![\"\"](\"https:\/\/staging.advancedrenaleducation.com\/wparep\/wp-content\/uploads\/2025\/07\/figure8.1-300x126.jpg\")
<\/span><\/p>\nFigure 8.1 | Factors impacting the substitution fluid volume generation in post-dilution hemodiafiltration. In green are the factors associated with the dialysis prescription, and in light blue the factors influencing the effective blood flow rate.<\/span><\/p>\n <\/p>\n The following items will be discussed in detail: A well-functioning vascular access is essential for the successful delivery of dialysis, regardless of the treatment modality. Vascular access dysfunction is a major cause of morbidity, requiring interventional procedures or hospitalization (310).<\/p>\n HVHDF can be performed using any type of vascular access, including AVFs, AVGs, or permanent CVCs. AVF and AVG with an access flow of >600 mL\/min can be considered sufficient to allow adequate blood flow (Qb).<\/p>\n Qb should not exceed 80% of the vascular access flow. Good vascular access is a prerequisite for performing post-dilution HVHDF, provided that adequately sized needles (15G or larger) are used. CVCs typically provide lower and more variable blood flow rates, which may impact treatment efficiency.<\/p>\n Regular vascular access blood flow monitoring can predict the need for interventions before unusability and significantly reduce the number of thrombosis events (311).<\/p>\n Qb is a fundamental determinant of dialysis adequacy in both high-flux HD and HDF treatment. The achieved blood flow is the most crucial predictor of convective volume achievement, as it facilitates ultrafiltration flow rate while limiting the filtration fraction to less than 30%<\/em> (96, 308, 309, 312, 313).\u00a0 Most studies rely on prescribed Qb (pQb) rather than effective Qb (eQb), which may introduce inaccuracies in assessing dialysis efficacy. The eQb\u2014the actual blood flow reaching the dialyzer\u2014can be substantially lower than the pQb due to factors such as low arterial bloodline pressure, resistance in AVF, AVG, or CVC, vascular access recirculation, cardiopulmonary recirculation, needle size, long catheter lumens (which may increase blood viscosity), and anticoagulation (314). The degree of discrepancy between pQb and eQb varies among individuals, making eQb a more accurate parameter for evaluating the relationship between Qb and clinical outcomes. In pre-dilution HDF, the substitution fluid dilutes the blood, effectively reducing the volume of undiluted blood reaching the dialyzer. In post-dilution HDF, there is no reduction in eQb because substitution fluid is added after the dialyzer. The eQb is effectively used for solute clearance, making post-dilution more efficient than pre-dilution in removing uremic toxins. The Qb exhibits a positive correlation with shear rate, which plays a crucial role in mitigating the formation of the secondary protein layer. Higher Qb reduces membrane fouling by enhancing shear forces, thereby preserving dialyzer membrane permeability and sustaining its sieving capacity over time. A vascular access with blood flow rates of 350\u2013400 mL\/min will be most\u00a0 successful in achieving the high convective volume associated with improved outcomes without the need to increase the dialysis treatment time (96, 315). To achieve full perfusion of all capillary fibers and optimize shear rate, a Qb of at least 200 mL\/min per 1.0 m\u00b2 of dialyzer surface area is required (308, 309). This flow rate ensures an adequate shear stress per fiber, effectively minimizing membrane fouling and maintaining dialyzer efficiency in currently available capillary dialyzers (309).<\/p>\n The internal lumen diameter of fistula needles is a critical determinant of vascular access resistance, as governed by the Hagen-Poiseuille law, where resistance to blood flow is inversely proportional to the fourth power of the lumen radius (309). For prevalent patients, at least 15 G needles are usually recommended<\/em> for both the arterial and the venous cannulation sites. A smaller needle should only be used in exceptional cases, e.g., if the vascular access flow rate is below 400 mL \/min, the vessel is too small to be cannulated with a 15 G needle, the fistula is not yet mature, or if shortly after fistula revision a hematoma is present and bleeding time is prolonged. By switching to a bigger needle (e.g., from 17 G to 15 G) at constant arterial pressure (PART<\/sub>, e.g. -200 mmHg), the blood flow increases (Figure 8.2). CVC must have an inner lumen diameter of \u2265 2 mm to ensure adequate flow dynamics and minimize resistance (12, 316).