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Background and objectivesAnemia management changed substantially among dialysis patients in the United States around the time of implementation of the new Centers for Medicare & Medicaid Services bundled payment system and erythropoiesis-stimulating agent (ESA) label change in 2011. Among these, average ferritin levels increased dramatically and have remained high since; this study sought to gain understanding of this sustained rise in ferritin levels.Design, setting, participants, & measurementsTrends in mean ferritin, hemoglobin, IV iron dose, and ESA dose from 2009 to 2013 were examined in 9735 patients from 91 United States Dialysis Outcomes and Practice Patterns Study facilities. Linear mixed models were used to assess the extent to which intravenous (IV) iron and ESA dose accounted for patients' changes in ferritin over time.ResultsMean ESA dose and hemoglobin levels declined throughout the study. Mean IV iron dose increased from 210 mg/mo in 2009-2010 to a peak of 280 mg/mo in 2011, then declined back to 200 mg/mo and remained stable from 2012 to 2013. Mean ferritin increased from 601 ng/ml in the third quarter of 2009 to 887 ng/ml in the first quarter of 2012; models suggest that higher IV iron dosing was a primary determinant during 2011, but lower ESA doses contributed to the sustained high ferritin levels thereafter. In a subset of 17 facilities that decreased IV iron dose in 2011, mean ferritin rose by 120 ng/ml to 764 ng/ml, which appeared to be primarily due to ESA reduction. Together, changes in IV iron and ESA doses accounted for 46% of the increase in ferritin over the study period.ConclusionsIn contrast to expectations, the rise in average IV iron dose did not persist beyond 2011. The sustained rise in ferritin levels in United States dialysis patients after policy changes in 2011, to average levels well in excess of 800 ng/ml, appeared to be partly due to reductions in ESA dosing and not solely IV iron dosing practices. The effect of these changes in ferritin on health outcomes requires further investigation.

The UV absorption spectrum of all-trans-octatetraene is reinvestigated theoretically, focussing on the strongly dipole-allowed 1 A g – 1 B u transition. The dynamical calculations rely on ab initio multistate CASPT2 (MS-CASPT2) computations of the underlying potential energy surfaces and coupling elements, and the multiconfiguration time-dependent Hartree (MCTDH) method for solving the time-dependent Schrödinger equation for the nuclear motion. The vibronic structure of the absorption band near 2700 Å is well reproduced, better than ever before by a purely ab initio approach. The C–C single bond and C = C double bond stretching modes dominate the vibrational structure of the transition. While the latter resembles nearly harmonic motion on weakly coupled potential energy surfaces, the time-dependent calculations reveal a subpicosecond electronic population transfer from the 1 B u state to the lower-lying 2 A g state proceeding on a time scale of ∼ 50 fs . The details of this internal conversion process and its relation to the conical intersection between the two excited states are discussed, paying particular attention to the impact of the 1 B u – 2 A g energy gap on the dynamics. [ABSTRACT FROM AUTHOR]

Uremic malnutrition and chronic inflammation are important comorbid conditions that predict poor clinical outcome in end-stage renal disease (ESRD) patients. These conditions are also closely associated with cardiovascular disease, the major cause of death in ESRD patients. A pathophysiologic link between malnutrition, inflammation, and atherosclerosis has been proposed in this patient population. Indeed, multiple lines of evidence suggest that chronic inflammation can predispose ESRD patients to a catabolic and atherogenic state. Malnutrition can also result from chronic inflammation and can accelerate the progression of cardiovascular disease. Whereas a single common etiology has not been identified in this complex process, nutritional and anti-inflammatory interventions provide potential treatment options to counter the high mortality and morbidity in ESRD patients. Key Words: end-stage renal disease, uremic malnutrition, chronic inflammation, atherosclerosis

Hemodialysis stimulates muscle and whole body protein loss and alters substrate oxidation. Am J Physiol Endocrinol Metab 282: E107-E116, 2002.--The hemodialysis (HD) procedure has been implicated as a potential catabolic factor predisposing the chronic HD (CHD) patients to protein calorie malnutrition. To assess the potential effects of HD on protein and energy metabolism, we studied 11 CHD patients 2 h before, during, and 2 h after HD by use of primed constant infusion of L-[1-[sup.13]C]leucine and L-[ring-[sup.2][H.sub.5]]phenylalanine. Our results showed that HD led to increased whole body (10%) and muscle protein (133%) proteolysis. Simultaneously, whole body protein synthesis did not change, and forearm synthesis increased (120%). The net result was increased net whole body protein loss (96%) and net forearm protein loss (164%). During the 2-h post-HD period, the muscle protein breakdown trended toward baseline, whereas whole body protein breakdown increased further. Substrate oxidation during the post-HD was significantly altered, with diminished carbohydrate and accelerated lipid and amino acid oxidation. These data demonstrate that hemodialysis is an overall catabolic event, decreasing the circulating amino acids, accelerating rates of whole body and muscle proteolysis, stimulating muscle release of amino acids, and elevating net whole body and muscle protein loss. catabolism; malnutrition; inflammation; energy expenditure; metabolism

A synthetic membrane used in dialysis treatments may be more effective than the standard cuprophane membrane in improving kidney function. A study of 72 patients with acute kidney failure undergoing hemodialysis to cleanse their blood found the synthetic polymethyl methacrylate membrane to be associated with a higher survival rate than the cuprophane membrane (80% versus 40%). The synthetic membrane may be more compatible with the body than the cuprophane membrane. This may enable patients with acute kidney failure to recover kidney function, and enable long-term dialysis patients to retain some kidney function for a longer period of time. The synthetic membrane may not activate the body's white blood cells as does the cuprophane membrane. This could may make a difference in the success of dialysis for patients with oliguria (reduced urine output). The synthetic membrane may cost more than the cuprophane membrane, but the improved treatment rate may more than pay for the difference.