In hemodialysis patients, blood pressure variability (BPV) is associated with cardiovascular events and all-cause mortality. However, previous research has predominantly concentrated on the predialysis BPV. In contrast, intradialytic BPV, reflecting the cardiovascular regulatory function during the process of rapid clearance of volume overload, holds greater relevance to the prognosis of patients. In this study, a latent category trajectory model was used to identify the patterns of intradialytic BPV and analyze the association between intradialytic BPV and the cardio-cerebrovascular events and other clinical outcomes. We found the variation of intradialytic systolic blood pressure (SBP) was associated with the risk of cardio-cerebrovascular events in hemodialysis patients. Patients in "SBP Class 4" and "SBP Class 3" subgroups were associated with the occurrence of cardio-cerebrovascular events and the number of cardio-cerebrovascular event hospitalizations during the follow-up period. This indicates that the variation pattern of intradialytic SBP results from the comprehensive action of various BP regulatory mechanisms in the body, which can reflect the level of cardiovascular regulatory function in hemodialysis patients and serve as a predictor of recent adverse cardio-cerebrovascular events.

Abnormal fluid and plasma sodium concentrations are established prognostic factors for patients on hemodialysis. However, the cumulative effects of abnormal salt and water and potential effect modifications and the effect of dialysate sodium remain incompletely understood.

The study followed 68,196 patients on incident hemodialysis from 875 dialysis clinics in 25 countries over 10 years (2010–2020) investigating dose-response patterns between cumulative exposure time of fluid overload/depletion (measured by bioimpedance spectroscopy using the Fresenius Body Composition Monitor), abnormal plasma sodium levels, low dialysate sodium, and all-cause mortality. We calculated time-varying cumulative exposure (in months) of relative fluid overload (any degree; >7% or severe; >13 or >15% in women or men, respectively) and fluid depletion (<−7%), hypo- or hypernatremia (sodium <135 or >145 mmol/L, respectively), low dialysate sodium (≤138 mmol/L), and estimated hazard ratios for all-cause mortality using a multivariable Cox model.

Of 2,123,957 patient-months, 61% were spent in any degree of fluid overload, 4% in fluid depletion, 11% in hyponatremia, and 1% in hypernatremia. Any degree of fluid overload was associated with higher all-cause mortality (hazard ratio peak at 3.42 [95% confidence intervals, 3.12 to 3.75] relative to no exposure), and this association with all-cause mortality seemed to be stronger with severe fluid overload. The risk pattern associated with hyponatremia was approximately linear in the first four patient-months and then plateaued after the fourth patient-month. We did not observe effect modification between fluid overload and hyponatremia.

Even mild fluid overload was associated with higher mortality in patients on hemodialysis. Whether more stringent fluid management results in clinical improvement requires further investigation.

To examine the relationship between cognitive impairment and body composition indicators in chronic kidney disease (CKD) patients post-hemodialysis.

This retrospective study included 110 CKD patients admitted to Beijing Luhe Hospital, Capital Medical University between January 2019 and January 2023. General clinical data and body composition indicators were compared between patients with and without cognitive impairment. Multiple logistic regression and ROC curve analysis were used to identify influencing factors and to develop a predictive model.

Cognitive impairment occurred in 50% of the patients post-hemodialysis. No significant differences were found in demographics, disease duration, comorbidities, or hemodialysis duration between the groups (all P > 0.05). However, significant differences were observed in body mass index (BMI) (P < 0.001), lean body mass index (LTI) (P = 0.007), fat tissue index (FTI) (P = 0.024), and total body water (TBW) (P < 0.001). Multiple logistic regression identified TBW (OR 4.900, 95% CI 3.062-7.511, P < 0.001), the TBW/extracellular water (ECW) ratio (OR 7.244, 95% CI 5.092-8.7613, P = 0.016), and the ECW/body cell mass (BCM) ratio (OR 6.720, 95% CI 4.564-8.692, P = 0.030) as independent risk factors for cognitive impairment post-hemodialysis. ROC analysis confirmed their predictive capacity, with AUC values of 0.840, 0.840, and 0.850 respectively. A predictive model incorporating these indicators was developed, showing good calibration (Hosmer-Lemeshow test, P = 0.912) and discrimination (C-index 0.974, 95% CI 0.952-0.997).