<\/p>\n Figure 8.2 |\u00a0Selection of needle size. Unpublished FME data.<\/span><\/p>\n A typical arterial pressure (PART<\/sub>) value in AVF or AVG is around -200 mmHg, usually resulting in venous pressures around +230 mmHg. To individually maximize Qb for dialysis, increase the Qb until the patient\u00adindividual limit for arterial or venous pressure is reached. The PART<\/sub> is measured at the arterial line before the blood pump.<\/p>\n It is suggested to increase the Qb until one of the following conditions is fulfilled, whichever is fulfilled first:<\/p>\n In patients with vascular access limitations, achieving high substitution volumes via increasing blood flow rate (Qb) may not always be feasible. In such cases, an automated regulation system, such as AutoSub plus<\/em> (FME), becomes particularly valuable. This system optimizes substitution volume delivery, enabling higher convective clearances even when Qb cannot be increased. By implementing AutoSub plus<\/em>, more patients could achieve a target substitution volume of \u2265 21 L per treatment, thereby enhancing the efficacy of HVHDF therapy (28).<\/p>\n Dialysis treatment time, quantified as the product of individual session length and weekly frequency, is a pivotal and autonomous determinant of blood purification efficacy. Substitution volume and processed blood volume increase<\/u> with dialysis time.<\/p>\n Prolonged treatment durations have been empirically validated to confer multiple clinical advantages, notably enhancing the clearance of solutes characterized by low intrinsic mass transfer coefficients, mitigating osmotic fluctuations, reducing the requisite UFR, and augmenting the convective dose administered (309). These benefits are equally pertinent to HDF (309, 317-319). Consequently, individualized optimization of treatment parameters is imperative for both high-flux HD and HDF modalities. Personalized treatment adjustments are essential for maximizing the benefits of both HD and HDF.<\/p>\n Increasing the treatment time or the Qb proportionally increases the substitution volume, potentially enhancing the convective clearance of middle- and large-molecular-weight solutes (Figure 8.3).<\/p>\n Figure 8.3 |\u00a0Examples for the calculation of the substitution volume considering a Filtration Fraction (FF) 30% and a Blood Flow Rate (Qb) of 350 ml\/min: Treatment time (TrT) 210 min:\u00a0 Substitution volume (QSub) = 22.0 L; TrT 225 min:\u00a0 Qsub = 23.6 L; TrT 240 min:\u00a0 Qsub = 25.2 L. FF 30% and a Qb of 370 ml\/min: TrT 210 min:\u00a0 QSub = 23.1 L; TrT 225 min: QSub = 24.5 L; TrT 240 min:\u00a0 QSub = 26.6 L. FF 30% and a Qb of 400 ml\/min: TrT 210 min:\u00a0 QSub = 25.2 L; TrT 225 min:\u00a0 QSub = 27.0 L; TrT 240 min:\u00a0 QSub = 28.8 L<\/span><\/p>\n These calculations demonstrate that increasing the treatment time or the Qb proportionally elevates the substitution volume, potentially enhancing the convective clearance of middle- and large-molecular-weight solutes.<\/p>\n During HD, the coagulation system is activated, necessitating the use of anticoagulation to prevent clot formation within the extracorporeal circuit (ECC). Preventing clotting within the extracorporeal circuit is fundamental to optimizing HDF efficacy and ensuring patient safety.<\/p>\n In routine practice, one of the following anticoagulants is usually prescribed to prevent the coagulation of the blood:<\/p>\n UFHs carry a higher negative charge than LMWH (320). Given that most dialyzer membranes are also negatively charged, the electrostatic repulsion between UFH and the membrane likely reduces UFH adsorption during HDF. This suggests that UFH removal during HDF may be less than anticipated based solely on its molecular size. As a result, UFH dose during this type of treatment may be lower than anticipated. Despite this, the specific conditions within the dialyzer during HDF, such as increased convective transport and higher FFs, can elevate the risk of clot formation within the extracorporeal circuit (320). No specific modifications are necessary compared to its use in high-flux HD, as both the loading dose and maintenance infusion remain unchanged. UFH dosing in both HDF and HD is typically individualized, guided by activated partial thromboplastin time (aPTT) measurements and visual inspection for clot formation in the air trap chamber. These monitoring practices are consistent across both modalities, ensuring appropriate anticoagulation tailored to each patient’s needs (320).