Idiopathic granulomatous mastitis (IGM) is a rare, benign, chronic inflammatory condition of the breast, which usually mimics breast carcinoma. The aim of this study was to analyze the clinical features of IGM by identifying a more reliable diagnostic protocol, and evaluating the treatment methods and patient outcomes on follow-up. We performed a retrospective analysis of 46 patients diagnosed with IGM and managed by the same surgical team between 1999 and 2011, at three high-volume hospitals. The median age of the patients was 33 years. The most common symptom was painful breast mass (n = 39), followed by abscess (n = 11). All patients underwent ultrasonography (USG). Mammography (MG) and magnetic resonance imaging (MRI) were also performed in 20 patients (43%) and 17 patients (37%), respectively. The mean size of the lesions was 32.8 ± 8.8 mm and ranged from 15 to 50 mm. Preoperative diagnosis of IGM was established by core needle biopsy (CNB) under USG guidance. Eighteen patients (39%) underwent complete excision of the lesion and 25 (54%) were treated with steroids. Three patients treated with steroids subsequently underwent local excision. The mean follow-up period was 35.4 ± 30.9 months. Eight patients (17%) developed disease recurrence; three of these were successfully treated with steroids, one with surgery, and four with both steroids and surgery. CNB in conjunction with high diagnostic accuracy has a significant role in distinctive diagnosis of IGM and hence, is useful for treatment planning. Treatment can be designated according to the extent and the severity of the disease, and the patient's general health and treatment preferences. Patients with IGM must be closely followed up due to the frequency of disease recurrence.

No abstract

The LDLT option in the pediatric population allows recipients to be transplanted early. A total of 202 consecutive pediatric liver transplants from two different institutions--108 (LDLT) and 94 (DDLT)--were retrospectively compared. Overall, one- and three-yr patient and graft survival were similar between DDLT and LDLT. ACR was greater in recipients of DDLT at one and three yr (50.8% and 61.0%) compared to LDLT (30.8% and 32.2%) (p = 0.002). When the data were stratified according to PELD/MELD score, LDLT with a low score had better one- and three-yr graft survival (96.2% and 96.2%) compared to DDLT (88.2% and 85.2%) (p = 0.02), with comparable patient survival (p = 0.75). Patient and graft survival were similar between DDLT and LDLT in the high PELD/MELD group. Lower incidence of ACR in both low and high PELD/MELD groups was (29.6% and 34.3%) for LDLT compared to DDLT (50.3% and 53.3%, p = 0.002 and p = 0.028, respectively). Regardless of PELD/MELD score, status, age group, and recipient weight, LDLT provides excellent patient and graft survival with a lower incidence of rejection compared to DDLT.

Delayed graft function (DGF) in renal transplant is associated with reduced graft survival and increased immunogenicity. The complement-driven inflammatory response after brain death (BD) and posttransplant reperfusion injury play significant roles in the pathogenesis of DGF. In a nonhuman primate model, we tested complement-blockade in BD donors to prevent DGF and improve graft survival.BD donors were maintained for 20 hours; kidneys were procured and stored at 4°C for 43-48 hours prior to implantation into ABO-compatible, nonsensitized, MHC-mismatched recipients. Animals were divided into 3 donor-treatment groups: G1 -vehicle, G2 -rhC1INH+heparin, and G3 -heparin. G2 donors showed significant reduction in classical complement pathway activation and decreased levels of tumor necrosis factor α and monocyte chemoattractant protein 1. DGF was diagnosed in 4/6 (67%) G1 recipients, 3/3 (100%) G3 recipients, and 0/6 (0%) G2 recipients (P = .008). In addition, G2 recipients showed superior renal function, reduced sC5b-9, and reduced urinary neutrophil gelatinase-associated lipocalin in the first week posttransplant. We observed no differences in incidence or severity of graft rejection between groups. Collectively, the data indicate that donor-management targeting complement activation prevents the development of DGF. Our results suggest a pivotal role for complement activation in BD-induced renal injury and postulate complement blockade as a promising strategy for the prevention of DGF after transplantation. 1514 | DANOBEITIA ET Al. K E Y W O R D S animal models: nonhuman primate, complement biology, delayed graft function (DGF), donors and donation: donation after brain death (DBD), immunosuppression/immune modulation, ischemia reperfusion injury (IRI), kidney transplantation/nephrology, translational research/ science 1 | INTRODUC TI ON Delayed graft function (DGF) manifests as a consequence of ischemia-reperfusion injury (IRI) and is characterized by acute kidney injury (AKI) within 7 days of transplant, requiring life-sustaining dialysis. 1 The incidence of DGF in kidney transplants from brain dead (BD) donors is approximately 26% in the United States, and this rate can reach as high as 37% in kidneys from older donors and those subjected to extended cold ischemia >36 hours. 2-4 In addition to complications related to AKI in the peritransplant period, development of DGF is an important risk factor for acute cellular rejection, antibody-mediated rejection (AMR), and reduced