Total body water, the TBW/ECW ratio, and the ECW/BCM ratio are independently associated with cognitive impairment in CKD patients post-hemodialysis. Body composition analysis serves as a valuable tool for predicting cognitive impairment in this population, guiding clinicians in assessing cognitive function and planning interventions for these patients.

Defining the optimal hydration status in patients with chronic kidney disease (CKD) is challenging, and the quest for an objective accurate method continues. Lung ultrasound (LUS) is a well-validated technique to estimate volume status. Previous studies examining the relationship between LUS and physical examination demonstrated conflicting results. We aimed to evaluate the correlation between LUS results and physical examination for assessing volume status in patients with CKD, and to compare different LUS protocols.

A prospective, single-center trial correlating physical examination findings to LUS results in different CKD groups, including non-dialysis and dialysis patients. Hemodialysis patients were tested twice, before and after dialysis, to compare results with ultrafiltration volume. Different LUS protocols were performed and compared, including 16-, 12-, and 8-zone measurements.

We recruited 175 participants. A strong positive correlation was demonstrated between 16- and 12-zone protocols [r = .91 (P < .001)] and between 12- and 8-zone protocols (r = .951, P < .001). Correlation was significant in various CKD groups. While blood pressure did not correlate with LUS score, there was a significant correlation between LUS and other components of the physical examination including lung crackles (OR = 1.15 (95%CI 1.096-1.22), P < .01), pleural effusion (OR = 1.15 (95%CI 1.09-2.13), P < .01) and peripheral edema (r = .24, P < .001). Ultrafiltration volume did not correlate significantly with change in LUS scores pre- and post-dialysis (r = .169, P = .065).

Most components of physical examination findings correlated with extravascular lung water assessment on LUS in CKD patients. The use of a simplified pragmatic LUS protocol may facilitate LUS use in clinical practice.

This large observational cohort study aimed to investigate the relationship between dialysate and plasma sodium concentrations and mortality among maintenance hemodialysis patients. Using a large multinational cohort of 68,196 patients, we found that lower dialysate sodium concentrations (≤138 mmol/L) were independently associated with higher mortality compared with higher dialysate sodium concentrations (>138 mmol/L). The risk of death was lower among patients exposed to higher dialysate sodium concentrations, regardless of plasma sodium levels. These results challenge the prevailing assumption that lower dialysate sodium concentrations improve outcomes in hemodialysis patients. The study confirms that until robust evidence from randomized trials that are underway is available, nephrologists should remain cautious in reconsideration of dialysate sodium prescribing practices to optimize cardiovascular outcomes and reduce mortality in this population.

Excess mortality in hemodialysis (HD) patients is largely due to cardiovascular disease and is associated with abnormal fluid status and plasma sodium concentrations. Ultrafiltration facilitates the removal of fluid and sodium, whereas diffusive exchange of sodium plays a pivotal role in sodium removal and tonicity adjustment. Lower dialysate sodium may increase sodium removal at the expense of hypotonicity, reduced blood volume refilling, and intradialytic hypotension risk. Higher dialysate sodium preserves blood volume and hemodynamic stability but reduces sodium removal. In this retrospective cohort, we aimed to assess whether prescribing a dialysate sodium ≤138 mmol/L has an effect on survival outcomes compared with dialysate sodium >138 mmol/L after adjusting for plasma sodium concentration.