<\/p>\n LMWHs are categorized as middle-molecular-weight compounds. As such, they are susceptible to enhanced removal through convection, the principal mechanism of solute clearance in HDF. The CONTRAST study reported approximately 10% higher LMWH dose in HDF patients compared to HD patients (321). However, studies have shown that the clearance of LMWHs like enoxaparin and dalteparin remains relatively low during both HD and HDF. This is likely due to their negative charge, which reduces adsorption onto the similarly charged dialyzer membranes (320, 322, 323). Therefore, membrane characteristics, particularly electrical charge, play a significant role in LMWH removal during dialysis. The LMWH\u2019s infusion as a single bolus at treatment initiation requires careful consideration of the injection site to maintain optimal antithrombotic activity. Empirical evidence has demonstrated that immediate injection of LMWH into the arterial bloodline results in a 20% to 30% loss of the active compound, leading to diminished anticoagulant efficacy. Consequently, higher doses may be required to achieve equivalent anticoagulant effects (324). To mitigate this loss and preserve LMWH’s full anticoagulant potential, the preferred method of administration is direct injection into the venous needle or venous bloodline (309). If arterial line administration is necessary, delaying the injection can significantly enhance the bioavailability and efficacy of LMWH (309). Implementing these evidence-based strategies ensures adequate anticoagulation during HDF, reducing the risk of clotting-related complications, and maintaining circuit patency. Please note that most LMWHs are licensed for arterial bloodline administration. Nevertheless, the consumption of LMWHs is usually lower when administered to the venous side of the bloodline.<\/p>\n For dalteparin, a starting dose of 60 IU\/kg has been found adequate in HDF patients (320, 325). Given the increased coagulation activation in HDF, future monitoring may benefit from assessing thrombin-antithrombin (TAT) complex levels in addition to anti-factor Xa activity to better evaluate anticoagulation efficacy (320).<\/p>\n Patients receiving oral anticoagulant therapy (e.g., warfarin) represent special cases. However, in patients already receiving coumarin therapy, the heparin (UFH\/LMWH) starting dose for extracorporeal therapy may be reduced to 50% of the standard dose to mitigate the cumulative anticoagulant effect and reduce the risk of bleeding, as supported by clinical guidance (320, 326).<\/p>\n It is recommended to adopt the following Qd:Qb ratio prescription (29):<\/p>\n Qd:Qb = 1.2: All patients. <\/em>If:<\/p>\n HDF combines diffusion and convection to enhance solute clearance and improve patient outcomes. While Qb and substitution volume are often the primary focus in optimizing HDF, dialysate flow rate (Qd) plays a critical role in increasing treatment efficacy. Qd is the rate at which dialysate is delivered to the dialyzer and serves as the driving force for diffusive clearance, primarily removing small molecular weight uremic toxins, such as urea and creatinine. However, in HDF, combining high-volume ultrafiltration (convective transport) with diffusive clearance requires careful balancing of Qd to optimize both mechanisms. Determining the ideal Qd for HDF involves balancing dialysis efficiency with cost-effectiveness and machine capabilities. Typical Qd values in HDF settings range between 500 and 800 mL\/min, depending on the HDF modality. In post-dilution HDF, substitution fluid is infused after the dialyzer, maximizing convective clearance. Since diffusion remains unaffected, Qd can be maintained at 500\u2013600 mL\/min.