Introduction: Pregnancy post allo-islet transplant (IT) is generally discouraged due to presumed risks to mother, fetus and graft. There are 4 published cases of childbirth in allo-IT recipients, all of which required insulin during pregnancy or within 2 years (y) post-partum (PP). Here we report the first known case of long-term, uninterrupted insulin independence post allo-IT and childbirth. Method: A 35 y/o Caucasian female with T1D since age 18y, complicated by hypoglycemia and diabetic eye disease (DED), received 3 ITs. Pre-IT, C-peptide was undetectable and daily insulin use was 41 units/d (0.62 units/kg/d) with A1c of 7.3%. Islets were infused intraportally (total islet dose: 849,265 IEQ; 12,751 IEQ/kg). Immunosuppression consisted of basiliximab/daclizumab, etanercept, tacrolimus (TAC) and sirolimus (SIRO), with intermittent MMF. Patient (pt) became insulin free. At Y5, A1c was 5.7% and stimulated c-peptide of 5.59 ng/ml. At age 41y (6y post-IT), pt conceived with ovarian stimulation. Pre-conception, SIRO was discontinued and TAC was increased. Azathioprine (AZA) was added during the 1st trimester. OGTT and immune studies were performed at 7, 15 and 25 wks of gestation and 24 wks PP. This report summarizes observations through 13.5y post-IT and 7y PP. Results: Throughout pregnancy, 1st morning BG was 99±14 mg/dl and A1c was maintained between 5.1-5.3% without insulin. Glyburide was started at 20 wks to achieve target fasting BG<105 mg/dl. At 15 and 25 wks, plasma glucose (PG) 2-hrs post 75g OGTT was 149 and 138 mg/dl, with peak C-peptide responses of 12.5 and 8.85 ng/ml; respectively. Blood pressure, renal function and DED were stable. At 36 wks, pt vaginally delivered a healthy 6.0lb baby girl without complication. The infant received 3 days of UV light therapy for hyperbilirubinemia, but was otherwise in good health. At 24 wks PP (7y post-IT), pt remained off insulin with A1c of 5.5% and normal OGTT response (2-hr PG=149 mg/dl; peak C-peptide=8.46 ng/ml). Glyburide was discontinued 6-mo PP due to hypoglycemia. In the years PP, pt has maintained uninterrupted insulin independence and A1c < 6.5%. Mildly elevated FBG were observed starting ~1y PP (113-133 mg/dl) and prompted resuming oral diabetes medication. Between Y9.5-10 post-IT, AZA was discontinued and low dose SIRO re-started. At Y13.5 post-IT, immunosuppression includes low dose SIRO (< 2.0 ng/ml) and TAC (3.7 ng/ml). Pt remains off insulin and on metformin and linagliptin with an A1c of 6.1% and no hypoglycemia. Pre-existing DED continues with slow, progressive loss of vision in the left eye. Per pt, the child, now almost 7y, is in good health. Conclusion: This is the 1st reported case of uninterrupted, long-term insulin independence for 13.5y post-IT and 7y PP with only oral DM medication support. While pregnancy in T1D and immunosuppression remains high risk, this suggests that successful childbirth post-IT can be safely achieved without significantly compromising graft function. NIH Grant U42R16607 (Southern California Islet Cell Resources Center). NIH Grant M01 RR-43 (General Clinical Research Center). Beckman Research Institute of the City of Hope. References: 1. Schive SW, Scholz H, Sahraoui A, Kloster-Jensen K, Hafsahl G, Korsgren O, Foss A, Jenssen TG. Graft function 1 year after pregnancy in an islet-transplanted patient. Transpl Int. 2015 Oct;28(10):1235-9. doi: 10.1111/tri.12596. Epub 2015 May 11. PMID: 25903157. 2. Assalino M, Podetta M, Demuylder-Mischler S, Francini K, Pernin N, Randin JP, Bosco D, Andres A, Berney T. Successful pregnancy and delivery after simultaneous islet-kidney transplantation. Am J Transplant. 2018 Aug;18(8):2075-2078. doi: 10.1111/ajt.14884. Epub 2018 May 10. PMID: 29673064. 3. Rickels MR, Markmann E, Naji A. Successful pregnancies after islet transplantation for type 1 diabetes. Am J Transplant. 2019 Jan;19(1):298-299. doi: 10.1111/ajt.14972. Epub 2018 Jul 13. PMID: 29920931; PMCID: PMC6364294. 4. Birrell K, Ali M, Shaw J, MacDougall M, Williams S, Napier C. Pregnancy following islet cell transplantation in a woman with type 1 diabetes and autoimmune Addison’s disease. Endocrine Abstracts (2022) 86 P221. doi: 10.1530/endoabs.86.P221