The study population included incident HD patients from 875 Fresenius Medical Care Nephrocare clinics in 25 countries between 2010 and 2019. Baseline dialysate sodium (≤138 or >138 mmol/L) and plasma sodium (<135, 135-142, >142 mmol/L) concentrations defined exposure status. We used multivariable Cox regression model stratified by country to model the association between time-varying dialysate and plasma sodium exposure and all-cause mortality, adjusted for demographic and treatment variables, including bioimpedance measures of fluid status.

In 2,123,957 patient-months from 68,196 incident HD patients with on average three HD sessions per week dialysate sodium of 138 mmol/L was prescribed in 63.2%, 139 mmol/L in 15.8%, 140 mmol/L in 20.7%, and other concentrations in 0.4% of patients. Most clinical centers (78.6%) used a standardized concentration. During a median follow-up of 40 months, one third of patients ( n =21,644) died. Dialysate sodium ≤138 mmol/L was associated with higher mortality (multivariate hazard ratio for the total population (1.57, 95% confidence interval, 1.25 to 1.98), adjusted for plasma sodium concentrations and other confounding variables. Subgroup analysis did not show any evidence of effect modification by plasma sodium concentrations or other patient-specific variables.

These observational findings stress the need for randomized evidence to reliably define optimal standard dialysate sodium prescribing practices.

Alport syndrome is a rare genetic disease that results in disordered basement membrane type IV collagen resulting in haematuria, proteinuria and often development of renal fibrosis leading to progressive kidney disease. The therapeutic blockage of the renin-angiotensin-aldosterone system, which slows the progression to kidney failure, is supported by strong evidence. Recent clinical trials using sodium-glucose co-transporter-2 (SGLT2) inhibitors and mineralocorticoid receptor antagonists (MRA) in patients with chronic kidney disease have changed the therapeutic landscape. Patients with Alport syndrome and progressive kidney disease may benefit from treatment with MRAs because research has shown that these drugs are nephroprotective through a variety of mechanisms, including by preventing fibrosis. Ongoing clinical trials show great promise in order to help establish the long-term safety and efficacy of Finerenone, a MRA. This review discusses the evidence for the use of MRAs as a potential treatment in Alport syndrome that may slow the progression of chronic kidney disease and prevent patients reaching kidney failure.

The 5-year mortality rate for haemodialysis patients is over 50%. Acute and chronic disturbances in salt and fluid homeostasis contribute to poor survival and are established as individual mortality risk factors. However, their interaction in relation to mortality is unclear.

We used the European Clinical Database 5 to investigate in a retrospective cohort analysis the relationship between transient hypo- and hypernatremia, fluid status and mortality risk of 72 163 haemodialysis patients from 25 countries. Incident haemodialysis patients with at least one valid measurement of bioimpedance spectroscopy were followed until death or administrative censoring from 1 January 2010 to 4 December 2019. Fluid overload and depletion were defined as >2.5 L above, and -1.1 L below normal fluid status, respectively. N = 2 272 041 recorded plasma sodium and fluid status measurements were available over a monthly time grid and analysed in a Cox regression model for time-to-death.

Mortality risk of hyponatremia (plasma sodium <135 mmol/L) was slightly increased when fluid status was normal [hazard ratio (HR) 1.26, 95% confidence interval (CI) 1.18-1.35], increased by half when patients were fluid depleted (HR 1.56, 95% CI 1.27-1.93) and accelerated during fluid overload (HR 1.97, 95% CI 1.82-2.12).

Plasma sodium and fluid status act independently as risk factors on mortality. Patient surveillance of fluid status is especially important in the high-risk subpopulation of patients with hyponatremia. Prospective patient-level studies should examine the effects of chronic hypo- and hypernatremia, risk determinants, and their outcome risk.

Machine Learning has been increasingly used in the medical field, including managing patients undergoing hemodialysis. The random forest classifier is a Machine Learning method that can generate high accuracy and interpretability in the data analysis of various diseases. We attempted to apply Machine Learning to adjust dry weight, the appropriate volume status of patients undergoing hemodialysis, which requires a complex decision-making process considering multiple indicators and the patient's physical conditions.

