Sodium hypochlorite (NaOCl) is the active ingredient in household bleach and is a very common chemical. It has been used in medical and commercial situations dating back to the 18th century for its disinfectant properties, including topical use in medicine as an antiseptic. For this indication, NaOCl is a proven and safe chemical. However, exposure of NaOCl beyond topical use, whether it is intentional or accidental, is associated with significant risks due to its strong oxidizing properties. Potentially damaging scenarios include ingestion, inhalation, deposition into tissue or injection into the bloodstream. All of these scenarios can lead to significant morbidity and even mortality. In this review, we examine the toxicity associated with NaOCl exposure and analyze potential mechanisms of injury, placing special emphasis on the potential for renal toxicity. Due to the extreme ease of access to household bleach products and its use in medicine, it is important for the clinician to understand the potential damage that can occur in NaOCl exposures so that complications can be prevented before they arise.

Although current therapies for pretransplant desensitization and treatment of antibody-mediated rejection (AMR) have had some success, they do not specifically deplete plasma cells that produce antihuman leukocyte antigen (HLA) antibodies. Bortezomib, a proteasome inhibitor approved for the treatment of multiple myeloma (a plasma cell neoplasm), induces plasma cell apoptosis. In this paper we review the current body of literature regarding the use of this biological agent in the field of transplantation. Although limited experience with bortezomib may seem to show promise in the realm of transplant recipients desensitization and treatment of AMR, there is also experience that may suggest otherwise. Bortezomib's role in desensitization protocols and treatment of AMR will be defined better as more clinical data and trials become available.

There is increasing evidence that a low vitamin D status may be an important and hitherto neglected factor of cardiovascular disease. This review is an overview of the current body of literature, and presents evidence of the mechanisms through which vitamin D deficiency affects the cardiovascular system in general and the heart in particular. Available data indicate that the majority of congestive heart failure patients have 25-hydroxyvitamin D deficiency. Furthermore, the low serum 25-hydroxyvitamin D level has a higher impact on hypertension, coronary artery disease an on the occurrence of relevant cardiac events. A serum 25-hydroxyvitamin D level below 75 nmol/l (30 ng/l) is generally regarded as vitamin D insufficiency in both adults and children, while a level below 50 nmol/l (20 ng/l) is considered deficiency. Levels below 50 nmol/l (20 ng/l) are linked independently to cardiovascular morbidity and mortality.

Background: Vitamin D deficiency/insufficiency (VDDI) is common in CKD patients and may be associated with abnormal mineral metabolism. It is not clear whether the K/DOQI recommended doses of ergocalciferol are adequate for correction of VDDI and hyperparathyroidism. Methods: Retrospective study of 88 patients with CKD Stages 1-5 and baseline 25-hydroxyvitamin D level < 30 ng/ml (< 75 nmol/l). Patients treated with ergocalciferol as recommended by K/DOQI guidelines. Only 53 patients had elevated baseline PTH level for the CKD stage. Patients were excluded if they received vitamin D preparations other than ergocalciferol or phosphate binders. 25-hydroxyvitamin D level, intact PTH level (iPTH), and other parameters of mineral metabolism were measured at baseline and after completion of ergocalciferol course. Results: 88 patients with CKD were treated with ergocalciferol. Mean age 56.8 ± 9.5 years and 41% were males. The mean (± SD) GFR was 28.3 ± 16.6 ml/min. At the end of the 6-month period of ergocalciferol treatment, the mean 25-hydroxyvitamin D level increased from 15.1 ± 5.8 to 23.3 ± 11.8 ng/ml (37.75 ± 14.5 to 58.25 ± 29.5 nmol/l) (p < 0.001). Treatment lead to ³ 5 ng/ml (12.5 nmol/l) increases in 25-hydroxyvitamin D level in 54% of treated patients, and only 25% achieved levels ³ 30 ng/ml (75 nmol/l). Mean iPTH level decreased from 157.9 ± 125.9 to 150.7 ± 127.5 pg/ml (p = 0.5). Only 26% of patients had ³ 30% decrease in their iPTH level after treatment with ergocalciferol. Conclusions: Current K/DOQI guidelines are inadequate for correcting VDDI or secondary hyperparathyroidism in CKD patients. Future studies should examine the effects of higher or more frequent dosing of ergocalciferol on these clinical endpoints.

Recipients over 60 yr receiving rATG induction have acceptable renal function and a low risk of rejection; however, reduced survival was noted among those receiving >6 mg/kg. These data suggest that when used, lower cumulative dosages of rATG are preferable in the older recipient.