Genetic variation in recipient B-cell activating factor modulates phenotype of GVHD.

B-cell activating factor (BAFF) single nucleotide polymorphisms (SNPs) are associated with autoimmune diseases. Because patients with classic and overlap chronic GVHD (cGVHD) have features of autoimmune diseases, we studied the association of recipient and/or donor BAFF SNPs with the phenotype of GVHD after allogeneic stem cell transplantation. Twenty tagSNPs of the BAFF gene were genotyped in 164 recipient/donor pairs. GVHD after day 100 occurred in 124 (76%) patients: acute GVHD (aGVHD) subtypes (n = 23), overlap GVHD (n = 29), and classic cGVHD (n = 72). In SNP analyses, 9 of the 20 tag SNPs were significant comparing classic/overlap cGVHD versus aGVHD subtypes/no GVHD. In multivariate analyses, 4 recipient BAFF SNPs (rs16972217 [odds ratio = 2.72, P = .004], rs7993590 [odds ratio = 2.35, P = .011], rs12428930 [odds ratio2.53, P = .008], and rs2893321 [odds ratio = 2.48, P = .009]) were independent predictors of GVHD subtypes, adjusted for conventional predictors of cGVHD. This study shows that genetic variation of BAFF modulates GVHD phenotype after allogeneic stem cell transplantation.

Hyperhomocysteinemia in end stage renal disease: is treatment necessary?

Hyperhomocysteinemia occurs in 85% of patients with end stage renal disease (ESRD) and may contribute to their increased risk of cardiovascular disease (CVD). This population experiences excess morbidity and mortality due to CVD, presenting a unique challenge in terms of preventative medicine. The treatment of hyperhomocysteinemia in the renal population has been a topic recently considered in published studies. It is thought, but not yet supported by evidence, that lowering homocysteine (Hcy) levels in ESRD patients will decrease the incidence of CVD. Nephrology nurses need to be aware of the pathophysiology, treatment, and current research regarding hyperhomocysteinemia in patients with ESRD and integrate this knowledge into clinical practice.