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Background: Hyperhomocysteinemia (Hhcy) occurs in about 85% of chronic kidney disease (CKD) patients because of impaired renal metabolism and reduced renal excretion. Folic acid (FA), the synthetic form of vitamin B₉, is critical in the conversion of homocysteine (Hcy) to methionine. If there is not enough intake of FA, there is not enough conversion, and Hcy levels are raised. Summary: Hhcy is regarded as an independent predictor of cardiovascular morbidity and mortality in end-stage renal disease. Hhcy exerts its pathogenic action on the main processes involved in the progression of vascular damage. Research has shown Hhcy suggests enhanced risks for inflammation and endothelial injury which lead to cardiovascular disease (CVD), stroke, and CKD. FA has also been shown to improve endothelial function without lowering Hcy, suggesting an alternative explanation for the effect of FA on endothelial function. Recently, the role of FA and Hhcy in CVD and in CKD progression was renewed in some randomized trials. Key Messages: In the general population and in CKD patients, it remains a topic of discussion whether any beneficial effects of FA therapy are to be referred to its direct effect or to a reduction of Hhcy. While waiting for the results of confirmatory trials, it is reasonable to consider FA with or without methylcobalamin supplementation as appropriate adjunctive therapy in patients with CKD.

No abstract

TGF-beta1 was significantly reduced in hemodialysis patients, in particular in those with severe cardiovascular disease. Baseline TGF-beta1, diabetes mellitus and serum albumin levels proved to be the only independent contributors to atherosclerotic risk in dialysis patients.

A mathematical model of solute kinetics oriented to the simulation of hemodialysis is presented. It includes a three-compartment model of body fluids (plasma, interstitial and intracellular), a two-compartment description of the main solutes (K+, Na+, Cl-, urea, HCO3-, H+), and acid-base equilibrium through two buffer systems (bicarbonate and noncarbonic buffers). Tentative values for the main model parameters can be given a priori, on the basis of body weight and plasma concentration values measured before beginning the session. The model allows computation of the amount of sodium removed during hemodialysis, and may enable the prediction of plasma volume and osmolarity changes induced by a given sodium concentration profile in the dialysate and by a given ultrafiltration profile. Model predictions are compared with clinical data obtained during 11 different profiled hemodialysis sessions, both with all parameters assigned a priori, and after individual estimation of dialysances and mass-transfer coefficients. In most cases, the agreement between the time pattern of model solute concentrations in plasma and clinical data was satisfactory. In two sessions, blood volume changes were directly measured in the patient, and in both cases the agreement with model predictions was acceptable. The present model can be used to improve the dialysis session taking some characteristics of individual patients into account, in order to minimize intradialytic unbalances (such as hypotension or disequilibrium syndrome).

Platelet activation and platelet release reactions are lower with PS than with CDA membranes. PDGF-AB, released during and after dialysis, represents a clear biocompatibility marker. Its slow return to basal values and its action on vascular cells make it a potential risk factor for atherosclerosis in uraemic patients.

The newly developed sodium‐glucose cotransporter 2 inhibitors (SGLT2is) effectively modulate glucose metabolism in diabetes. Although clinical data suggest that SGLT2is (empagliflozin, dapagliflozin, ertugliflozin, canagliflozin, ipragliflozin) are safe and protect against renal and cardiovascular events, very little attention has been dedicated to the effects of these compounds on different electrolytes. As with other antidiabetic compounds, some effects on water and electrolytes balance have been documented. Although the natriuretic effect and osmotic diuresis are expected with SGLT2is, these compounds may also modulate urinary potassium, magnesium, phosphate, and calcium excretion. Notably, they have had no effect on plasma sodium levels and promoted only small increases in serum potassium and magnesium concentrations in clinical trials. Moreover, SGLT2is may induce an increase in serum phosphate, FGF‐23, and PTH; reduce 1,25‐dihydroxyvitamin D; and generate normal serum calcium. Some published and preliminary reports, as well as unconfirmed reports have suggested an association with bone fractures. Some homeostasis perturbations are transient, whereas others may persist, suggesting that the administration of SGLT2is may affect electrolyte balances in exposed subjects. Although current evidence supports their safety, additional efforts are needed to elucidate the long‐term impact of these compounds on chronic kidney disease, mineral metabolism, and bone health. Indeed, the limited follow‐up studies and the heterogeneity of the case‐mix of different randomized controlled trials preclude a definitive answer on the impact of these compounds on long‐term outcomes such as the risk of bone fracture. Here we review the current understanding of the mechanisms involved in electrolyte handling and the available data on the clinical implications of electrolytes and mineral metabolism perturbations induced by SGLT2i administration. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

In recent years the high prevalence of diabetes and atherosclerosis in elderly uremic patients starting hemodialysis (HD) has led to the increase in the risk of vascular access (VA) failure caused by pre-existing arterial diseases, including both VA slow maturation and early failure, and upper limb ischemic symptoms. Recently, in performing radial (R), brachial (B) and ulnar (U) artery (A) percutaneous transluminal angioplasty (PTA) in HD patients affected by access thrombosis, with insufficient blood flow and severe upper limb ischemia, good outcomes have been reported. Nevertheless, these procedures were performed after arteriovenous fistula (AVF) creation. About 2 years ago, we approached an intra-operative ultrasound-guided transluminal angioplasty (IUTA) performed during AVF creation, using the arterial incision, necessary because of the anastomosis, to introduce the necessary devices for the IUTA. The arterial stenosis having undergone IUTA was diagnosed by a preliminary ultrasound examination. Ultrasound guidance during the procedure is necessary for correct balloon location in the stenosis site. We treated seven patients (four diabetics), mean age 76 + 5 yrs. In all cases, the radial arteries because of hyposphygmia, were unfit for AVF creation. Four distal radio-cephalic AVFs at the wrist were created in patients 1, 3, 4 and 5; in the other three patients (2, 6 and 7), with failure or thrombosis of previous distal AVFs, an immediately upstream anastomosis was performed. In all cases, first, the area selected to perform the AV anastomosis was exposed, then the AR was incised, and the introductory metallic guide wire and the angioplasty catheter (with dimensions decided after PUS), were introduced. The balloon was inflated to 8-13 atm for 30-35 sec. In two patients a stent was also positioned. Later, a side-to-side AVF was created, closing the distal venous vessel. Patient follow-up ranged from 6-22 months. The ultrasound evaluation after IUTA showed the correction of all the stenosis treated. AVF maturation was good, except for the stented ones, which were inadequate. In conclusion, our early experience shows IUTA could be an adequate and effective procedure allowing the use of the stenotic arteries (otherwise unsuitable) for AVF creation. In our experience, stenting after IUTA does not add any other advantages.