meanwhile, we found that treatment of 3-MA (autophagy inhibitor) could enhance the protective effects of Ginsenoside Rb1 on H9C2 cells during H/R. Moreover, Ginsenoside Rb1 treatment resulted in the activation of the PI3K/Akt/mTOR pathway, and treatment of LY294002 (PI3K/Akt pathway repressor) abolished the protective effects of Ginsenoside Rb1 on myocardial in vitro and in vivo. Our results suggest that Ginsenoside Rb1 functions as a protector against MIRI by repressing cardiomyocyte autophagy through the PI3K/Akt/mTOR signaling pathway.

Children's visits to the ICU are still restricted, and more focus on the child's own needs and experiences are needed. The aim of this study is to illustrate the meaning of being a visiting child of a seriously ill parent receiving care at the ICU.

A qualitative descriptive design was used, with open-ended interviews with seven children (6-18years) performed and analysed using a phenomenological research approach.

Being a visiting child of a seriously ill parent receiving care at the ICU is described as a life situation taking place in an unfamiliar environment, characterized by a heartfelt, genuine desire to be there, in an interdependence entailing offering a loved one the help they need while at the same time being seen in a compassionate way and being able to share, revealing a sudden awakening of an inner truth of reality and a sense of a healing wisdom of understanding.

The children felt good when they visited their ill parent, but at the same time not fully involved, and desired a more compassionate, caring approach by the nurses.