Potential Benefits of Renal Diets on Cardiovascular Risk Factors in Chronic Kidney Disease Patients

Dietary manipulation, including protein, phosphorus, and sodium restriction, when coupled with the vegetarian nature of the renal diet and ketoacid supplementation can potentially exert a cardiovascular protective effect in chronic renal failure patients by acting on both traditional and nontraditional cardiovascular risk factors. Blood pressure control may be favored by the reduction of sodium intake and by the vegetarian nature of the diet, which is very important also for lowering serum cholesterol and improving plasma lipid profile. The low protein and phosphorus intake has a crucial role for reducing proteinuria and preventing and reversing hyperphosphatemia and secondary hyperparathyroidism, which are major causes of the vascular calcifications, cardiac damage, and mortality risk of uremic patients. The reduction of nitrogenous waste products and lowering of serum PTH levels may also help ameliorate insulin sensitivity and metabolic control in diabetic patients, as well as increase the responsiveness to erythropoietin therapy, thus allowing greater control of anemia. Protein-restricted diets may have also anti-inflammatory and anti-oxidant properties. Thus, putting aside the still debatable effects on the progression of renal disease and the more admitted effects on uremic signs and symptoms, it is possible that a proper nutritional treatment early in the course of renal disease may be useful also to reduce the cardiovascular risk in the renal patient. However, conclusive data cannot yet be drawn because quality studies are lacking in this field; future studies should be planned to assess the effect of renal diets on hard outcomes, as cardiovascular events or mortality

Review—Innovative Polymeric Materials for Better RechargeableBatteries: Strategies from CIC Energigune

The need for sustainable energy sources and their efficient utilization has motivated extensive explorations of new electrolytes, electrodes, and alternative battery chemistries departing from current lithium-ion battery ( LIB) technologies. The evolution and development of rechargeable batteries are tightly linked to the research of polymeric materials, such as polymer electrolytes and redox-active polymeric electrodes, separators, and binders, etc. In this contribution, we review the recent progresses on polymer electrolytes and redox-active polymeric electrodes developed in CIC Energigune with particular attention paid to the molecular designing and engineering. On the basis of our knowledge and experience accumulated in rechargeable batteries, further developments and improvements on the properties of these polymeric materials for building better rechargeable batteries are discussed. (c) The Author(s) 2019. Published by ECS.This work was supported by GV-ELKARTEK-2016 from the Basque Government, and MINECO RETOS (Ref: ENE2015-64907-C2-1-R) from Spanish Government. H.Z. thanks the Basque Government for the Berrikertu program (1-AFW-2017-2). This manuscript is dedicated to the 73th birthday of Prof. Dr. Michel Armand, who ushered theoretical concepts leading to practical applications in energy-related electrochemistry

Reduced parathyroid functional mass after successful kidney transplantation

Reduced parathyroid functional mass after successful kidney transplantation.BackgroundChronic uremia is responsible for secondary hyperparathyroidism (HPT II). Parathyroid secretion usually tends to normalize after kidney transplantation (KT), but the parameters of the reversibility of HPT II remain poorly defined, particularly the intrinsic mechanisms underlying the improvement of parathyroid function.MethodsThe kinetic functional parameters of the ionized calcium (iCa)/parathormone (PTH) relationship curve were studied in 11 patients with mild to moderate HPT II one and six months after successful KT. Hypercalcemia and hypocalcemia were induced, respectively, by CaCl2 and Na2-ethylenediaminetetraacetic acid (Na2-EDTA) infusions.ResultsThe mean glomerular filtration rate remained stable during follow-up. Basal PTH decreased from 195 ± 54 pg/ml before KT to 70 ± 12 pg/ml six months later (P < 0.005). During the tests, mean PTH levels decreased significantly between the two measured times for all iCa levels, indicating an improved parathyroid function. An analysis of the kinetic parameters of the curves showed significant decreases of the mean maximal and minimal PTH levels, respectively, from 340 ± 91 to 220 ± 30 pg/ml (P = 0.03) and from 25 ± 6 to 15 ± 5 pg/ml (P = 0.005). On the other hand, no change was noted in the parathyroid-cell calcium-sensitivity parameters (slope, set point) assessed using two different approaches, either the entire curve or the limited calcium-mediated suppression curve.ConclusionImprovement of the parathyroid function between the first and sixth months post-KT seems mainly attributable to a reduction of the parathyroid functional mass

Nutrition in hemodialysis patients previously on a supplemented very low protein diet