Background.A large number of procured kidneys continue not to be transplanted, while the waiting list remains high. Methods.We analyzed donor characteristics for unutilized kidneys in our large organ procurement organization (OPO) service area in a single year to determine the reasonableness of their nonuse and to identify how we might increase the transplant rate of these kidneys. Five experienced local transplant physicians independently reviewed unutilized kidneys to identify which kidneys they would consider transplanting in the future. Biopsy results, donor age, kidney donor profile index, positive serologies, diabetes, and hypertension were risk factors for nonuse. Results.Two-thirds of nonused kidneys had biopsies with high degree of glomerulosclerosis and interstitial fibrosis. Reviewers identified 33 kidneys as potentially transplantable (12%). Conclusions.Reducing the rate of unutilized kidneys in this OPO service area will be achieved by setting acceptable expanded donor characteristics, identifying suitable well-informed recipients, defining acceptable outcomes, and systematically evaluating the results of these transplants. Because the improvement opportunity will vary by region, to achieve a significant impact on improving the national nonuse rate, it would be useful for all OPOs, in collaboration with their transplant centers, to conduct a similar analysis.

Introduction: Achieving long term glycemic control after islet transplantation depends, in part, on quantity and quality of used islets. This requires achieving an optimal balance of enzymatic digestion to free islets from surrounding acinar tissue. Underexposure of digestive enzymes to the pancreas results in trapped or embedded islets, whereas excess digestion can lead to islet fragmentation, injury, and poor islet survival. Methods: We have developed a machine learning model to define the most suitable levels of digestive enzyme exposure using results from function assays, gene signature, and isolation parameters to maximize islet yield and in vivo function. To predict islet yield, the model was trained based on transplant outcome, where the threshold for successful islet isolation was defined as 300,000 IEQ. Independent parameters were comprised of donor/organ characteristics including BMI, age, HbA1c, cold ischemia time (CI), pancreas weight (PW), and enzyme exposure parameters included amount and duration of Wunsch enzyme used. To predict in vivo islet function, stabilized blood glucose (BG) averages from NOD/skid mice transplanted with donor islets, within 7 to 30 days post-transplant using the integral area under the curve (AUC) were used as a training set. Independent variables included isolation parameters used for yield prediction, as well as functional assay results from oxygen consumption rate (OCR)1 and genetic expression markers shown to be reflective of islet function2. Results: From 246 islet isolations the algorithm correctly identified unsuccessful digests with a hold-out accuracy of 89%, and islet function by predicting when a transplant would fail to reverse diabetes in mice in 84% of cases. Cluster analysis identified 3 classifications of islet function based on similarity in donor and digest characteristics, OCR, and gene expression. Group 1 (HbA1c= 5.4% ±0.53, purity = 80% ±6.99%, CI = 395 ±116 minutes) reversed diabetes in 10.6 ±5.5 days with a stabilized BG of 183.6 mg/dl ±125.0; group 2 (HbA1c= 6.6% ±2.17, purity = 77% ±7.47%, CI = 431 ±100 minutes) showed a maximum response at 13.5 ±6.0 days, where the most stabilized BG averaged 404.9 mg/dl ±176.0, and group 3 (HbA1c= 5.3% ±0.32, purity = 81% ±6.48%, CI = 491 ±152 minutes) showed a maximum response at 10.9 ±6.2 days, where the most stabilized BG averaged 300.5 ±163.9 mg/dl. Group 1 had lower Wunsch exposure, PW, and HbA1c (p=*, **, ***, respectively), and had higher OCR and gene expression for the functional islet gene marker MNX12 (p=***, ***, respectively) than group 2. Group 3 also had levels indicative of good islet function compared to group 2 (HbA1c, MNX1, OCR p=***, ***, ***, respectively), but may have been susceptible to poor islet function due to high Wunsch amount, CI, and PW (**, **, ***, respectively). Conclusion: The model can make inferences on the most suitable levels of digestive enzyme exposure to maximize islet yield and in vivo function. References: 1. Sweet IR, Gilbert M, Scott S, Todorov I, Jensen R, Nair I, Al-Abdullah I, Rawson J, Kandeel F, Ferreri K. Glucose-stimulated increment in oxygen consumption rate as a standardized test of human islet quality. Am J Transplant. 2008 Jan;8(1):183-92. doi: 10.1111/j.1600-6143.2007.02041.x. Epub 2007 Nov 12. PMID: 18021279. 2. Kurian SM, Ferreri K, Wang CH, Todorov I, Al-Abdullah IH, Rawson J, Mullen Y, Salomon DR, Kandeel F. Gene expression signature predicts human islet integrity and transplant functionality in diabetic mice. PLoS One. 2017 Oct 2;12(10):e0185331. doi: 10.1371/journal.pone.0185331. PMID: 28968432; PMCID: PMC5624587.

