404A ANNUAL MEETING ABSTRACTS Kidney/Renal Pathology (including Transplantation) 1614 Molecular Assessment of Transplant Renal Biopsies and Comparison with Histology John Aird, Claire Kennedy, Donal Sexton, Jeff Reeve, Philip Halloran, Declan de Freitas, Brendan Doyle. Royal College of Surgeons in Ireland, Dublin, Ireland; Beaumont Hospital, Dublin, Ireland; University of Alberta, Edmonton, AB, Canada. Background: “The Molecular Microscope ® ” utilises a combined microarray and reference biopsy library to determine a probability score for disease activity, stage and prognosis in renal transplant biopsies. Here we describe an audit of our initial experience using this approach to complement traditional biopsies. Design: At the time of renal biopsy, an additional core was taken and shipped to the University of Alberta in RNALater. Renal biopsies were reported by 2 renal pathologists using the Banff Classifcation, without knowledge of the molecular results. “The Molecular Microscope ® ” assay was performed without clinical or histological information. Both techniques were then compared and ultimately a histo-molecular phenotype was arrived at. Results: To date we have collected data from 6 patients. A molecular report was returned between 3-6 days after the biopsy depending on day of shipping. Table 1 shows the histological, molecular and clinical diagnoses. In two of the cases which showed rejection the biopsy for histology was sub-optimal and the correlation with the molecular phenotype provided extra evidence on which to base clinical decisions. Table 1. TCMR: T-cell mediated rejection, BKN: BK Nephropathy, ATI: Acute tubular injury, AKI: Acute kidney injury, ABMR: Acute antibody mediated rejection Histology Molecular Clinical 1 TCMR TCMR TCMR 2 BKN AKI BKN 3 Infarction AKI AKI 4 ATI AKI AKI 5 Mixed rejection ABMR ABMR 6 ATI AKI AKI Interestingly, the biopsy which was infarcted was read molecularly as all medulla, based on a lack of podocin expression. It remains to be seen if this genuinely represents medulla or an artefact of the infarction. In this case the molecular phenotype was of acute kidney injury. On this basis no treatment was instigated and the patient’s renal function improved spontaneously, supporting the molecular diagnosis. In general, the molecular assay also predicted the histological scores of the biopsies. Conclusions: The use of molecular techniques is well established in tumour pathology, but remains at an early stage in transplant renal pathology. We have seen in this series that the results generally correlated well with histology and can add value in terms of clinical decision making. It is important that clinical phenotype, histology and molecular techniques are integrated, in order to reach the optimal diagnosis. 1615 Renal Pathology Findings in POEMS Syndrome Mariam P Alexander, Lynn D Cornell, Thomas Czeczok. Mayo Clinic, Rochester, MN. Background: Individuals with polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes (POEMS) syndrome often have renal dysfunction. Renal biopsy fndings in a Caucasian population is not well described. This study aims to describe presentation, rbx fndings, & outcomes in the setting of POEMS syndrome. Design: The renal pathology database was searched for POEMS syndrome from 2001- 2016. Chart review was performed including clinical presentation, laboratory testing, and follow-up. Pathology was reviewed when available. Results: Nine biopsies were identifed; all were Caucasian. Findings are presented in Table1. There was a male dominance (n=7). Indications for biopsy included proteinuria (n=4; 2 with nephrotic range), chronic renal failure (n=2), and acute kidney injury (n=2). VEGF and IL-6 were elevated in 6 and 5 individuals, respectively. Biopsies showed thrombotic microangiopathy (TM) (n=8), membranous nephropathy (n=1), crescentic and endocapillary proliferative glomerulonephritis with linear IgA λ (n=1), diabetic glomerulosclerosis with resolving post infectious GN (n=1), and immunotactoid glomerulopathy (n=1). Interstitial fbrosis was mild (0-30%). Electron