All medical data and 69,375 dialysis records of 314 Asian patients undergoing hemodialysis at a single dialysis center in Japan between July 2018 and April 2020 were collected from the electronic medical record system. Using the random forest classifier, we developed models to predict the probabilities of adjusting the dry weight at each dialysis session.

The areas under the receiver-operating-characteristic curves of the models for adjusting the dry weight upward and downward were 0.70 and 0.74, respectively. The average probability of upward adjustment of the dry weight had sharp a peak around the actual change over time, while the average probability of downward adjustment of the dry weight formed a gradual peak. Feature importance analysis revealed that median blood pressure decline was a strong predictor for adjusting the dry weight upward. In contrast, elevated serum levels of C-reactive protein and hypoalbuminemia were important indicators for adjusting the dry weight downward.

The random forest classifier should provide a helpful guide to predict the optimal changes to the dry weight with relative accuracy and may be useful in clinical practice.

Hemodialysis is life-sustaining in kidney failure. However, proper regulation of body fluids depends on an accurate estimate of target weight. This trial aims to compare clinical endpoints between target weight estimation guided by bioimpedance spectroscopy and usual care in hemodialysis patients.

This is an open-label, parallel-group, controlled trial that randomized, through a table of random numbers, adult patients on maintenance hemodialysis to target weight estimation based on monthly clinical evaluation alone or added to evaluation by bioimpedance twice a year. The primary outcome was survival, and the secondary outcomes were the rate of hospital admissions, change in blood pressure (BP), and antihypertensive drugs load. Participants were followed for 2 years. Survival analysis was performed using Kaplan-Meier estimator and Log-rank test, and hospital admissions were analyzed by the incidence-rate ratio.

One hundred and ten patients were randomized to the usual care (52) or bioimpedance (58) groups, with a mean age of 57.4 (15.4) years, 64 (58%) males. There was no difference between the groups at baseline. Survival was not significantly different between groups (log-rank test p = 0.68), but the trial was underpowered for this outcome. There was also no difference between the groups in the change in systolic or diastolic BP or in the number of antihypertensive drugs being used. The incidence rate of hospital admissions was 3.1 and 2.1 per person-year in usual care and bioimpedance groups, respectively, with a time-adjusted incidence rate ratio of 1.48 (95% CI: 1.20-1.82, p = 0.0001) and attributable fraction of risk among exposed individuals of 0.32 (95% CI: 0.17-0.45).

The inclusion of bioimpedance data to guide the estimation of target weight in hemodialysis patients had no detectable impact on survival or BP control, but significantly reduced the incidence rate of hospital admissions. The study was registered at ClinicalTrials.gov Identifier: NCT05272800.

New physiologic findings related to sodium homeostasis and pathophysiologic associations require a new vision for sodium, fluid and blood pressure management in dialysis-dependent chronic kidney disease patients. The traditional dry weight probing approach that has prevailed for many years must be reviewed in light of these findings and enriched by availability of new tools for monitoring and handling sodium and water imbalances. A comprehensive and integrated approach is needed to improve further cardiac health in hemodialysis (HD) patients. Adequate management of sodium, water, volume and hemodynamic control of HD patients relies on a stepwise approach: the first entails assessment and monitoring of fluid status and relies on clinical judgement supported by specific tools that are online embedded in the HD machine or devices used offline; the second consists of acting on correcting fluid imbalance mainly through dialysis prescription (treatment time, active tools embedded on HD machine) but also on guidance related to diet and thirst management; the third consist of fine tuning treatment prescription to patient responses and tolerance with the support of innovative tools such as artificial intelligence and remote pervasive health trackers. It is time to come back to sodium and water imbalance as the root cause of the problem and not to act primarily on their consequences (fluid overload, hypertension) or organ damage (heart; atherosclerosis, brain). We know the problem and have the tools to assess and manage in a more precise way sodium and fluid in HD patients. We strongly call for a sodium first approach to reduce disease burden and improve cardiac health in dialysis-dependent chronic kidney disease patients.