Islet cell transplantation has become a favorable therapeutic approach in the treatment of Type 1 Diabetes due to the lower surgical risks and potential complications compared to conventional pancreas transplantation. Despite significant improvements in islet cell transplantation outcomes, several limitations hamper long-term graft survival due to tremendous damage and loss of islet cells during the islet cell transplantation process. Oxidative stress has been identified as an omnipresent stressor that negatively affects both the viability and function of isolated islets. Furthermore, it has been established that at baseline, pancreatic β cells exhibit reduced antioxidative capacity, rendering them even more susceptible to oxidative stress during metabolic stress. Thus, identifying antioxidants capable of conferring protection against oxidative stressors present throughout the islet transplantation process is a valuable approach to improving the overall outcomes of islet cell transplantation. In this review we discuss the potential application of antioxidative therapy during each step of islet cell transplantation.

Introduction: Human Leukocyte Antigen (HLA) alleles have been shown to affect both the susceptibility and severity of viral infections. [1] Recently, seasonal coronavirus-specific CD8+ T cells were found to cross-react with HLA-A24 high binding epitope from SARS-COV2 spike protein in healthy persons with HLA A-24 alleles. [2] Considering that HLA-A24 antigen has been found in high frequency in Asian countries that have experienced the lowest death per capita, HLA-A24 allele may confer protection against COVID 19. Therefore, in this study, we examined the association of HLA-A24 allele and COVID19 susceptibility and severity in kidney transplant recipients (KTR). Methods: A single-center cross-sectional study included 530 patients who received a kidney transplant between 2/1/2017 to 1/31/2022. The exposure was HLA-A24 allele and primary outcomes were COVID19 infection and COVID-19-related hospitalization or COVID-19-associated death. All positive COVID-19 KTR were either self-reported or were from PCR tests indicated for patients with COVID-19 symptoms. For further analysis, patients were stratified by vaccination status prior to COVID-19 infection. Data was analyzed using student’s T test, Chi square test, and Fischer exact test. Results: Of the 509 KTR, 139 (27%) patients had at least one HLA-A24 antigen of which 13 patients were double-positive for HLA-A24. There were no significant differences in age, gender, race, ethnicity, BMI, and prevalence of comorbidities including coronary artery disease, diabetes, and heart failure between patients with and without HLA-A24 allele. Of 139 KTR with HLA-A24 alleles, 35 patients became infected with COVID-19; while 139 of 370 KTR without HLA-A24 had COVID-19 (25.2% vs. 37.5%; P <0.01). After stratified by vaccination status prior to COVID-19 infection, while the ratio of KTR with COVID-19 prior to vaccination did not differ between the two groups (20.1% vs. 22.4%, P =0.58), the proportion of patients who had COVID-19 after vaccination was significantly lower in the HLA-A24 group (5.0% vs. 15.1%; P <0.01). There was no difference in hospitalization and mortality related to COVID-19 between the two groups.Conclusion: COVID-19 vaccination is more effective in KTR with HLA-A24allele. Further studies are required to elucidate the mechanism of protective effect of HLA-A24 on COVID-19 in high-risk immunocompromised host such as in KTR. References: 1.Tavasolian, F., M. Rashidi, G. R. Hatam, M. Jeddi, A. Z. Hosseini, S. H. Mosawi, E. Abdollahi, and R. D. Inman. “Hla, Immune Response, and Susceptibility to Covid-19.” Front Immunol 11 (2020): 601886. 2.Shimizu, K., T. Iyoda, A. Sanpei, H. Nakazato, M. Okada, S. Ueda, M. Kato-Murayama, K. Murayama, M. Shirouzu, N. Harada, M. Hidaka, and S. I. Fujii. “Identification of Tcr Repertoires in Functionally Competent Cytotoxic T Cells Cross-Reactive to Sars-Cov-2.” Commun Biol 4, no. 1 (2021): 1365.

