Search

Aims: Direct oral anticoagulant (DOAC) has been recently introduced in the clinical practice. Rather than interfering with vitamin K-dependent posttranscriptional modification of various proteins, DOACs selectively inhibit factors involved in the coagulation cascade. In particular, in contrastwithWarfarin, Rivaroxabn does not interfere with activation of matrix Gla Protein (MGP), a potent vascular calcification Inhibitor. We herein sought to investigate the impact of Rivaroxaban and Warfarin on cardiac valve calcifications in a cohort of moderate-to advanced CKD patients. Methods and results: This is amulticenter, observational, retrospective, longitudinal study. Consecutive CKD stage 3b – 4 (according to KDIGO guidelines) patients from8 cardiologic outpatient clinicswere enrolled betweenMay 2015 and October 2017. All patients received anticoagulation (100Warfarin vs 247 Rivaroxaban) as part of their non-valvular atrial fibrillation management. Cardiac valve calcificationwas evaluated via standard trans-thoracic echocardiogram. 347 patients (mean age: 66 years;mean eGFR: 37 ml/min/1.73m2) were studied. Over a mean follow-up period of 16 months, Rivaroxaban compared toWarfarin reduced both mitral and aortic valve calcifications (p b 0.001) independently of the degree of calcifications at baseline and potential confounders. Notably, Rivaroxaban use was also associated with a significant reduction in C reactive protein (CRP) (p b 0.001) during follow-up. Conclusion: This study generates the hypothesis that the use of Rivaroxaban associateswith a reduction of cardiac valve calcification deposition and progression as compared to Warfarin, in a cohort of CKD stage 3b-4 patients. Future endeavors are needed to confirm and to establish the mechanisms responsible for these findings.

Postdialytic rebound (PDR) of plasma solutes is a relevant drawback of intermittent hemodialysis, but its pathophysiological process remains undefined. We assessed the independent effects of efficiency and length of dialytic session on PDR of urea, phosphate, and potassium.Uremic patients were evaluated at the beginning and end of dialysis and after 180 minutes in 2 randomized crossover studies. In study 1, we compared the effect of standard versus higher efficiency acetate-free biofiltration (AFB) while maintaining the same duration of 4 hours. In study 2, we compared the effect of 3- versus 5-hour AFB sessions while maintaining similar efficiency.In study 1, greater Kt/V (1.49 +/- 0.20 versus 1.22 +/- 0.15; P0.0001) was coupled with significant increases in both absolute removal and PDR of urea and phosphate (PDR of urea, +45% versus +29%; PDR of phosphate, +79% versus +52%), but not of potassium. Similarly, in study 2, shortening the AFB session while maintaining similar absolute removal and Kt/V (1.28 +/- 0.09 versus 1.31 +/- 0.09) significantly increased PDR of urea and phosphate (PDR of urea, +32% versus +19%; PDR of phosphate, +63% versus +36%), but not of potassium. In both studies, greater PDRs of urea and phosphate were associated with estimated greater removal of these solutes per hour.The rate of removal of phosphate and urea is a critical determinant of their PDR; conversely, potassium is not influenced by removal rate, likely because of its marked cell compartmentalization.

Supplemented very low protein diet ameliorates responsiveness to erythropoietin in chronic renal failure.BackgroundThe aim of this study was to evaluate the relationship between uremic state and erythropoiesis in patients with predialytic chronic renal failure (CRF).MethodsWe monitored for 2years the erythropoietin (EPO) requirement in patients with advanced CRF (creatinine clearance ≤25mL/min), randomized to either low protein diet (LPD) group (0.6g/kg body weight/day, N = 10) or very low protein diet (VLPD) group (0.3g/kg body weight/day, N = 10) supplemented with a mixture of ketoanalogs and essential amino acids, both kept at target hemoglobin levels.ResultsThe achieved protein intake after 6months was 0.79 ± 0.02g/kg body weight/day and 0.50 ± 0.02g/kg body weight/day in LPD and VLPD, respectively; such a difference was maintained up to the end of follow up. The final hemoglobin values did not differ from the basal values in either group (11.5 ± 0.2g/dL and 11.5 ± 0.3g/dL). EPO dose, that was similar at baseline (62.4 ± 9.6 UI/kg body weight/week and 61.8 ± 8.8 UI/kg body weight/week subcutaneously), remained unchanged in LPD but progressively decreased in VLPD down to the final value of 41.2 ± 7.0 UI/kg body weight/week (P < 0.0001 vs. basal and LPD). VLPD was associated with a decrease of urinary excretion and serum levels of urea nitrogen and phosphate; however, EPO requirement was not correlated with the changes of these parameters. On the contrary, the variation of EPO dose directly correlated with the modification of parathyroid hormone (PTH) levels, that diminished from 229 ± 55pg/mL to 118 ± 16pg/mL (P < 0.0001) in VLPD and did not change in LPD.ConclusionIn patients with advanced CRF, an effective decrease of protein intake of 0.3g/kg body weight/day induces a reduction of about 35% of the EPO dose required to maintain the target hemoglobin levels. This effect appears dependent on the correction of a moderate secondary hyperparathyroidism.

To the Editor: We read with interest the recent article by Ikizler et al demonstrating that, in a 15-month follow-up period, the relative risk of hospitalization determined in 73 unselected hemodialysis (HD) patients increased to 9% and 14% as their reactance (Xc) values decreased from 70 ohm to Xc = 43 and Xc = 31 ohm, respectively1. With equal interest we read the Letter to the Editor by Piccoli et al, which demonstrated that the Xc distribution in either healthy or uremic patients is dependent on race-ethnicity, gender, body mass and soft tissue hydration2. Piccoli et al demonstrated that low Xc is found not only in malnutrition patients, but, for example, also in obese HD patients.