The development of maintenance hemodialysis (HD) for end stage kidney disease patients is a success story that continues to save many lives. Nevertheless, intermittent renal replacement therapy is also a source of recurrent stress for patients. Conventional thrice weekly short HD is an imperfect treatment that only partially corrects uremic abnormalities, increases cardiovascular risk, and exacerbates disease burden. Altering cycles of fluid loading associated with cardiac stretching (interdialytic phase) and then fluid unloading (intradialytic phase) likely contribute to cardiac and vascular damage. This unphysiologic treatment profile combined with cyclic disturbances including osmotic and electrolytic shifts may contribute to morbidity in dialysis patients and augment the health burden of treatment. As such, HD patients are exposed to multiple stressors including cardiocirculatory, inflammatory, biologic, hypoxemic, and nutritional. This cascade of events can be termed the dialysis stress storm and sickness syndrome. Mitigating cardiovascular risk and morbidity associated with conventional intermittent HD appears to be a priority for improving patient experience and reducing disease burden. In this in-depth review, we summarize the hidden effects of intermittent HD therapy, and call for action to improve delivered HD and develop treatment schedules that are better tolerated and associated with fewer adverse effects.

The relationship between Na+ balance and cardiovascular disease (CVD) in hemodialysis (HD) patients is not yet fully understood. We hypothesized that HD patients co-diagnosed with CVD show increased tissue Na+ accumulation compared to HD patients without CVD.

In our observational study 52 HD patients were divided into a group with (23 subjects) or without (29 subjects) a positive history of cardiovascular events. We used 23Na-Magnetic Resonance Imaging (23Na-MRI) at 3.0 Tesla to quantify Na+ content in skin and muscle of both groups directly before and after HD. Additionally, total body fluid distribution was determined by Bioimpedance Spectroscopy (BIS) and laboratory parameters were assessed.

Compared to HD patients without CVD, 23Na-MRI detected an increased Na+ content in skin (21.7 ± 7.3 vs. 30.2 ± 9.8 arbitrary units, a.u., p < 0.01) and muscle tissue (21.5 ± 3.6 vs 24.7 ± 6.0 a.u., p < 0.05) in patients with previous CVD events. Simultaneously measured fluid amount by BIS, including excess extracellular water (1.8 ± 1.7 vs. 2.2 ± 1.7 L, p = 0.44), was not significantly different between both groups. Tissue Na+ accumulation in HD-CVD patients was paralleled by a higher plasma concentration of the inflammation marker Interleukin-6 (5.1, IQR 5.8 vs. 8.5, IQR 7.9 pg/ml, p < 0.05).

In our cohort, HD patients with CVD showed higher tissue Na+ content than HD patients without CVD, while no difference in body water distribution could be detected between both groups. Our findings provide evidence that the history of a cardiovascular event is associated with disturbances in tissue Na+ content in HD patients.

Chronic kidney disease (CKD) is associated with a higher prevalence of vascular calcification (VC) and cardiovascular disease. VC in CKD patients showed different pathophysiological features from those of the general population. The pathogenesis of VC in CKD is a highly organized process, and prior studies have suggested that patients with CKD have their own specific contributors to the phenotypic change of vascular smooth muscle cells (VSMCs), including uremic toxins, CKD-mineral and bone disease (CKD-MBD), inflammation, and oxidative stress. For the diagnosis and monitoring of VC in CKD, several imaging modalities, including plain radiography, ultrasound, and computed tomography have been utilized. VC in CKD patients has distinct clinical features and implications. CKD patients revealed a more intense and more prevalent calcification on the intimal and medial layers, whereas intimal calcification is predominantly observed in the general population. While a higher VC score is clearly associated with a higher risk of all-cause mortality and cardiovascular events, a greater VC score in CKD patients does not fully reflect the burden of atherosclerosis, because they have more calcification at equal volumes of atheromatous plaques. The primary goal of VC treatment in CKD is the prevention of VC progression, and the main management is to control the biochemical components of CKD-MBD. Cinacalcet and non-calcium-containing phosphate binders are the mainstay of VC prevention in CKD-MBD management. VC in patients with CKD is an ongoing area of research and is expected to advance soon.