Diabetes mellitus (DM) is a metabolic disorder characterized by chronic hyperglycemia as a result of insufficient insulin levels and/or impaired function as a result of autoimmune destruction or insulin resistance. While Type 1 DM (T1DM) and Type 2 DM (T2DM) occur through different pathological processes, both result in β-cell destruction and/or dysfunction, which ultimately lead to insufficient β-cell mass to maintain normoglycemia. Therefore, therapeutic agents capable of inducing β-cell proliferation is crucial in treating and reversing diabetes; unfortunately, adult human β-cell proliferation has been shown to be very limited (~0.2% of β-cells/24 h) and poorly responsive to many mitogens. Furthermore, diabetogenic insults result in damage to β cells, making it ever more difficult to induce proliferation. In this review, we discuss β-cell mass/proliferation pathways dysregulated in diabetes and current therapeutic agents studied to induce β-cell proliferation. Furthermore, we discuss possible combination therapies of proliferation agents with immunosuppressants and antioxidative therapy to improve overall long-term outcomes of diabetes.

Introduction: The risk for morbidity and mortality from coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), is high in transplant recipients due to the continued immunosuppression regimen for allograft maintenance. While SARS-CoV-2 primarily affects the lungs and causes pulmonary sequelae, evidence suggests that infection by the virus affects other organ systems as well. Simultaneous pancreas-kidney (SPK) transplantation is a treatment for patients with insulin-dependent diabetes and end-stage renal failure. Management of COVID-19 is especially challenging in patients who received SPK transplantation due to the complex interaction between the viral pathogenesis, pancreas and kidney allografts, and immunosuppressive therapies. Therefore, examining the clinical management and recovery process of allograft damage in post-SPK transplant patients who contacted COVID-19 could be valuable in establishing optimal treatment guidelines for this vulnerable population. Methods: We present a series of patients who contacted COVID-19 and developed allograft damage after receiving SPK transplantation at our institution. The following information was retrieved and collated: demographics, baseline health following transplantation, clinical management of COVID-19 infection and allograft damage. Results: Out of 10 post-SPK transplant patients who tested positive for COVID-19, 5 patients (50%) also developed elevation of amylase and/or lipase levels 3 times the upper limit of normal. The average AlloSure level of these 5 patients was 5.67% at the time of pancreatic damage. One patient contacted COVID-19 after being admitted for acute rejection and inflammation of the pancreas, and recovered after receiving remdisivir, dexamethasone, plasmapheresis, and high dose prednisone with aggressive diuresis. The other patient was diagnosed with pancreatitis and acute kidney injury on admission and had symptomatic improvements after receiving thymoglobulin induction, IVIG, and rituximab. The patient subsequently contacted COVID-19 after discharge and fully recovered after receiving Bamlanivimab infusion, which occurred concurrently with a precipitous decline in amylase and lipase levels. The remaining 3 patients did not meet the criteria for acute pancreatitis, and they recovered after receiving tixagevimab with cilgavimab, remdisivir with dexamethasone, and Bamlanivimab infusion, respectively, along with supportive treatments. Conclusion: Damage to the allograft via immunological processes and infectious agents is a recurring concern for patients who received SPK transplantation. Notwithstanding the clinical overlap of COVID-19 infection and allograft damage in the reported patients, it is still unclear if COVID-19 infection directly elicits damage. Further research is required to clarify the relationship between these two phenomena and establish an optimal treatment guideline.

