Tadashi Uramatsu

De novo minimal change disease after ABO-incompatible kidney transplantation.

We report the clinical and pathological findings of a case of de novo minimal change disease (MCD) after ABO‐incompatible living kidney transplantation. A 62‐yr‐old man with end‐stage renal disease associated with type I diabetes received ABO‐incompatible kidney transplantation from his 58‐yr‐old wife. Although allograft function was excellent immediately after surgery, massive proteinuria (35 g/d) appeared on post‐transplantation day 5. After the allograft biopsy taken on post‐transplantation day 6, he was treated with 12 cycles of plasma exchange, but the nephrotic‐range proteinuria showed no remission. The biopsy specimen showed no significant pathological findings on light microscopy, but electron microscopy showed diffuse effacement of podocyte foot processes. Based on the diagnosis of de novo MCD, the patient received intravenous methylprednisolone pulse therapy, followed by high‐dose steroid maintenance therapy. The steroid therapy induced complete remission of nephrotic syndrome and stable allograft function immediately, which was also maintained at one yr after the transplantation.

Membranous Nephropathy with Crescent after ematopoietic Cell Transplantation: A Case Report

A 44-year-old man who received allogenic hematopoietic stem cell transplantation after being diagnosed with acute myeloid leukemia developed nephrosis when the dose of tacrolimus was tapered. A renal biopsy showed the granular deposition of immunoglobulin G in the glomerular basement membrane and subepithelial electron-dense deposits, crescent formation, C4d-positive staining of the peritubular capillary, and subendothelial swelling, suggesting that the main pathological diagnosis was membranous nephropathy and that chronic graft-versus-host disease played a role in the etiology of nephrosis. We herein report a case of membranous nephropathy with various pathological findings. C4d deposition suggests complement activation and the involvement of humoral factors.

Methotrexate-induced acute kidney injury in patients with hematological malignancies: three case reports with literature review

BackgroundHigh-dose methotrexate (HD-MTX) therapy has been used to treat a wide range of oncological malignancies. While the therapy can be tolerated with hydration, urine pH control, and leucovorin rescue therapy, HD-MTX is cytotoxic and can cause renal failure. There have been several case reports of HD-MTX toxicity in patients with solid tumors; however, few case series of hematological malignancies have been published. Patients with hematological malignancies tend to be administered many concomitant drugs, which can affect the elimination of MTX and result in acute kidney injury.Case presentationHere, we present three cases of HD-MTX-induced acute kidney injury in patients with hematological malignancies. Several blood purification methods were used to attempt to eliminate MTX.ConclusionsRapid elimination of MTX is needed for patients with higher serum MTX concentrations to avoid additional cytotoxic effects, especially in patients who have experienced many complications. Although the most effective method for MTX elimination remains unknown, the results of our retrospective survey suggest that combined modalities, such as hemodialysis and plasma exchange, may be suitable for treatment of patients with hematological malignancies.

Serum Endocan as a Predictive Marker for Decreased Urine Volume in Peritoneal Dialysis Patients

Background Endocan is expressed in vascular endothelial cells, and its expression is enhanced following endothelial injury via inflammatory cytokines. Subsequently, endocan is secreted into the circulation. Thus, serum endocan levels are considered a marker of endothelial injury. However, to the best of our knowledge, no data on the serum endocan levels in peritoneal dialysis (PD) patients are available. Material/Methods This study included 21 PD patients who underwent peritoneal equilibration test (PET) more than once between 2011 and 2015. Serum samples were collected from each patient, and the 24-h urine volume was measured at the time of PET. Serum endocan levels were measured using enzyme-linked immunosorbent assay (ELISA) at the time of the first PET, and their relationship with clinical data or the extent of urine volume decline (mL/year) was analyzed retrospectively. Results Serum endocan levels were positively correlated with proteinuria level, serum creatinine level, serum tumor necrosis factor (TNF)-α level, β2-microglobulin level, and PD drainage volume, but not with urine volume at baseline. The extent of decline in urine volume was significantly associated with serum endocan level, proteinuria level, serum creatinine level, and serum TNF-α level at baseline in a simple linear regression analysis. Moreover, multiple linear regression analysis showed that the serum endocan level and proteinuria level at baseline were independent predictors for the extent of decline in urine volume. Conclusions The results of this study indicate that serum endocan level and proteinuria level may be useful predictive markers for decreased urine volume in PD patients.

A case of mild phenotype Alport syndrome caused by COL4A3 mutations

In a case of 41-year-old man with mild nephropathy, Alport syndrome (AS) was diagnosed from the renal biopsy. However, the α5 chain of type IV collagen expressed in the glomerular basement membrane, which was the atypical staining pattern of AS. Genetic testing suggested autosomal recessive AS from heterozygous mutations at two positions in the type IV collagen α3 chain. These two gene mutations represented a new pattern of mutation and was suggested the association with an atypical α5 chain expression and mild phenotype.