Hemodialysis (HD) is a life-sustaining therapy as well as an intermittent and repetitive stress condition for the patient. In ridding the blood of unwanted substances and excess fluid from the blood, the extracorporeal procedure simultaneously induces persistent physiological changes that adversely affect several organs. Dialysis patients experience this systemic stress condition usually thrice weekly and sometimes more frequently depending on the treatment schedule. Dialysis-induced systemic stress results from multifactorial components that include treatment schedule (i.e. modality, treatment time), hemodynamic management (i.e. ultrafiltration, weight loss), intensity of solute fluxes, osmotic and electrolytic shifts and interaction of blood with components of the extracorporeal circuit. Intradialytic morbidity (i.e. hypovolemia, intradialytic hypotension, hypoxia) is the clinical expression of this systemic stress that may act as a disease modifier, resulting in multiorgan injury and long-term morbidity. Thus, while lifesaving, HD exposes the patient to several systemic stressors, both hemodynamic and non-hemodynamic in origin. In addition, a combination of cardiocirculatory stress, greatly conditioned by the switch from hypervolemia to hypovolemia, hypoxemia and electrolyte changes may create pro-arrhythmogenic conditions. Moreover, contact of blood with components of the extracorporeal circuit directly activate circulating cells (i.e. macrophages-monocytes or platelets) and protein systems (i.e. coagulation, complement, contact phase kallikrein-kinin system), leading to induction of pro-inflammatory cytokines and resulting in chronic low-grade inflammation, further contributing to poor outcomes. The multifactorial, repetitive HD-induced stress that globally reduces tissue perfusion and oxygenation could have deleterious long-term consequences on the functionality of vital organs such as heart, brain, liver and kidney. In this article, we summarize the multisystemic pathophysiological consequences of the main circulatory stress factors. Strategies to mitigate their effects to provide more cardioprotective and personalized dialytic therapies are proposed to reduce the systemic burden of HD.

Online hemodiafiltration (HDF) is an established renal replacement modality for patients with end stage chronic kidney disease that is now gaining rapid clinical acceptance worldwide. Currently, there is a growing body of evidence indicating that treatment with HDF is associated with better outcomes and reduced cardiovascular mortality for dialysis patients. In this comprehensive review, we provide an update on the potential mechanisms which may improve survival in HDF treated patients. The strongest evidence is for better hemodynamic stability and reduced endothelial dysfunction associated with HDF treatments. Clinically, this is marked by a reduced incidence of intradialytic hypotensive episodes, with a better hemodynamic response to ultrafiltration, mediated by an increase in total peripheral vascular resistance and extra-vascular fluid recruitment, most likely driven by the negative thermal balance associated with online HDF therapy. In addition, endothelial function appears to be improved due to a combination of a reduction of the inflammatory and oxidative stress complex syndrome and exposure to circulating cardiovascular uremic toxins. Reports of reversed cardiovascular remodeling effects with HDF may be confounded by volume and blood pressure management, which are strongly linked to center clinical practices. Currently, treatment with HDF appears to improve the survival of dialysis patients predominantly due to a reduction in their cardiovascular burden, and this reduction is linked to the sessional convection volume exchanged.

Excess sodium intake and consequent volume overload are major clinical problems in hemodialysis (HD) contributing to adverse outcomes. Saline used for priming and rinsing of the extracorporeal circuit is a potentially underappreciated source of intradialytic sodium gain. We aimed to examine the feasibility and clinical effects of replacing saline as the priming and rinsing fluid by a 5% dextrose solution.