<\/em><\/p>\n Mesic et al. investigated the impact of automated adjustment of dialysate flow rates based on blood flow in optimizing dialysate consumption while maintaining or improving dialysis dose (327). Conducted as a randomized crossover trial across multiple dialysis centers, the research compared conventional HD with HDF, applying an automated Qd:Qb ratio of 1.2. This led to 8.5% lower dialysate consumption while still achieving a 3.5% increase in dialysis dose (Kt\/V) (327). \u00a0More recently, Canaud et al. evaluated dialysis fluid consumption and efficiency in post-dilution HVHDF compared to high-flux HD, aiming to optimize resource use while maintaining or improving dialysis efficacy (29). Conventional high-flux HD typically sets the Qd:Qb ratio between 1.4 and 1.5, leading to substantial dialysate consumption, averaging around 125 liters per session (29). When HVHDF is optimized with a reduced Qd:Qb of 1.2, HVHDF achieves the same or better solute clearance while reducing total dialysis fluid consumption to approximately 99 liters per session, representing a 26% reduction compared to traditional HDF (29) (Figure 8.4).<\/p>\n Figure 8.4 | Graphic adapted from Canaud et al. (29). *Estimates are based on presumed prescription during the CONVINCE trial (Qd:Qb 1.4) and observed Qb and substitution volumes (assuming no net UF). The dialysate volume consumption\/session is shown in dark green, and the convective volume\/ session in light green.<\/span><\/p>\n The impact of these optimizations is evident in both water savings and treatment effectiveness. Despite reducing dialysate volume, optimized HDF maintains urea clearance comparable to HD, with a Kt\/V ranging from 1.65 to 1.71 (29) (Figure 8.4). Moreover, \u03b22M removal was enhanced due to convective transport, making HVHDF a superior modality for eliminating small and larger uremic toxins and a more sustainable alternative to high-flux HD (29).<\/p>\n Independent of the treatment modality, dialysate and substitution fluid electrolytes such as potassium (K+<\/sup>), sodium (Na+<\/sup>), calcium (Ca2+<\/sup>), magnesium (Mg2+<\/sup>), and bicarbonate (HCO3-<\/sub>) should be prescribed in a reasonable range based on clinical basis, tolerance, and outcomes, and must be monitored regularly.<\/p>\n The electrolyte concentrations in the dialysate and substitution fluid are identical, making it impossible to have two different concentrations.<\/em><\/p>\n The electrolyte levels in the dialysate and substitution fluid used for HVHDF may need to be adjusted compared to those used in conventional HD to prevent electrolyte imbalances. Indeed, in HVHDF, the initial electrolyte shift is greater than in conventional HD treatments. In conventional dialysis, electrolytes back-diffuse from the dialysate into the patient\u2019s blood within the dialyzer.<\/p>\n However, in post-dilution HDF, electrolytes are directly infused with the substitution fluid into the patient\u2019s blood via the venous drip chamber<\/em>. One key consideration is the bicarbonate concentration, which may need to be reduced to avoid overcorrection of the metabolic acidosis commonly observed in ESKD patients<\/em> (308, 328).<\/p>\n The bicarbonate exchange also influences the serum potassium concentration. A rapid increase in serum bicarbonate is associated with a faster decline in serum potassium because increasing the blood’s pH causes the movement of K+<\/sup> into the intracellular space.<\/p>\n Sodium balance is another critical factor that requires careful modulation in post-dilution HVHDF. The sodium concentration in the dialysis fluid (and substitution fluid) should be adjusted to a level lower than that of the patient\u2019s plasma water.<\/p>\n These findings underscore the importance of tailoring dialysis fluid composition to optimize electrolyte homeostasis in HVHDF while mitigating potential complications related to bicarbonate and sodium handling.<\/p>\n Electrolyte serum concentration:<\/strong> The electrolyte serum concentration at the end of dialysis depends mainly on the concentration of respective electrolytes in the dialysis fluid and not on the dialysis modality (329).<\/p>\n Electrolyte shift:<\/strong> In high-flux HD and HVHDF, the initial electrolyte shift is greater than in low-efficiency HD treatments, i.e., in treatments with low blood flow rate.<\/p>\n For patients initiating hemodialysis therapy, a gradual correction of chronic uremic acidosis is recommended. This approach prioritizes cardiovascular stability during the early treatment phase, while minimizing the risk of complications associated with rapid alkalization, such as post-dialysis alkalosis, particularly in the context of both HD and online HDF (77). In prevalent patients, the dialysate bicarbonate concentration may be progressively increased to 30\u201332\u202fmEq\/L, with adjustments based on pre- and post-dialysis bicarbonate levels and the patient\u2019s overall metabolic status (77). Montagud-Marrahi et al., in a prospective cohort study of patients on stable chronic HDF, analyzed the impact of reducing dialysate bicarbonate concentration from 35 to 32\u202fmEq\/L on plasma bicarbonate levels (328). A 3\u202fmEq\/L reduction in dialysate bicarbonate significantly and safely decreased both pre- and post-dialysis total carbon dioxide (TCO\u2082) levels, thereby preventing overcorrection of acidosis and contributing to improved control of secondary hyperparathyroidism (328).