Living donor kidney transplantation is an effective strategy to mitigate the challenges of solid organ shortage. However, being a living kidney donor is not without risk, as donors may encounter short- and long-term complications including the risk of developing chronic kidney disease, end-stage kidney disease, hypertension, and possible pregnancy-related complications. Although the evaluation of potential living donors is a thorough and meticulous process with the intention of decreasing the chance of complications, particularly in donors who have lifetime risk projection, risk factors for kidney disease including genetic predispositions may be missed because they are not routinely investigated. This type of testing may not be offered to patients due to variability and decreased penetrance of symptoms and lack of availability of appropriate genetic testing and genetic specialists. We report a case of a middle-aged woman with a history of gestational diabetes and preeclampsia who underwent an uneventful living kidney donation. She developed postdonation nonnephrotic range proteinuria and microscopic hematuria. Given the risk of biopsy with a solitary kidney, genetic testing was performed and revealed autosomal dominant Alport syndrome. Our case underscores the utility of genetic testing. Hopefully, future research will examine the incorporation of predonation genetic testing into living kidney donor evaluation.

OBJECTIVE To evaluate the efficacy of interactive virtual reality (iVR) in providing a three-dimensional (3D) experience with the donor's anatomy for surgeons and patients, we present a retrospective, case controlled study assessing the impact of iVR renal models prior to LDN on both surgical outcomes and patients' understanding of the procedure. MATERIALS AND METHODS Twenty patients undergoing LDN were prospectively recruited; their contrast-enhanced CT scans were transformed into iVR models. An iVR platform allowed the surgeons to rotate and deconstruct the renal anatomy; patients could also view their anatomy as the procedure was explained to them. Questionnaires assessed surgeons' understanding of renal anatomy after CT alone and after CT+iVR. Surgeons also commented on whether iVR impacted their preoperative plan. Patients assessed their anatomical understanding and anxiety level before and after iVR. Surgical outcomes for the iVR cohort were compared to a retrospectively matched, non-iVR cohort of LDN patients. RESULTS Surgeons altered their preoperative plan in 18 of 20 LDNs after viewing iVR models. Patients reported better understanding of their anatomy (5/5) and noted decreased preoperative anxiety (5/5) after viewing iVR. When compared to the non-iVR group, the iVR group had a 25% reduction in median operative time (P < .001). In terms of surgical outcomes, patients in the iVR group had a 40% lower median relative change in postoperative creatinine (P < .001). CONCLUSION Preoperative viewing of iVR models altered the operative approach, decreased the operative time, and improved donor patient outcomes. iVR models also reduced patients' preoperative anxiety. (C) 2021 Elsevier Inc.

Kidney allograft infarction is rare, but an urgent condition that requires prompt intervention to avoid allograft loss.Renal artery thrombosis is the leading cause of infarction.Apart from traditional risk factors for thrombosis, emerging SARS-CoV-2 predisposes patients to thrombotic diseases both in arterial and venous vasculatures.We report a case of kidney transplant recipient with known transplant renal artery stenosis (TRAS) status post angioplasty with severe COVID-19, complicated by oliguric acute kidney injury requiring continuous renal replacement therapy (CRRT).She did not have a history of thromboembolic disease.The hospital course was complicated by newonset atrial and ventricular fibrillation and cardiac arrest requiring multiple rounds of cardiopulmonary resuscitation.She had no signs of renal recovery, and an abdominal CT scan showed evidence of allograft infarcts.She underwent an allograft nephrectomy.Pathology revealed diffuse thrombotic microangiopathy involving glomeruli, arterioles, and arteries associated with diffuse cortical infarction with negative SARS-CoV-2 immunostain and in situ hybridization.This is the first case of kidney allograft infarct with a history of TRAS in a COVID-19 patient.Underlying TRAS and COVID-19-associated thrombosis in this patient are unique and likely play a key role in allograft infarction from arterial thrombosis.Recognizing risk factors and early therapy for allograft infarction may improve transplant outcomes.