We enrolled non-diabetic and anuric stable HD patients. First, the extracorporeal circuit was primed and rinsed with approximately 200-250 mL of isotonic saline during 4 weeks (Phase 1), subsequently a similar volume of a 5% dextrose solution replaced the saline for another 4 weeks (Phase 2), followed by another 4 weeks of saline (Phase 3). We collected data on interdialytic weight gain (IDWG), pre- and post-dialysis blood pressure, intradialytic symptoms, and thirst.

Seventeen chronic HD patients (11 males, age 54.1 ± 18.7 years) completed the study. The average priming and rinsing volumes were 236.7 ± 77.5 and 245.0 ± 91.8 mL respectively. The mean IDWG did not significantly change (2.52 ± 0.88 kg in Phase 1; 2.28 ± 0.70 kg in Phase 2; and 2.51 ± 1.2 kg in Phase 3). No differences in blood pressures, intradialytic symptoms or thirst were observed.

Replacing saline by 5% dextrose for priming and rinsing is feasible in stable HD patients and may reduce intradialytic sodium loading. A non-significant trend toward a lower IDWG was observed when 5% dextrose was used. Prospective studies with a larger sample size and longer follow-up are needed to gain further insight into the possible effects of using alternate priming and rinsing solutions lowering intradialytic sodium loading.

Identifier NCT01168947 (ClinicalTrials.gov).

Hemodialysis (HD) is a life-saving therapy for patients with end-stage renal disease. In dialyzed patients, the prevalence of multi-morbidity is rising driven by various factors, such as the population aging, the incomplete correction of uremia, and the side effects of the dialysis therapy itself. Each dialyzed patient has their own specific clinical and biochemical problems. It is therefore unthinkable that the same dialysis procedure can be able to meet the needs of every patient on chronic dialysis. We have very sophisticated dialysis machines and different dialysis techniques and procedures beyond conventional HD, such as hemodiafiltration (HDF) with pre- and post-dilution, acetate-free biofiltration (AFB), hemofiltration (HF), and expanded HD. Each of these techniques has its own specific characteristics. To solve some intradialytic clinical issues, such as arterial hypotension and arrhythmias, we have biofeedback systems with automatic regulation of the blood volume, body temperature, arterial pressure, as well as potassium profiling techniques in the dialysis bath. New technical innovations, such as citrate-containing dialysate or heparin-coated membranes, could reduce the risk of bleeding. To better address to patient needs, the strengths and weaknesses of each of these systems must be well-known, in order to have a personalized dialysis prescription for each patient.

Vascular calcification is a known complication of chronic kidney disease (CKD). The prevalence of vascular calcification in patients with non-dialysis-dependent CKD stages 3-5 has been shown to be as high as 79% (20). Vascular calcification has been associated with increased risk for mortality, hospital admissions, and cardiovascular disease (6, 20, 50, 55). Alterations in mineral and bone metabolism play a pivotal role in the pathogenesis of vascular calcification in CKD. As CKD progresses, levels of fibroblast growth factor-23, parathyroid hormone, and serum phosphorus increase and levels of 1,25-(OH)₂ vitamin D decrease. These imbalances have been linked to the development of vascular calcification. More recently, additional factors have been found to play a role in vascular calcification. Matrix G1a protein (MGP) in its carboxylated form (cMGP) is a potent inhibitor of vascular calcification. Importantly, carboxylation of MGP is dependent on the cofactor vitamin K. In patients with CKD, vitamin K deficiency is prevalent and is exacerbated by warfarin, which is frequently used for anticoagulation. Insufficient bioavailability of vitamin K reduces the amount of cMGP available, and, therefore, it may lead to increased risk of vascular calcification. In vitro studies have shown that in the setting of a high-phosphate environment and vitamin K antagonism, human aortic valve interstitial cells become calcified. In this article, we discuss the pathophysiological consequence of vitamin K deficiency in the setting of altered mineral and bone metabolism, its prevalence, and clinical implications in patients with CKD.