<\/p>\n Independent of the treatment modality, dialysis fluid bicarbonate should be prescribed based on regularly monitoring the pre\u00addialysis serum bicarbonate level.<\/p>\n There is no exclusive (or single) international guideline for metabolic acidosis correction in maintenance ESKD patients, and recommendations in national guidelines vary by country.<\/em><\/p>\n Excessively high bicarbonate concentrations in the dialysate, and in the substitution fluid in the case of HDF, can cause metabolic alkalosis. Conversely, insufficient bicarbonate levels may lead to metabolic acidosis. At the start of HD, the bicarbonate shift is more pronounced in HVHDF compared to low-efficiency HD treatments. This larger bicarbonate shift leads to a more rapid correction of acidosis. Serum bicarbonate levels are influenced by the back-diffusion of bicarbonate across the dialyzer membrane and by the infusion of substitution fluid. One key consideration is the bicarbonate concentration, which may need to be reduced to avoid overcorrection of the metabolic acidosis commonly observed in HD patients (308, 328).<\/p>\n Patients undergoing high-flux HD and HDF with elevated dialysate bicarbonate concentrations are at an increased risk of adverse effects due to rapid correction of acidosis and the potential development of an alkalotic state. These risks include hypokalemia, caused by potassium clearance via dialysis and its intracellular shift due to rising pH, hypocalcemia, hypomagnesemia, prolonged QT interval on the electrocardiogram, vasodilation, hypotension, suppression of minute ventilation, cerebral ischemia, and accelerated vascular calcification (337-345). Tentori et al. demonstrated a positive association between higher dialysate bicarbonate concentrations and increased mortality, cardiovascular hospitalizations, and IDH (335). Another study found that reducing the dialysate HCO3<\/sub>–<\/sup> concentration decreased IDH (346).<\/p>\n During treatment, the principle of diffusion regulates serum bicarbonate levels, preventing them from exceeding the dialysis fluid’s bicarbonate concentration, as set by the machine\u2019s \u201cbicarbonate\u201d setting. To achieve the desired serum bicarbonate concentration, physicians should individually adjust the dialysate or replacement fluid levels using the dialysis machine, whether in HD or HDF.<\/p>\n Dialysis fluid and substitution fluid typically contain a combination of bicarbonate and acetate\/citrate. The type and concentration of acetate\/citrate are determined by the acid concentrate used, which varies between formulations. In both HD and HDF, bicarbonate and acetate\/citrate diffuse across the dialyzer membrane into the blood. In HDF, these components also reach the blood via the substitution fluid. Once in the patient\u2019s blood, acetate\/citrate is metabolized into bicarbonate, contributing to the overall circulating bicarbonate concentration. S\u00e1nchez-Canel et al. investigated the acid-base status of patients undergoing HDF with bicarbonate dialysate containing 3 mEq\/L of acetate or Acetate-Free Biofiltration (AFB) (347). The study found that acetate concentrations remained stable during and after AFB. In contrast, acetate concentrations increased by approximately 0.05 mmol\/L during HDF at the midpoint of treatment, remained unchanged post-HDF, and returned to baseline levels after the session. Bicarbonate concentrations were comparable between HDF and AFB, though AFB demonstrated slightly greater bicarbonate replenishment. These findings align with the results of Smith et al., indicating that only a minimal amount of dialysate acetate is transferred to the patient during HDF. This small acetate load does not significantly impact blood bicarbonate concentrations or the bicarbonate administered during treatment (348).<\/p>\n For prevalent patients, the dialysate potassium concentration may be adjusted to a range of 2-3\u202fmEq\/L, based on pre- and post-dialysis plasma potassium levels (77).