Association between Vitamin D Deficiency and Anemia in Patients with End-Stage Renal Disease: A Cross-Sectional Study

PURPOSE: Despite new treatment strategies, anemia remains the most prevalent complication in patients with end-stage renal disease (ESRD). We investigated whether 25-hydroxyvitamin D [25(OH)D3] deficiency was associated with anemia in ESRD patients. MATERIALS AND METHODS: We reviewed the medical records of 410 ESRD patients who had undergone renal transplantation (RTx) at Yonsei University Health System and who had 25(OH)D3 levels measured at the time of RTx. Patients were divided into two groups based on baseline 25(OH)D3 concentrations: group 1, 25(OH)D3 levels <10 ng/mL; and group 2, 25(OH)D3 levels ≥10 ng/mL. RESULTS: Using multivariate regression models, 25(OH)D3, age, and erythrocyte-stimulating agent (ESA) dose were found to be significantly associated with hemoglobin (Hb) levels [25(OH)D3: β=0.263, p<0.001; age: β=0.122, p=0.010; ESA dose: β=-0.069, p=0.005]. In addition, logistic regression analysis revealed that patients in group 1 had a significantly higher risk for developing anemia (Hb level <10 g/dL) compared to group 2 patients, even after adjusting for potential risk factors for anemia (odds ratio=3.857; confidence interval=1.091-13.632; p=0.036). CONCLUSION: 25(OH)D3 deficiency was significantly associated with anemia in patients with ESRD. Randomized controlled trials are needed to determine whether vitamin D supplementation can improve anemia in these patients.

A Case of Acute Renal Failure Associated with Acute Fulminant Hepatitis A / 대한신장학회잡지

Hepatitis A is a common cause of acute hepatitis throughout the world and is usually a mild self-limiting disease of the liver, but rarely presents as fulminant hepatitis in 0.14-0.35% of acute hepatitis A. Acute renal failure requiring dialysis in acute hepatitis A is also exceeding rare. We here report an unusual case of acute renal failure associated with acute fulminant hepatitis A. A previously healthy 22-year-old female was admitted to our hospital with nausea and vomiting of 1 day duration. Biochemical tests on admission revealed a marked increase of serum AST 19,810 IU/L, ALT 10,340 IU/L, total bilirubin 5.7 mg/dL, BUN 32.7 mg/dL and creatinine 4.4 mg/dL. Prothrombin time was prolonged to 40.3 seconds (INR 5.85). Random urine Na+ was 121.5 mmol/L and fractional excretion of sodium 22%. IgM antibody to hepatitis A virus was positive, while serology tests for hepatitis B and C virus, HIV, cytomegalovirus and Epstein-Barr virus were negative. On the 4th day of admission, hepatic encephalopathy and diuretics-resistant pulmonary edema developed. Lactulose treatment was performed for hepatic encephalopathy, and intermittent hemodialysis and continuous venovenous hemodialysis for pulmonary edema and uremia. On day 21, her urine output increased up to 1,000 cc with progressive improvement in renal function. She was discharged on day 32, with her serum creatinine of 2.0 mg/dL and total bilirubin of 4.7 mg/dL.

Partial agenesis of dorsal pancreas with Castleman's disease in pancreatic tail area / 대한내과학회지

Agenesis of dorsal pancreas is a very rare congenital anomaly which comes from the failure of development of the body and tail of pancreas in embryogenesis. Castleman's disease is a rare lymphoid tumor which usually occurred in the mediastinum, but it is very uncommon in the retroperitoneal pancreatic tail area. We report a case of partial agenesis of dorsal pancreas with Castleman's disease in pancreatic tail area, mimicking a pancreatic tumor. A 46-year-old woman was admitted to our hospital with intermittent abdominal discomfort for 2 months. Computed tomography, magnetic resonance imaging, and endoscopic retrograde cholangiopancreatography (ERCP) revealed a tumor at distal pancreatic tail area, short pancreatic duct, and absence of pancreatic body and tail. The surgical excision of the tumor revealed hyaline-vascular type Castleman's disease.

Complete Resolution of Posttransplant Lymphoproliferative Disorder (Diffuse Large B-cell Lymphoma) with Reduction of Immunosuppressive Therapy

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication of organ transplantation. PTLD is the disorder arising from the combined effects of Epstein-Barr virus associated lymphoid proliferation with the disruption of the normal immune control by the cytotoxic T cells. The treatment for PTLD is one of the most controversial topics in solid organ transplantation. It is well known that the initial management of PTLD is a reduction of immunosuppression. Early diagnosis and the early reduction in immunosuppression are essential even for monomorphic lymphoma. We report here on a case of the complete resolution of PTLD (diffuse large B cell lymphoma) which occurred after a drastic reduction of immunosuppression in a renal transplant recipient.