Search

Background: The nonuse rate for kidneys recovered from deceased donors is increasing, rising to 27% in 2023. In 10% of these cases, 1 kidney is transplanted but the mate kidney is not., Study Design: We conducted a retrospective, single-center cohort study from December 2001 to May 2023 comparing single kidneys transplanted at our center (where the contralateral kidney was not used) to kidneys where both were transplanted separately, at least 1 of which was at our center., Results: We performed 395 single deceased-donor kidney transplants in which the mate kidney was not transplanted. Primary reasons for mate kidney nonuse were as follows: no recipient located or list exhausted (33.4%), kidney trauma or injury or anatomic abnormalities (18.7%), biopsy findings (16.7%), and poor renal function (13.7%). Mean donor and recipient ages were 51.5 ± 14.2 and 60 ± 12.6 years, respectively. Mean kidney donor profile index was 73% ± 22%, and 104 donors (26.3%) had kidney donor profile index >85%. Mean cold ischemia was 25.6 ± 7.4 hours, and 280 kidneys (70.7%) were imported. Compared with 2,303 concurrent control transplants performed at our center, primary nonfunction or thrombosis (5.1% single vs 2.8% control) and delayed graft function (35.4% single vs 30.1% control) were greater with single-kidney use (both p < 0.05). Median patient and death-censored graft survival were shorter in the single group (11.6 vs 13.5 years, p = 0.03 and 11.6 vs 19 years, p = 0.003), although the former was at least double median survival on the waiting list. In patients with functioning grafts in the single-kidney group, 1-year mean serum creatinine was 1.77 ± 0.8 mg/dL and estimated glomerular filtration rate was 44.8 ± 20 mL/min/1.73 m 2 ., Conclusions: These findings suggest that many mate kidneys are being inappropriately rejected, given the acceptable outcomes that can be achieved by transplanting the single kidney in appropriately selected recipients., (Copyright © 2024 by the American College of Surgeons. Published by Wolters Kluwer Health, Inc. All rights reserved.)

BACKGROUND Takotsubo syndrome is a transient, reversible, stress-induced cardiomyopathy that affects only 1.4% of liver transplant patients and can cause complications, including cardiogenic shock, arrhythmia, and thromboembolism. Hepatic artery thrombosis is also rare, affecting just 2-4% of these patients, but can have disastrous consequences. Here, we describe a case of concurrent takotsubo syndrome and hepatic artery thrombosis in a postoperative liver transplant recipient. CASE REPORT The patient was a 66-year-old man who underwent living donor liver transplantation for non-alcoholic steatohepatitis. On postoperative day 3, he became lethargic and tachycardic to the 120 s. Work-up, including EKG, troponin I, BNP, and transthoracic echocardiogram, was characteristic for takotsubo syndrome. His LVEF of 15-20% was markedly reduced compared to his baseline of 50-55% from 6 months prior. Hepatic ultrasonography showed no hepatic arterial flow, prompting emergent return to the OR, where intraoperative evaluation revealed hepatic artery thrombosis. The graft was salvaged after hepatic artery thrombectomy and arterial anastomosis revision. We are unable to determine which event caused the other in this case, as both takotsubo syndrome and hepatic artery thrombosis manifested within the same time frame. CONCLUSIONS It is important to recognize takotsubo syndrome as a potential cause of cardiac dysfunction and hepatic artery thrombosis in liver transplant patients, and also be aware that hepatic artery thrombosis can precipitate takotsubo syndrome.

Background: Approximately 38% of patients with colorectal cancer will develop isolated liver metastases. Sidedness of colon tumor is identified in non-metastatic and unresected metastatic cancers as predictive of survival, yet its dedicated analysis in resected liver metastases is minimal. Our primary aim was to assess whether left-sided primary tumors improve prognosis in stage IV cancer patients undergoing curative-intent liver metastasectomy; it was hypothesized that it would., Methods: This is a retrospective, observational cohort study from 1996 to 2016 in a single tertiary-care facility. Survival from diagnosis was calculated via Kaplan-Meier method and compared between the right and left sides via log-rank analysis., Results: Median survival differs significantly between colorectal tumors of the right and left origins after hepatic metastasectomy in 612 patients. In patients with right-sided tumors, median survival from diagnosis was 4.5 years (IQR 4.1-5.3), and 6.3 years (IQR 5.6-6.9) in those with left tumors (HR 1.5, 95% CI 1.38-1.60, p < 0.001)., Conclusion: As in studies on earlier-stage or unresected metastatic disease, tumor sidedness is an important prognostic factor in patient survival with liver metastasectomy. Clinical risk scores should include side of primary tumor. Further work is needed to determine the molecular basis for this difference., (Copyright © 2019. Published by Elsevier Ltd.)

A pilot study is underway to quantify in vivo the uptake and distribution of Tc-99m Sestamibi in subjects without previous history of breast cancer using a dedicated SPECT-CT breast imaging system. Subjects undergoing diagnostic parathyroid imaging studies were consented and imaged as part of this IRB-approved breast imaging study. For each of the seven subjects, one randomly selected breast was imaged prone-pendant using the dedicated, compact breast SPECT-CT system underneath the shielded patient support. Iteratively reconstructed and attenuation and/or scatter corrected images were coregistered; CT images were segmented into glandular and fatty tissue by three different methods; the average concentration of Sestamibi was determined from the SPECT data using the CT-based segmentation and previously established quantification techniques. Very minor differences between the segmentation methods were observed, and the results indicate an average image-based in vivo Sestamibi concentration of 0.10 ± 0.16 μCi/mL with no preferential uptake by glandular or fatty tissues.

Heparin-induced thrombocytopenia (HIT) is a life-threatening, thrombotic disorder associated with development of anti-platelet factor 4 (anti-PF4)/heparin autoantibodies. Little is known about the antigenic and cellular requirements that initiate the immune response to these complexes. To begin to delineate mechanisms of autoantibody formation in HIT, we studied the immunizing effects of murine PF4 (mPF4)/heparin in mice with and without thymic function. Euthymic mice were injected with mPF4/heparin complexes, mPF4, heparin, or buffer. Mice injected with mPF4/heparin, but not mPF4 or heparin alone, developed heparin-dependent autoantibodies that shared serologic and functional characteristics of human HIT antibodies, including preferential binding to mPF4/heparin complexes and causing heparin- and FcRgammaIIA-dependent platelet activation. In contrast, athymic mice did not develop HIT-like antibodies. Taken together, these studies establish that PF4/heparin complexes are highly immunogenic and elicit self-reacting anti-PF4/heparin antibodies in a T cell-dependent manner.