<\/p>\n After a prolonged interdialytic interval, serum K+<\/sup> levels should ideally range between \u22654.0 and \u22646.0 mEq\/L (333). Potassium plays a critical role in maintaining the resting cell membrane potential, neuromuscular excitability, and the rhythmicity of cardiac pacemaker activity (349). HD and HDF treatments induce a rapid decline in serum K+<\/sup> concentration, most notably during the first 60 minutes of therapy. Subsequently, plasma K+<\/sup> levels stabilize, reaching a steady state during the final hour of dialysis (211, 350-352).<\/p>\n A lower dialysate potassium concentration facilitates greater potassium removal from the bloodstream, resulting in reduced post-dialysis serum potassium levels (353). Additionally, the bicarbonate exchange also affects the serum K+<\/sup> concentration. A rapid increase in serum bicarbonate is associated with a faster decline in serum K+<\/sup> because increasing the blood’s pH causes the movement of K+<\/sup> into the intracellular space.<\/p>\n This abrupt reduction in plasma K+<\/sup> alters the intracellular-to-extracellular potassium concentration gradient, transmembrane potential, and cardiac cell repolarization. These changes predispose patients to IDH by reducing cardiac output and increasing the risk of arrhythmias, prolonged QT interval on the electrocardiogram, and ectopic ventricular beats (354, 355).<\/p>\n Hypokalemia during dialysis sessions has been associated with brief episodes of paroxysmal atrial fibrillation, particularly during the last two hours of treatment (356, 357). Dialysate K+<\/sup> levels < 2 mEq\/L have been linked to an elevated incidence of cardiac events (358-360).<\/p>\n To mitigate the risk of intradialytic hypokalemia, strict dietary potassium control may reduce the necessity for low dialysate K+<\/sup> levels (361).<\/p>\n Studies evaluating total sodium mass have consistently ruled out the presence of a positive sodium balance in patients undergoing HDF (246, 362). During HDF, where significant convective volumes are removed, albumin\u2014acting as a non-removable anion\u2014becomes increasingly concentrated on the blood side of the dialysis membrane. This concentration gradient promotes sodium retention, which binds to albumin to maintain electrical equilibrium as dictated by the Gibbs\u2013Donnan effect (159, 161).<\/p>\n The Gibbs-Donnan effect results in a lower Na+<\/sup> concentration in the ultrafiltrate compared to the plasma water from which it is derived, leading to an increase in plasma water Na+<\/sup> concentration along the dialyzer length. In conventional HD, this Na+<\/sup> accumulation is mitigated by concurrent diffusive Na+<\/sup> transfer into the dialysis fluid. However, in post-dilution HDF, where UFRs are significantly higher, diffusive Na+<\/sup> loss may be insufficient to offset the Gibbs-Donnan driven increase in plasma Na+<\/sup> concentration. This results in a higher Na+<\/sup> burden for the patient, with the magnitude of the effect being directly proportional to the convection rate (308, 363).<\/p>\n The retention of Na+<\/sup> in this context results in elevated osmolarity within the blood compartment, thereby enhancing fluid refilling from the interstitial compartment (162). This mechanism may contribute to the improved hemodynamic stability observed during HDF. Furthermore, the enhanced hemodynamic tolerance might also be attributed to an increase in pre-dialysis systolic blood pressure, as reported in several studies (92, 154). While this potential benefit could theoretically lead to hydrosaline overload, clinical trials have not demonstrated a sustained increase in natremia (37), nor have they identified markers indicative of fluid overload in patients treated with HVHDF.<\/p>\n A recent study investigating sodium removal in post-dilution HDF versus high-flux HD found no significant difference in Na+<\/sup> balance when a dialysis fluid sodium concentration of 1 mmol\/L lower than the pre-dialysis plasma Na+<\/sup> concentration (138 and 139 mmol\/L, respectively) was used (246, 308).<\/p>\n The online HDF parameters have a negligible effect on ionized calcium and magnesium (364). Independent of the treatment modality, dialysis fluid Ca++<\/sup> should be prescribed based on regularly monitoring the pre\u00addialysis serum calcium level.