Allocation of donated organs for transplantation is a complex process that considers numerous factors such as donor, organ and candidate characteristics and practical issues such as geography. Whole pancreas and isolated islet transplantation are lifesaving for certain individuals with diabetes. Herein, we suggest a revised allocation schema that matches donor characteristics with candidate medical condition while allowing for geographic considerations. It is hoped that adoption of this schema will shorten allocation time, decrease organ waste and optimize the parity between organ donor characteristics and candidate state of health.

Hyperglycemia after kidney transplantation is common in both diabetic and non-diabetic patients. Both pretransplant and post-transplant diabetes mellitus are associated with increased kidney allograft failure and mortality. Glucose management may be challenging for kidney transplant recipients. The pathophysiology and pattern of hyperglycemia in patients following kidney transplantation is different from those with type 2 diabetes mellitus. In patients with pre-existing and post-transplant diabetes mellitus, there is limited data on the management of hyperglycemia after kidney transplantation. The following article discusses the nomenclature and diagnosis of pre- and post-transplant diabetes mellitus, the impact of transplant-related hyperglycemia on patient and kidney allograft outcomes, risk factors and potential pathogenic mechanisms of hyperglycemia after kidney transplantation, glucose management before and after transplantation, and modalities for prevention of post-transplant diabetes mellitus.

IMPORTANCE There are over 2 million undocumented immigrants (UI) in California, where currently, all individuals regardless of immigration status have access to kidney transplant. There is a medical perception that UI face a higher risk of transplant failure due to language barriers and lack of access to immunosuppressive medication and health care when compared with US residents (UR). OBJECTIVE To elucidate the kidney transplant outcomes of UI at an academic medical center in California. DESIGN, SETTING, AND PARTICIPANTS A retrospective cohort study was conducted from a single transplant center during an 8-year study period. Patients who received a kidney transplant at the University of California, Irvine, between January 1, 2012, and September 1, 2019, were included in this study. Data were analyzed from October 2020 to August 2021. EXPOSURES The primary exposure of this study was citizenship status. UI were defined as immigrants residing in the US without permission or legal documentation. MAIN OUTCOMES AND MEASURES The primary end point was all-cause graft loss defined as the return to dialysis, need for a second kidney transplant, or death. The secondary end points of this study were all-cause mortality and rejection. All-cause mortality between the 2 groups was compared using multiple Cox proportional hazard regression analysis. Other transplant outcomes, including all-cause graft loss and acute rejection, were examined by competing risks regressions with mortality and mortality plus graft loss serving as competing risks, respectively. RESULTS Of all 446 consecutive kidney transplant recipients, the mean (SD) age was 47 (13) years; 261 patients (59%) were male, and 114 (26%) were UI. During a median (IQR) follow-up time of 3.39 (0.04-8.11) years, 6 UI and 48 UR experienced all-cause graft loss. UR had a 192%(hazard ratio, 2.92; 95% CI, 1.21-6.85; P =.01) and 343%(hazard ratio, 4.34; 95% CI, 1.05-18.69; P =.04) significantly increased unadjusted risk for all-cause graft loss and all-cause mortality, respectively. These results became nonsignificant and were mostly attenuated when adjusted for age and ethnicity. Finally, there was no difference in incidence rate of kidney allograft rejection between the 2 groups (UR, 3.5 per 100 person-years vs UI, 2.4 per 100 person-years; rate ratio, 1.45; 95% CI, 0.90-5.05; P =.08). CONCLUSIONS AND RELEVANCE This single-center cohort study found that kidney transplant outcomes of UI were not inferior to those of UR. Across the US, however, UI have consistently had unequal access to transplantation. These findings suggest that extending kidney transplants to UI is safe and does not portend worse outcomes. As a result, denying transplant according to immigration status not only results in higher costs but also worse end stage kidney disease outcomes for an already underserved population.