Nutrition in hemodialysis patients previously on a supplemented very low protein diet.BackgroundNutritional safety of protein-restricted diets in patients with chronic renal failure is controversial. In the present study, we have assessed the evolution of nutritional status after initiation of hemodialysis in patients previously treated by a supplemented very low protein diet (SVLPD).MethodsNutritional data were prospectively collected during the first year of hemodialysis from 15 consecutive patients treated with a SVLPD (0.3 g protein/kg/day supplemented with essential amino acids, calcium, iron, and vitamins) and compared to 15 age- and gender-matched end-stage renal disease (ESRD) patients previously on a less-restricted diet (0.90 ± 0.21 g protein/kg/day) who started hemodialysis during the same period. Dual-energy x-ray absorptiometry (DEXA) was used to assess body composition at 0, 6, and 12 months. Hemodialysis prescriptions, biologic data and 3-day food records were collected every 3 months.ResultsProtein intake was higher than 1.2 g/kg/day in both groups as soon as 3 months after the start of hemodialysis. Albumin and prealbumin increased significantly during the first 6 months in all patients. Body mass index (BMI) increased in all patients (+0.97 ± 1.31 kg/m2; P < 0.001) reflecting a gain in fat mass in the overall population (+2.36 ± 2.94 kg/m2; P < 0.001) while lean body mass remained stable overall.ConclusionOnce on hemodialysis, SVLPD patients rapidly increased protein intake. Nutritional status improved in all patients, with a gain in fat mass in all, and a gain in lean body mass in SVLPD men only. These data indicate that treatment with a SVLPD prior to hemodialysis initiation is nutritionally safe

Improvement of leucocytic Na+K+ pump activity in uremic patients on low protein diet

Improvement of leucocytic Na+ K+ pump activity in uremic patients on low protein diet. Leucocytic Na+K+ pump activity was assessed in 20 patients with advanced renal failure. Na+K+-ATPase activity was reduced when compared with the values obtained from normal subjects (101.8 ± 48.6 versus 165.13 ± 8.9 µM of Pi hr-1 · g-1 P < 0.001) and the mean 86Rb uptake by U 937 cells was depressed by 38% after the addition of patients' sera. Subsequently, patients were put on a diet providing 0.3g protein/kg body weight daily and supplemented with ketoacids. After three months of dietary treatment Na+K+-ATPase activity increased to 142 ± 48.3 (P < 0.01) and reached normal values at the sixth month (162.8 ± 54.70 µM of Pi hr-1 · g-1; P < 0.001) whereas 86Rb uptake increased by 23 percent when compared to initial values. These data suggest that among the different mechanisms which have been advanced to explain the defects in the Na+ pump observed in uremic patients, circulating inhibitors deriving from alimentary protein intake may affect cation transport

A Central Nervous System Focused Treatment Program for People with Frozen Shoulder: A Feasibility Study

Background: Frozen shoulder (FS) is a highly disabling pathology of poorly understood etiology, which is characterized by the presence of intense pain and progressive loss of range of motion (ROM). The aim of this study is to evaluate the feasibility and clinical impact of a CNS-focused treatment program for people with FS. Methods: 10 subjects with primary FS received a 10-week CNS-focused intervention including sensory discrimination training and graded motor imagery techniques delivered as clinic sessions (60 min) and home therapy (30 min five times per week). Measurements were taken at baseline, after a 2-week 'washout' period, after treatment, and at three months followup. The Shoulder Pain and Disability Index (SPADI) was the primary outcome. Secondary measures were feasibility-related outcomes, self-reported shoulder pain, active and passive range of motion, two-point discrimination threshold (TPDT), left/right judgement task (LRJT), fear-avoidance (Tampa Scale for Kinesiophobia), pain catastrophization (Pain Catastrophizing Scale), and pain sensitization (Central Sensitization Inventory). A Student's t-test was used to assess the 'washout' period. A repeated measure analysis of variance (ANOVA) was used to evaluate within-subjects' differences for all outcome measures in the different assessment periods and a pairwise analysis was used to compare between the different assessment points. Statistical significance was set at p < 0.05. Results: 70% of participants completed the treatment. No significant changes were found after 'washout' period except for TPDT (p = 0.02) and SPADI (p = 0.025). Improvements in self-reported shoulder pain (p = 0.028) and active shoulder flexion (p = 0.016) were shown after treatment (p = 0.028) and follow-up (p = 0.001) and in SPADI at follow-up (p = 0.008). No significant changes were observed in TPDT, LRJT, fear-avoidance, pain catastrophization, and pain sensitization. Conclusions: a CNS-focused treatment program might be a suitable approach to improve pain and disability in FS, but further research is needed to draw firm conclusions

Pathogenic Mouse Hepatitis Virus or Poly(I:C) Induce IL-33 in Hepatocytes in Murine Models of Hepatitis.

International audienceThe IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33