<\/p>\n Both HD and HDF require careful dialysate Ca++<\/sup> adjustment to optimize calcium balance, support cardiovascular stability, and minimize long-term complications such as vascular calcification and bone disorders. Maintaining an optimal Ca++<\/sup> balance in ESKD patients is a complex process influenced by several factors, including plasma calcium levels, PTH, the use of phosphate binders and vitamin D analogs, and IDH risk and cardiac arrhythmias. These factors act in concert and require careful consideration for optimal outcomes. Therefore, dialysate Ca++<\/sup> prescription should be carefully individualized (365).<\/p>\n The KDOQI guidelines recommend a corrected total serum Ca++<\/sup> \u00a0goal range of 8.4\u201310.2 mg\/dL (2.1\u20132.54 mmol\/L) (366). The correction of acidosis and the development of post-dialysis alkalosis can lead to hypocalcemia, particularly when low dialysate Ca++<\/sup> concentrations are used. Hypocalcemia is associated with pro-arrhythmogenic effects that may induce IDH (367-369).<\/p>\n In patients undergoing HD and HDF, intradialytic reductions in plasma Ca++<\/sup> \u00a0levels have been inversely correlated with prolonged QTc interval on the electrocardiogram, suggesting that larger reductions in plasma calcium are associated with more significant increases in QTc at the end of the dialysis session (367-369). The KDIGO 2017 guidelines recommend a dialysate Ca++<\/sup> range of 1.25\u20131.5 mmol\/L (370, 371). However, dialysate Ca++<\/sup> levels within this range have distinct physiological effects:<\/p>\n Leenders et al. conducted a systematic review and meta-analysis demonstrating that higher circulating magnesium (Mg) levels are inversely associated with all-cause and cardiovascular mortality in patients with chronic kidney disease (379). These findings suggest that increasing serum magnesium may help reduce cardiovascular risk in this population (379). In HD patients, modification of this risk factor may be readily achieved by increasing dialysate Mg concentration (379).<\/p>\n In HD patients, the use of dialysate Mg concentrations of 0.75 to 1.0 mEq\/L has been associated with improved hemodynamic stability, reduced IDH, and enhanced cardiovascular safety. Kyriazis et al. identified a dialysis solution containing 0.25 mmol\/L Mg and 1.25 mmol\/L Ca++<\/sup> as a major cause of IDH due to an impairment of myocardial contractility, and showed that increasing dialysate Mg level to 0.75 mmol\/L could prevent IDH frequently seen with the use of 1.25 mmol\/L dialysate Ca (380).<\/p>\n Both hypoglycemia and hyperglycemia should be avoided to ensure hemodynamic stability during HD, emphasizing the importance of tight glycemic control and regular blood glucose monitoring. While glucose-free dialysate has been proposed to prevent hypertriglyceridemia and minimize the potential risk of bacterial proliferation in the dialysate (211), its use poses a significant risk of hypoglycemia, particularly in diabetic patients receiving insulin therapy (381, 382).<\/p>\n To mitigate these risks, a dialysate glucose concentration of 5.55 mmol\/L (1 g\/L) is recommended as an optimal balance to maintain glucose homeostasis during HD.<\/p>\n For HD and HDF treatments, dialysis fluid containing glucose is recommended. Ideally, the dialysis treatment does not alter the blood glucose level. In the Turkish (36) and the Catalonian HVHDF (37) studies, 5.55 mmol \/L (1 g \/L) of dialysis fluid glucose were prescribed with satisfactory results.<\/p>\n Independent of the treatment modality, potassium removal may be higher with glucose-free dialysis fluid because glucose can induce insulin production, which promotes K+<\/sup> entry into cells. Subsequently, less K+<\/sup> is available for removal during dialysis. Caloric loss with glucose-free dialysis fluid may be increased. Maintaining stable blood glucose levels is essential in patients with ESKD to reduce the risk of IDH.<\/p>\n Modern dialysis membranes must meet a comprehensive set of criteria to ensure safety, efficacy, and biocompatibility in dialysis treatments. This is particularly relevant for HVHDF due to its substantially increased transmembrane filtration. The following are the key criteria that collectively define the ideal dialysis membrane for HVHDF (383):<\/p>\n Dialysis treatment for adult patients with ESKD may be initiated with HDF support (77, 309). In such cases, it is recommended to implement HDF stepwise while monitoring patient response and tolerance. Recently, Stuard et al. documented the HD procedures adopted in FME EMEA NephroCare clinics for initiating HD and HDF therapy in stable incident patients (77).