Flow cytometric analysis is superior to the Ham test and permits concomitant diagnosis of PNH in about 20% of patients with myelodysplasia (a rate similar to that seen in patients with aplastic anemia). The presence of GPI-anchored protein-deficient cells in myelodysplasia predicts responsiveness to immunosuppressive therapy. Early emergence of GPI-anchored protein-deficient hematopoiesis in a patient with marrow failure may point to an underlying immune pathogenesis.

Two-day steroid withdrawal in kidney transplant recipients did not affect BPAR, SCAR, CAN, graft function and patient and graft survival compared to control group up to 3 years. NODM was significantly less in steroid withdrawal group. Two-day steroid withdrawal is safe and beneficial in kidney transplant recipients.

Background New-onset diabetes after transplantation (NODAT) is a major post-transplant complication associated with lower allograft and recipient survival. Our objective was to determine if metabolic syndrome pre-transplant is independently associated with NODAT development. Methods We recruited 640 consecutive incident non-diabetic renal transplant recipients from 3 academic centers between 1999 and 2004. NODAT was defined as use of hypoglycemic medication, a random plasma glucose >200 mg/dL, or 2 fasting glucose levels ≥126 mg/dL beyond 30 days post-transplant. Results Metabolic syndrome was common pre-transplant (57.2 %). NODAT developed in 31.4% of recipients one year post-transplant. Participants with metabolic syndrome were more likely to develop NODAT compared to recipients without metabolic syndrome (34.4% v. 27.4%, p=0.057). Recipients with increasing number of positive metabolic syndrome components were more likely to develop NODAT (metabolic syndrome score-prevalence at 1 year: 0-0.0%, 1-24.2, 2-29.3%, 3-31.0%, 4-34.8%, and 5-73.7%, p=0.001). After adjustment for demographics, age by decade (HR-1.34 (1.20-1.50), p<0.0001), African American race (HR-1.35 (1.01-1.82), p=0.043), cumulative prednisone dosage (HR-1.18 (1.07-1.30), p=0.001), and metabolic syndrome (HR-1.34 (1.00-1.79), p=0.047) were independent predictors of development of NODAT at 1 year post-transplant. In a multivariable analysis incorporating the individual metabolic syndrome components themselves as covariates, the only pre-transplant metabolic syndrome component to remain an independent predictor of NODAT was low HDL (HR-1.37 (1.01-1.85), p=0.042). Conclusions Metabolic syndrome is an independent predictor for NODAT and is a possible target for intervention to prevent NODAT. Future studies to evaluate if modification of metabolic syndrome factors pre-transplant reduces NODAT development are needed.