Pretransplant BMI Should Be <25 in Japanese Kidney Transplant Recipients: A Single-Center Experience.

BACKGROUND: The aim of this study was to determine the appropriate body mass index (BMI) in Japanese kidney transplant (KTx) recipients. We analyzed the effects of pre- and post-transplant (Tx) obesity on graft and patient survival, perioperative complications, post-transplant diabetes mellitus (PTDM), and cardiovascular disease (CVD) in Japanese KTx recipients. METHODS: This retrospective study included 269 recipients who underwent KTx from 2008 through 2020 at Niigata University Hospital. Obesity was defined as a body mass index (BMI) ≥25 kg/m2. We examined the association between pre- and post-Tx obesity and graft survival, patient survival, the incidence of PTDM and CVD, and perioperative surgical complications. RESULTS: The graft survival rate was lower in the pre-Tx BMI ≥25 kg/m2 group, although there was no significant difference in patient survival. There was no difference in graft and patient survival between the post-Tx BMI ≥25 kg/m2 group and the <25 kg/m2 group. A pre-Tx BMI ≥25 kg/m2 was an independent risk factor for biopsy-proven allograft rejection. New-onset DM after transplantation was significantly more common in the BMI ≥25 kg/m2 group than in the BMI <25 kg/m2 group (36% vs 13%; P = .002). The incidence of CVD was significantly higher in the post-Tx BMI ≥30 kg/m2 group than in the BMI <30 kg/m2 group (50% vs 11%; P = .023). There were no differences in surgical operating time, intraoperative blood loss, or perioperative complications between the obese and non-obese groups. CONCLUSION: Pre-Tx BMI ≥25 kg/m2 may be a risk factor for allograft rejection and graft loss. Post-Tx BMI should be <25 kg/m2 to reduce the risk for PTDM.

Analysis of the prevalence of systemic de novo thrombotic microangiopathy after ABO-incompatible kidney transplantation and the associated risk factors.

OBJECTIVES: To analyze the prevalence of systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation and risk factors associated with this condition. METHODS: A total of 201 patients who received living-donor kidney transplantation (114 patients with ABO-identical kidney transplantation and 87 patients with ABO-incompatible kidney transplantation) were retrospectively analyzed. Systemic de novo thrombotic microangiopathy was diagnosed clinically according to the presence of thrombocytopenia with microangiopathic hemolytic anemia and pathological findings of thrombotic microangiopathy. Anti-A and anti-B antibodies were purified from human plasma, and these antibodies' bindings to human kidney were investigated in vitro. RESULTS: ABO-incompatible kidney transplantation was a significant risk factor of systemic de novo thrombotic microangiopathy (odds ratio 55.9, 95% CI 1.8-8.9, P < 0.001) after transplantation. Multivariate logistic regression analysis showed that non-use of mycophenolate mofetil, pretreatment immunoglobulin G antibody titer ≥64-fold and pretransplant immunoglobulin M antibody titer ≥16-fold were significant risk factors for systemic de novo thrombotic microangiopathy in ABO-incompatible kidney transplantation. Microvascular inflammation of 1-h post-transplant biopsy could be observed more frequently in thrombotic microangiopathy patients than in non-thrombotic microangiopathy patients. Anti-A and anti-B antibodies purified from human plasma showed a strong in vitro reaction against human kidney when the antibody titer was ≥16-fold. CONCLUSIONS: Antibody titer should be decreased to ≤16-fold until the day of ABO-incompatible kidney transplantation by desensitization therapy including mycophenolate mofetil. The 1-h biopsy results might help to diagnose systemic de novo thrombotic microangiopathy.

[SMALL CELL PROSTATE CANCER PRODUCING SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDIURETIC HORMONE; A CASE REPORT].