<\/p>\n FME EMEA NephroCare has developed HD strategies and procedures to optimize the management and seamless transition of stable incident patients with ESKD. For these patients, a stepwise approach is recommended: progressively increasing the substitution volume, starting with 5 L in the second week of dialysis, then adding 5 L per week to reach a substitution volume \u2265 21 L \/ session by the fifth week of dialysis (Table 8.1 adapted from Stuard et al.) (77).<\/p>\n Table 8.1 |\u00a0Qb: Blood flow rate; Qd: Dialysate flow rate, Qsub: Substitution fluid \/session; D. Dialysate; | Qsub: Substitution Volume. AHTs: antihypertensive drugs. IDH: Intradialytic hypotension. RKF: residual kidney function.\u00a0 *Increase the dialyzer surface area according to patient characteristics. **Adjust the dialysate electrolyte prescription according to the patient\u2019s blood test results. ***Hemoglobin, urea, calcium, bicarbonate, potassium, and sodium. \u2020Increase in case spKt\/V <1.4.<\/span><\/p>\n Switching a stable prevalent patient from high-flux HD to post-dilution HVHDF can enhance the removal of middle molecules and potentially improve clinical outcomes, provided that high convective volumes (\u2265\u202f23\u202fL\/session) are achieved.<\/p>\n At FME Fresenius Kidney Care centers in the United States, a dedicated and structured algorithm has been developed, approved, and implemented to guide the transition of adult, stable ESKD patients, defined as those receiving high-flux HD for more than 30 days, from high-flux HD to HVHDF.<\/p>\n More broadly, it is recommended that the first HDF session be scheduled mid-week (e.g., Wednesday or Thursday). For prevalent patients, the probing period is shorter compared to stable incident patients starting HDF. In such cases, initiating HDF involves only a few key steps, making the transition process both streamlined and clinically feasible (309):<\/p>\n <\/p>\n","protected":false},"featured_media":0,"template":"","format":"standard","meta":{"_acf_changed":false},"categories":[5],"tags":[296],"language":[41],"articles":[162],"class_list":["post-7862","article","type-article","status-publish","format-standard","hentry","category-articles","tag-handbook-hdf","language-english","articles-hemodiafiltration","entry","no-media"],"acf":[],"yoast_head":"\n
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<\/p>\n8.1\u00a0 | Vascular access<\/h2>\n
8.2\u00a0 | Treatment prescription<\/h2>\n
8.2.A\u00a0 Blood flow<\/h4>\n
8.2.A1\u00a0 Needle size, catheter lumen<\/h4>\n
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<\/span><\/p>\n8.2.A2\u00a0 Extracorporeal pressure regimen<\/h4>\n
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8.2.A3\u00a0 How to achieve high substitution volume<\/h4>\n
8.2.A4 \u00a0Workflow: How to achieve the highest blood flow rate<\/h4>\n
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<\/h4>\n8.2.B\u00a0 Dialysis treatment time<\/h4>\n
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<\/span><\/p>\n8.2.C\u00a0 Prescription of anticoagulants<\/h4>\n
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8.2.D\u00a0 Prescription of dialysate flow rate<\/h4>\n
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<\/span><\/p>\n8.2.E\u00a0 Prescription of dialysate and substitution fluid electrolytes<\/h4>\n
8.2.E1\u00a0 Prescription of dialysate and substitution fluid bicarbonate<\/h4>\n
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8.2.E2\u00a0 Prescription of dialysate and substitution fluids potassium<\/h4>\n
8.2.E3\u00a0 Prescription of dialysate and substitution fluids sodium<\/h4>\n
8.2.E4\u00a0 Prescription of dialysate and substitution fluids calcium and magnesium<\/h4>\n
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8.2.F\u00a0 Prescription of dialysate and substitution fluids glucose<\/h4>\n
8.2.G\u00a0 Prescription of the hemodialyzer<\/h4>\n
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8.3\u00a0 | Dialysis procedures in stable incident patients starting HDF<\/h2>\n
![\"\"](\"https:\/\/staging.advancedrenaleducation.com\/wparep\/wp-content\/uploads\/2025\/07\/table8.1-1-300x293.png\")
<\/span><\/p>\n8.4\u00a0 | Switching stable and regularly dialyzed patients from high-flux HD to HVHDF<\/h2>\n
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