microscopy showed variable endothelial and subendothelial injury, glomerular basement membrane remodeling, and mesangiolysis. Serum creatinine and 24-hour urine proteins did not signifcantly improve with treatment. Case Age/ Gen- der Serum Cre- atinine (mg/ dL) at Presenta- tion 24-hr Urine Protein (g) Pathologic Di- agnosis Treatment Follow- Up Cre- atinine (mg/ dL) Follow- Up 24- hr Urine Protein (g) 1 59M 1.5 1,112 TM SCT 2.0 - 2 56F 1.5 500 TM Sacral Plas- macytoma Radiation, Prednisone 2.8 73 3 72M 2.3 123 TM Bortezomib, Cyclophospha- mide, Dexa- methasone 2.4 173 4 57M 1.1 16,200 Membranous Nephropathy SCT, Revlimid, Dexametha- zone 1.7 102 5 41M 1.2 7,500 TM, Crescentic and Endocapil- lary Prolifera- tive Glomeru- lonephritis with Linear IgA l SCT, Ixazomib, Dexametha- sone. 1.1 324 6 51M 1.9 72 Diabetic Ne- phropathy, TM SCT 2.0 - 7 69M 2.9 257 TM - - - 8 69M 2.2 146 TM Rituximab, Cyclophospha- mide, Predni- sone 2.1 126 9 64F - - Immunotactoid Glomerulopa- thy, TM - - - Conclusions: This is the frst series of renal biopsies in individuals with POEMS syndrome in a caucasian population. While thrombotic microangiopathy is the most common fnding, immune complex glomerulonephritis may occur. Elevated VEGF and IL-6 likely contribute to pathology. 1616 Chimerism in Allograft Kidney Tumors in Transplanted Patients Hussein Alnajar, Sahr Syed, David Cimbaluk, Lela Buckingham, Paolo Gattuso. Rush University Medical Center, Chicago, IL. Background: In renal transplant patients, tumors more commonly arise in native end- stage kidney, while allograft tumors are extremely rare. To date, genetic studies to trace the origin of these tumors have been performed in just a few cases. Design: We performed a retrospective analysis of allograft biopsies and transplant nephrectomies at our institution from 1993-2016, to elucidate donor versus recipient origin of native kidney tumors in renal transplant patients. Results: We identifed a total of 4521 specimens including 189 allograft nephrectomies and 4332 allograft renal biopsies. Nine cases of renal allograft tumors were identifed (0.2 % of allograft specimens). Of these, renal cortical adenoma was the most common tumor (4 cases, 44%), followed by urothelial cell carcinoma (UCC) of the renal pelvis (2 cases, 22%), post-transplant lymphoproliferative disorder (2 cases, 22%) and oncocytoma (1 case, 12%). The mean age was 50 years (range 28-73). Mean interval between the time of renal transplant and the development of neoplasm was 102 months (range 1 -255 months). Most solid-organ or hematopoietic stem-cell transplantations are allogeneic and chimerism studies can distinguish donor and recipient tissue origin. DNA extracts from eight tumors and benign tissue from the recipient were submitted for chimerism analysis. Donor reference tissue was not available. Six cases showed different allelic profles in donor and recipient DNA. Matching confrmed the recipient origin of tumor cells in the other two cases. Conclusions: Allograft renal tumors are extremely rare (0.2% of cases). Renal cortical adenoma was the most common neoplasm of the allograft renal tumors. Tumor cells developed in the allograft kidney may arise from the donor’s kidney, or may originate from a recipient origin. The possibility of development of malignancies in allograft kidney may actually have occurred prior to transplantation. A de novo origin can be assumed if the tumor occurs later than 6 months after the transplant. Only two patients developed tumor earlier than six months; however, the possibility of an occult slow growing tumor in allograft cannot be ruled out. Renal or bone marrow stem cells migrating to the allograft kidney with subsequent malignant transformation was proposed in tumor with recipient origin. A possibility of metastasis from the native kidney was excluded by imaging studies and follow up. Once the diagnosis of tumor in the allograft kidney is made, it is crucial to obtain information about tumor cell origin, especially to assess potential transmission of a neoplasm to other recipients from the same donor.