Hye-Eun Yoon

Influence of Sirolimus on Cyclosporine‐Induced Pancreas Islet Dysfunction in Rats

This study was performed to investigate the effect of sirolimus (SRL) on cyclosporine (CsA)‐induced pancreatic islet dysfunction in rats. Three separate studies were performed. First, diabetogenic effect of SRL was evaluated with three different doses (0.15, 0.3 and 0.6 mg/kg). Second, rats were treated with SRL (0.3 mg/kg) with or without CsA (15 mg/kg) for 4 weeks. Third, rats were treated with CsA for 4 weeks, and then switched to SRL for 4 weeks. The effect of SRL on CsA‐induced pancreatic islet dysfunction was evaluated by an intraperitoneal glucose tolerance test, plasma insulin concentration, HbA1c level, HOMA‐R index, immunohistochemistry of insulin and pancreatic beta islet cell mass. The SRL treatment increased blood glucose concentration in a dose‐dependent manner. The combined treatment with SRL and CsA increased blood glucose concentration, Hemoglobin A1c (HbA1c) level, HOMA‐R [fasting insulin (mU/mL) x fasting glucose (mmol/L)]/22.5] index and decreased plasma insulin concentration, immunoreactivity of insulin and pancreatic beta islet cell mass compared with rats treated with CsA. CsA withdrawal for 4 weeks improved pancreatic beta‐cell function and structure. However, conversion from CsA to SRL further increased blood glucose levels compared with the rats converted from vehicle to SRL. The results of our study demonstrate that SRL is diabetogenic and aggravates CsA‐induced pancreatic islet dysfunction.

Long-term risk of hypertension and chronic kidney disease in living kidney donors.

OBJECTIVE The aim of this study was to assess the long-term risks of chronic kidney disease and arterial hypertension in living kidney donors. METHODS Donors who were followed for more than 1 year after nephrectomy were included. We assessed each donors blood pressure, urine protein, and estimated glomerular filtration rate (eGFR). RESULTS The follow-up rate was 11% (154 out of 1,356 donors), only 19% of whom were followed by nephrologists. Blood pressure had increased from 113/75 to 116/77 mm Hg (P < .01), urinary protein excretion after donation did not increase, and renal function was well preserved after donor nephrectomy. However, 33 patients (21.4%) showed a decreased eGFR of <60 mL/min/1.73 m(2), and 3 donors developed end-stage renal disease that required renal replacement therapy. CONCLUSIONS The follow-up rate of living donors after donation was low, and we observed an increased risk of developing chronic kidney disease after donation.

Safety and Efficacy of a Quinolone-Based Regimen for Treatment of Tuberculosis in Renal Transplant Recipients

BACKGROUND Rifampin (RFP) is a first-line antituberculosis drug, but it increases the risk of acute rejection (AR) in transplant recipients. This study evaluated whether quinolone (QNL) can replace RFP in renal transplant recipients with tuberculosis. METHODS One hundred nine patients with active tuberculosis were included. Patients consisted of RFP (n = 91) and QNL (n = 18) groups based on the initial treatment regimen. Patients with RFP-associated adverse effects were subdivided into RFP-maintenance (RFP-M; n = 18) and QNL-conversion (QNL-C; n = 8) groups. Clinical outcomes were compared between groups. RESULTS The incidence of AR was higher in the RFP group than in the QNL group (24.2% vs 5.6%). The QNL group showed significantly higher 10-year graft survival rates than the RFP group (88.1% vs 66.5%; P = .022). The QNL-C group showed significantly higher 10-year graft survival rates than the RFP-M group (87.5% vs 27.8%; P = .011). The rate of complete functional recovery after AR was higher in the QNL-C group than in the RFP-M group (50% vs 22.2%). CONCLUSIONS A QNL-based regimen may be safe and effective for treatment of tuberculosis and may lower the risk of graft failure in renal transplant recipients.

Disseminated mucormycosis with myocardial involvement in a renal transplant recipient

We report the case of a renal transplant recipient with pulmonary and splenic mucormycosis whose demise was accelerated by a myocardial abscess. Once pulmonary and splenic mucormycosis was diagnosed, liposomal amphotericin B was started and immunosuppressant treatments were discontinued. The pulmonary cavities regressed during treatment, but new myocardial and peri‐allograft abscesses developed. The myocardial abscess diffusely infiltrated the left ventricular wall and was associated with akinesia, which led to sudden cardiac arrest. This case demonstrates a rare manifestation of mucormycosis and highlights the fatality and invasiveness of this infection.