The NT-ProBNP Test in Subjects with End-Stage Renal Disease on Hemodialysis Presenting with Acute Dyspnea: Is Knowing Worth the Cost?

Background. The NT-ProBNP/BNP test has been validated as a marker for determining the etiology of acute dyspnea. In the setting of end-stage renal disease on hemodialysis (ESRD on HD), the utility of the NT-ProBNP/BNP test has not been validated. This study examines the clinical utility of the NT-ProBNP test in the setting of ESRD on HD patients presenting with acute dyspnea. Methods. A retrospective case series of 250 subjects were admitted to Cooper University Hospital, 07/2010-03/2011, with ESRD and HD presenting with dyspnea. The incidences of echocardiography, cardiology consultation, and NT-ProBNP elevated and normal were examined. Correlation coefficients were calculated for NT-ProBNP with age (years), estimated dry weight (kg), amount of fluid removed (L), and ejection fraction (EF in %) among other echocardiography parameters. Results. Of the total sample 235 patients had NT-ProBNP levels performed. Cardiology consults were placed in 68.8% and 58% who underwent echocardiography. Of those for whom an echocardiography was performed estimated mean EFs of 54.6%, 50.8%, and 61.7% were observed among the NT-ProBNP elevated group, normal group, and no NT-ProBNP group, respectively. No differences were detected in all other echocardiography measurements. No correlation was observed between NT-ProBNP and age (r = 0.05), baseline EDW (r = -0.09), amount of fluid removed (r = 0.07), or EF (r = 0.02). Conclusion. In the setting of ESRD on HD, the NT-ProBNP test has no clinical utility in determining the etiology of acute dyspnea. This can be demonstrated through echocardiographic and therapeutic parameters measured in this study.

Pseudo-blood leak? A hemodialysis mystery.

Hydroxocobalamin is a treatment for cyanide toxicity with few side effects. We report a case of a hemodialysis patient whose treatment was compromised by hydroxocobalamin interference with the blood leak detector.

Trace minerals in patients with end-stage renal disease.

The kidneys are famously responsible for maintaining external balance of prevalent minerals, such as sodium, chloride, and potassium. The kidney's role in handling trace minerals is more obscure to most nephrologists. Similarly, the impact of kidney failure on trace mineral metabolism is difficult to anticipate. The associated dietary modifications and dialysis create the potential for trace mineral deficiencies and intoxications. Indeed, there are numerous reports of dialysis-associated mishaps causing mineral intoxication, notable for the challenge of assigning causation. Equally challenging has been the recognition of mineral deficiency syndromes, amid what is often a cacophony of multiple comorbidities that vie for the attention of clinicians who care for patients with chronic kidney disease. In this paper, I review a variety of minerals, some of which are required for maintenance of normal human physiology (the U.S. Food and Drug Administration's list of essential minerals), and some that have attracted attention in the care of dialysis patients. For each mineral, I will discuss its role in normal physiology and will review reported deficiency and toxicity states. I will point out the interesting inter-relationships between several of the elements. Finally, I will address the special concerns of aluminum and magnesium as they pertain to the dialysis population.

Henoch-Schönlein purpura after etanercept therapy for psoriasis.

Etanercept is a recombinant dimeric fusion protein consisting of a tumor necrosis factor-alpha receptor ligand-binding region linked to the Fc portion of human IgG. It is approved for use in the treatment of rheumatoid arthritis, ankylosing spondylitis, juvenile rheumatoid arthritis, psoriasis, and psoriatic arthritis. Since 1998, there have been reports of vasculitic adverse events, including necrotizing vasculitis and leukocytoclastic vasculitis. In addition, the adverse events reporting system of the U.S. Food and Drug Administration has recorded 35 cases of leukocytoclastic vasculitis, 20 after etanercept therapy and 15 after infliximab. Most cases of cutaneous vasculitis describe development of symptoms within 3 months of etanercept use. In only one case report was direct immunofluorescence performed on tissue and no specific immunoreactivity found. We describe the first case of Henoch-Schönlein purpura with acute renal failure associated with increase in etanercept dose after 11 months of use for treatment of psoriasis. Discontinuation of the drug and treatment with a course of systemic steroids led to the complete resolution of the vasculitis and improvement of renal function. Vasculitis occurring even during chronic use of antitumor necrosis factor agents must be considered as possibly related to the therapy.