A 73-year-old man with progressive prostate cancer visited our hospital after prostate biopsy performed at another hospital. His serum PSA level was 29.02 ng/ml. CT revealed invasion of the bladder, bilateral ureters, and rectum. Otherwise, there was no evidence of metastasis. Pathological findings showed a poorly differentiated adenocarcinoma (Gleason score 4+5) and small cell carcinoma component. Two months after administering combined androgen blockade therapy, he was admitted due to severe hyponatremia caused by the inappropriate secretion of antidiuretic hormone. Furthermore, CT revealed right ureter metastasis, although the PSA levels remained low. Therefore, the patient was put on fluid restriction and sodium administration. After the patient recovered from hyponatremia, chemotherapy, including VP-16 and CDDP, was initiated. However, CT after two chemotherapy cycles revealed disease progression, with multiple bone metastases. Second-line chemotherapy, including CPT-11 and CDDP, was less effective, and the patient died 9 months after the diagnosis.

Continuous remission of renal cell carcinoma with tumour thrombus after severe adverse events following short-term treatment with sunitinib.

A 64-year-old Japanese man with renal cell carcinoma (RCC) and tumour thrombus in the inferior vena cava was treated with sunitinib. Two weeks after treatment, he was hospitalised for disturbance of consciousness. Laboratory tests revealed high-grade hypoglycaemia, hyponatraemia, liver dysfunction and thrombocytopaenia with disseminated intravascular coagulation. Sunitinib was discontinued and the patient recovered after a protracted platelet transfusion. At 5 months after treatment, CT revealed that the tumour thrombus had disappeared and other lesions had regressed. MRI at 15 months revealed further regression and suggested the possibility of histological remission according to the signal intensity of fibrosis. A partial response persisted at 20 months after treatment, despite residual accumulation in the renal tumour evident on positron emission tomography. In summary, we present a case of locally advanced RCC accompanied by severe adverse events that showed a significant and durable response to treatment with sunitinib for just 2 weeks.

[Laparoscopic fenestration for a symptomatic lymphocele in renal graft after living-donor kidney transplantation].

A 36-year-old female received protocol biopsy at 1 month after living donor kidney transplantation. At 3 months post-transplantation, presence of a growing cystic mass in the kidney graft which had not been detected preoperatively, was demonstrated by ultrasound and computed tomography. The patient had an abdominal pain around the graft. Percutaneous drainage and sclerotherapy with minocyclin were performed twice, but the cystic mass, nevertheless, became enlarged and the abdominal pain recurred again. Laparoscopic fenestration was then performed. Immunohistochemistry of the cystic mass wall showed that it was CD34 (-), EMA (-), Megalin (-), but D2-40 (+). These results suggested that the cystic mass was derived from lymphatic vessels, which developed into lymphocele in the graft. We concluded that lymphatic vessels could have been injured and obstructed by the protocol biopsy. This is the first report of successful laparoscopic fenestration for lymphocele in the kidney graft.

Progression of ventricular remodeling and arrhythmia in the primary hyperoxidative state of glutathione-depleted rats.

BACKGROUND: Although oxidative stress is considered to promote arrhythmogenic substrates in diseased model animals, it is difficult to evaluate its primary role. In this study, we evaluated the promotion of arrhythmogenic substrates in the primary hyperoxidative state. METHODS AND RESULTS: Sprague-Dawley rats were treated with L-buthionine-sulfoximine (BSO, 30 mmol · L(-1) · day(-1)) for 14 days. On day 7 or 14, the serum levels of derivatives of reactive oxygen metabolites (d-ROM) were measured, and immune staining of 8-hydroxy-2'-deoxyguanosine (8O HdG) was performed to assess oxidative stress. The ventricular effective refractory period (ERP), monophasic action potential duration (MAPD), and the inducibility of ventricular arrhythmia were also evaluated. BSO rats exhibited higher serum d-ROM and clearer 8OHdG staining than the controls. The inducibility of ventricular arrhythmia was higher in the BSO rats than in the controls. The ERP was shorter in the BSO rats than the control (day 14, 32 ± 1 vs. 36 ± 1 ms, P<0.05), whereas the MAPD(90) was longer in the BSO rats (day 14, 76 ± 5 vs. 55 ± 4 ms, P<0.05). The mRNA levels of Kv4.2, erg, and SERCA2a were downregulated in the BSO rats (P < 0.05), and Western blot analysis exhibited the downregulation of erg and SERCA2 expression in the BSO rats (P < 0.05). CONCLUSIONS: Systemic oxidative stress might be one of the primary factors promoting cardiac electrophysiological remodeling and increasing the inducibility of arrhythmia independently of major organ disorders.