ABO-incompatible living kidney transplantation (ABO-ILKT) has steadily become more widespread. However, the optimal immunosuppressive regimen for ABO-ILKT remains uncertain. We aimed to determine the longitudinal changes in the outcomes from ABO-ILKT compared with those from ABO-compatible living kidney transplantation (ABO-CLKT) over the last 25 years. Of 1195 patients who underwent living kidney transplantations (LKT) at our institute between 1989 and 2013, 1032-including 247 ABO-ILKT and 785 ABO-CLKT cases-were evaluated for graft survival, patient survival, infectious adverse events, and renal function. The patients were divided into four groups according to the transplantation era and ABO-compatibility. In the past decade, ABO-ILKT and ABO-CLKT recipients yielded almost equivalent outcomes with respect to the 9-year graft survival rates, which were 86.9% and 92.0%, respectively (hazard ratio [HR] 1.38, 95% confidence interval [CI] 0.59-3.22, p ¼ 0.455). The graft survival rate for ABO-ILKT conducted between 2005 and 2013 was better than that for ABO-ILKT conducted between 1998 and 2004 (HR 0.30, 95% CI 0.13-0.72, p ¼ 0.007). ABO-ILKT recipients showed substantial improvements in the graft survival rate over time. Graft survival was almost identical over the past decade, regardless of ABO-incompatibility. Currently, ABO-ILKT is an acceptable treatment for patients with end-stage renal disease.

Study Type – Prognosis (case series)
Level of Evidence 4 OBJECTIVE To evaluate the clinical outcomes and histological types of renal cell carcinoma (RCC) arising in patients with end‐stage renal disease (ESRD), and to analyse the relationship of histopathological features with the duration of dialysis. PATIENTS AND METHODS Clinical characteristics and outcomes of 34 patients who had a radical nephrectomy for RCC arising in ESRD between November 1994 and June 2008 were investigated. Archive paraffin‐embedded tissue specimens obtained from 27 patients were histochemically and immunohistochemically analysed to determine the histopathological type. RESULTS There was one death from cancer and one patient with local progression within a median observation period of 29.5 months. Acquired cystic disease (ACD)‐associated RCC, clear cell‐papillary RCC, mucinous tubular and spindle‐cell carcinoma, and Xp11.2 translocation/TFE3 gene fusion were identified in eight, two, three and one patient, respectively. Conventional clear‐cell RCC was the predominant histological type (nine of 15) in patients with a duration of dialysis of <10 years, while ACD‐associated RCC was predominant (seven of 12) in those with dialysis for ≥10 years. Sarcomatoid foci were identified in three patients with dialysis for ≥10 years. Papillary adenoma was microscopically identified as a satellite tumour in 10 patients. CONCLUSION The spectrum of histological types of RCCs arising in ESRD is distinct from that of sporadic RCCs. Patients with a longer duration of dialysis should have particular attention for progression and metastasis. Immunohistochemical profiling is efficient in the histological classification of RCCs arising in ESRD, although knowledge about genetic changes remains to be accumulated.