Diabetes is a chronic metabolic disorder characterized by inappropriately elevated glucose levels as a result of impaired pancreatic β cell function and insulin resistance. Extensive studies have been conducted to elucidate the mechanism involved in the development of β cell failure and death under diabetic conditions such as hyperglycemia, hyperlipidemia, and inflammation. Of the plethora of proposed mechanisms, endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and oxidative stress have been shown to play a central role in promoting β cell dysfunction. It has become more evident in recent years that these 3 factors are closely interrelated and importantly aggravate each other. Oxidative stress in particular is of great interest to β cell health and survival as it has been shown that β cells exhibit lower antioxidative capacity. Therefore, this review will focus on discussing factors that contribute to the development of oxidative stress in pancreatic β cells and explore the downstream effects of oxidative stress on β cell function and health. Furthermore, antioxidative capacity of β cells to counteract these effects will be discussed along with new approaches focused on preserving β cells under oxidative conditions.

Conventional renal function markers are unable to measure renal allograft perfusion intraoperatively, leading to delayed recognition of initial allograft function. A handheld near-infrared spectroscopy (NIRS) device that can provide real-time assessment of renal allograft perfusion by quantifying regional tissue oxygen saturation levels (rSO2) was approved by the FDA. This pilot study evaluated the feasibility of intraoperative NIRS monitoring of allograft reperfusion in renal transplant recipients (RTR). Intraoperative renal allograft rSO2 and perfusion rates were measured in living (LDRT, n = 3) and deceased donor RTR (DDRT, n = 4) during the first 50 min post-reperfusion and correlated with renal function markers 30 days post-transplantation. Intraoperative renal allograft rSO2 for the DDRT group remained significantly lower than the LDRT group throughout the 50 min. Reperfusion rates were significantly faster in the LDRT group during the first 5 min post-reperfusion but remained stable thereafter in both groups. Intraoperative rSO2 were similar among the upper pole, renal hilum, and lower pole, and strongly correlated with allograft function and hemodynamic parameters up to 14 days post-transplantation. NIRS successfully detected differences in intraoperative renal allograft rSO2, warranting future studies to evaluate it as an objective method to measure ischemic injury and perfusion for the optimization of preservation/reperfusion protocols and early prediction of allograft function.

There is fast-emerging, cumulative clinical data on coronavirus disease 2019 (COVID-19) in kidney transplant recipients. Although respiratory tract symptoms are often the initial presentation among kidney transplant recipients who contract COVID-19, other clinical features which may indicate underlying SARS-CoV-2-related inflammation, such as gastrointestinal symptoms, are not uncommon. Hyponatremia can develop and may reflect underlying inflammation. Interferon-6 is an important pro-inflammatory cytokine involved in the pathogenesis of severe COVID-19 complications and may play a role in the inappropriately higher secretion of antidiuretic hormone leading to hyponatremia. This pathway is the so-called immuno-neuroendocrine interface. Hyponatremia in COVID-19 has been reported in a few case series of non-kidney transplant patients and only one reported kidney transplant recipient. However, the clinical course and prognostic value of hyponatremia in this population are not described in detail. We report a kidney transplant recipient who was infected with COVID-19 and exhibited severe hyponatremia secondary to the syndrome of inappropriate antidiuretic hormone secretion. Hyponatremia is one of the clinical presentations of COVID-19, although less common, and may occur more frequently in kidney transplant recipients. Thus, the possible underlying immuno-neuroendocrine relationship related to the inflammatory process of COVID-19 leading to hyponatremia and its prognostic value are reviewed.

Novel coronavirus disease 2019 (COVID-19) pandemic is a public health emergency with several million worldwide and a quarter of a million and soon half a million deaths including a third in the United States alone (as of May 10, 2020).1 It affects kidney transplantation and has caused mortality in waitlist dialysis and transplant patients.2,3 This inevitably raises questions about the practicality and direction of transplant surgeries during this critical period.