months). Both enzymes were negatively expressed in PrECs andPrSCs at mRNA and protein levels. ATX expression was higher than AGK in AILNCaP, DU-145, and PC-3 cell-lines, while AGK was mainly expressed in LNCaP cells. Immunohistochemically, ATX and AGK expressions were negative in non-neoplastic epithelia, while both were weakly expressed in the majority of high-grade intra-epithelial neoplasia (HG-PIN). In cancer foci, ATX and AGK expressions were strong in 49% and 62%, weak in 40% and 32%, and negative in 11% and 6%, respectively. Expressions of both enzymes were significantly correlated with primary Gleason grade of cancer foci (P < 0.0001) and capsular invasion (P = 0.03 and 0.003 respectively). ATX expression was significantly correlated with probability of prostate specific antigen (PSA)-failure after surgery (P < 0.0001). In conclusion, LPA-producing enzymes (ATX and AGK) were frequently expressed in prostate cancer cells and precancerous HG-PIN. In particular, high expression levels of ATX were associated with both malignant potentials and poor outcomes. (Cancer Sci 2009; 100: 1631-1638) L ysophosphatidic acid (1-or 2-acyl-lysophosphatidic acid; LPA) is an extracellular bioactive phospholipid that mediates diverse biological activities including platelet aggregation, smooth muscle contraction, cancer cell proliferation, invasion, angiogenesis, and cytoskeletal reorganization.(1,2) This action is mediated by several interactive mechanisms: (a) It activates RhoA and NF-κβ genes inducing prostate cancer progression. (3,4) (b) It enhances SRE activity in promoters of immediate early growth-related genes.(5) (c) It stimulates secretion of polypeptide growth factors such as EGF (epidermal growth factor) and sensitizes cells to their growth promoting effects.(6,7) (d) Finally, LPA suppresses apoptosis of cancer cells by reducing levels of apoptosispromoting proteins. (8,9) We previously examined LPA activity in various biologic fluids and found a high LPA activity exerted by a specific type of its receptors (Edg-7/LPA3) in human seminal fluids.(10) Furthermore, addition of 18:1 LPA (oleoyl-LPA) to prostate epithelial and stromal cells resulted in up-regulation of a novel extracellular matrix signaling protein CYR-61, that has a growth stimulating potential. (11) Several routes are proposed for LPA production. It is produced extracellularly by lipoprotein oxidation through the action of secretory phospholipase A2 on microvesicles released from activated cells. (12) In plasma, it is produced by thrombin-activated platelets through the stimulated release of phospholipase-A1 and A2 (13) and lysophospholipase D (LysoPLD). (14,15) LysoPLD is identical to autotaxin (nucleotide pyrophosphatase phosphodiesterase-2; ATX/NPP2, EC 3.1.1.5), a cell motility-stimulating factor originally identified in the culture cell supernatant of malignant melanoma cells. (16,17) We previously found that human seminal fluids contain a large amount of ATX, which hydrolyses lysophosphatidylcholine to produce LPA.(18) While LPA signaling had ...

Abstract:The incidence of venous extension to the inferior vena cava (IVC) in renal cell carcinoma (RCC) is markedly increased recently mostly due to the advances in diagnostic modalities. Such vascular invasion implies a heightened biologic behavior and a surgical challenge during the course of treatment. In this study, we reviewed the classifi cation guidelines, recent diagnostic tools and up-to-date therapeutic modalities for RCC with IVC tumor thrombi added to the prognostic signifi cance regarding the pathologic nature of vascular invasion; cephalad extent of thrombi and any associated distant metastasis. Also, we are providing our suggestion regarding the use of angioscopy for removal of IVC thrombi in a relatively bloodless fi eld without aggressive surgical manipulations or shunt techniques for maintenance of hemodynamic stability.

Introduction Latent mesangial immunoglobulin A (IgA) deposition in the donated kidney has been investigated in the context of kidney transplantation. However, few studies have examined the impact of mesangial expansion accompanied with IgA deposition. Therefore, we investigated the effects of latent IgA deposition and mesangial expansion on transplant prognosis following living‐donor kidney transplantation. Methods We retrospectively analyzed 68 consecutive adult living‐donor kidney transplantations performed at Kagawa University Hospital. Biopsies were performed at pre‐implantation and at one yr after transplantation. Results Twenty kidneys exhibited latent IgA deposition in pre‐implantation biopsies, including 14 with mesangial expansion. Latent IgA deposition was not associated with renal function or donor urinalysis after donation, irrespective of mesangial expansion. Latent IgA deposition was not significantly associated with graft survival rate, allograft function, abnormal urinalysis, or the recurrence of IgA nephropathy, irrespective of mesangial expansion. At one yr after transplantation, IgA deposition had disappeared in 14/20 allografts. Estimated glomerular function rate >40 mL/min/1.73 m2 was significantly associated with the disappearance of IgA deposition. Conclusions The present study showed that latent IgA deposition from the donor kidney, irrespective of mesangial expansion, does not affect transplant prognosis following living‐donor kidney transplantation.