Comparison of calcium phosphate product values using measurement of plasma total calcium and serum ionized calcium

Calcium phosphate product (Ca x Pi) is a clinically relevant tool to estimate the cardiovascular risk of patients with renal failure. In reports, mostly total serum calcium has been used. As measurement of serum ionized calcium has some benefits and is being used increasingly, we estimated the respective levels of calcium phosphate product using both total (t-Ca x Pi) and ionized calcium (ion-Ca x Pi). Fifty-eight healthy individuals and 180 hemodialysis (HD) patients from 2 centers were studied. Diagnostic accuracies for corresponding values of the t-Ca x Pi and ion-Ca x Pi were calculated using a GraphROC program. Of HD patients, 64% had t-Ca x Pi <4.4 mmol(2)/L(2) regarded as a desirable goal, and 10% had values over 5.6 mmol(2)/L(2) associated with a high cardiovascular risk. Based on GraphROC analysis, t-Ca x Pi of 4.4 mmol(2)/L(2) corresponded to a value of 2.2 mmol(2)/L(2) of ion-Ca x Pi and, respectively, t-Ca x Pi of 5.6 mmol(2)/L(2) corresponded 2.8 mmol(2)/L(2) of ion-Ca x Pi. Owing to the good agreement between the results in the 2 centers, these values for risk levels can be used in both centers. When measurement of ionized calcium is used, Ca x Pi values of 2.2 and 2.8 mmol(2)/L(2) can be used instead of generally used values of 4.4 and 5.6 mmol(2)/L(2) with total calcium.     

Calcium‐phosphate and parathyroid intradialytic profiles: A potential aid for tailoring the dialysate calcium content of patients on different hemodialysis schedules

Severe hyperparathyroidism is a challenge on hemodialysis. The definition of dialysate calcium (Ca) is a pending issue with renewed importance in cases of individualized dialysis schedules and of portable home dialysis machines with low‐flow dialysate. Direct measurement of calcium mass transfer is complex and is imprecisely reflected by differences in start‐to‐end of dialysis Ca levels. The study was performed in a dialysis unit dedicated to home hemodialysis and to critical patients with wide use of daily and tailored schedules. The Ca‐phosphate (P)‐parathyroid hormone (PTH) profile includes creatinine, urea, total and ionized Ca, albumin, sodium, potassium, P, PTH levels at start, mid, and end of dialysis. “Severe” secondary hyperparathyroidism was defined as PTH > 300 pg/mL for ≥3 months. Four schedules were tested: conventional dialysis (polysulfone dialyzer 1.8–2.1 m²), with dialysate Ca 1.5 or 1.75 mmol/L, NxStage (Ca 1.5 mmol/L), and NxStage plus intradialytic Ca infusion. Dosages of vitamin D, calcium, phosphate binders, and Ca mimetic agents were adjusted monthly. Eighty Ca‐P‐PTH profiles were collected in 12 patients. Serum phosphate was efficiently reduced by all techniques. No differences in start‐to‐end PTH and Ca levels on dialysis were observed in patients with PTH levels < 300 pg/mL. Conversely, Ca levels in “severe” secondary hyperparathyroid patients significantly increased and PTH decreased during dialysis on all schedules except on Nxstage (P < 0.05). Our data support the need for tailored dialysate Ca content, even on “low‐flow” daily home dialysis, in “severe” secondary hyperparathyroid patients in order to increase the therapeutic potentials of the new dialysis techniques.     

Dialysate bicarbonate variation in maintenance hemodiafiltration patients: Impact on serum bicarbonate,intradialytic hypotension and interdialytic weight gain

Introduction: The dialysate bicarbonate (DB) influences the acid‐base balance in dialysis patients. Very low and high serum bicarbonate (SB) have been related with a higher mortality. Acid‐base balance also has been associated with hemodynamic effects in these patients. The trial aim was to compare the effect of DB concentration variation on SB levels in maintenance hemodiafiltration (HDF) patients and the effect on intradialytic hypotension and interdialytic weight gain. Methods: A prospective study, with 9 months of follow‐up, involving 93 patients, divided in two groups: group 1 and group 2 with a DB of 34 mmol/L and 30 mmol/L, respectively, with monitoring of pre and post HDF SB, intradialytic hypotension, and interdialytic weight gain. Findings: Pre dialysis SB was higher in group 1: median concentration of 22.7 mmol/L vs. 21.1 mmol/L (P < 0.001). Post dialysis SB levels were higher in group 1: median concentration of 28.0 mmol/L vs. 25.3 mmol/L (P < 0.001). Post dialysis SB in alkalotic range was only detected in group 1 (51.2% of the patients). No significant differences were detected in intradialytic hypotension rate [28.0 vs. 27.4 episodes per 1000 sessions in group 1 and 2, respectively, (P = 0.906)] or in average interdialytic weight gain [2.9% vs. 3.0% in group 1 and 2, respectively, (P = 0.710)]. Discussion: DB of 30 mmol/L appears to be associated with SB levels closer to physiological levels than 34 mmol/L. The bicarbonate dialysate, in the tested concentrations, did not appear to have a significant impact on intradialytic hypotension and interdialytic weight gain in maintenance HDF patients.     

Dialysate calcium and calcium/phosphate balance in hemodialysis

The changing pattern of pharmaceutical use in dialysis patients has resulted in several alterations to dialysate calcium concentration over the past 40 years. Non‐calcium–containing phosphate binders and calcimimetics are the most recent examples of drugs that influence the overall calcium balance in dialysis patients. Renal osteodystrophy, vascular disease, and mortality are believed to be linked in patients with chronic kidney disease (CKD), although to date most of the evidence is based only on statistical associations. The precise pathophysiology of vascular calcification in end‐stage renal disease is unknown, but risk factors include age, hypertension, time on dialysis, and, most significantly, abnormalities in calcium and phosphate balance. Prospective studies are required before “cause and effect” can be established with certainty, but it is an active metabolic process with inhibitors and promoters. Serum calcium levels are clearly influenced by dialysate calcium and may therefore play an important role in influencing vascular calcification. Clinical management of hyperphosphatemia is being made easier by the introduction of potent non‐calcium–based oral phosphate binders such as lanthanum carbonate. Short‐term and long‐term studies have demonstrated its efficacy and safety. Vitamin D analogs have been a disappointment in the control of serum parathyroid hormone (PTH) levels, but evidence is emerging that vitamin D has other important metabolic effects apart from this, and may confer survival advantages to patients with CKD. Calcimimetics such as cinacalcet enable much more effective and precise control of PTH levels, but at the cost of a major financial burden. While it is unreasonable to expect that any one of these recent pharmacological developments will be a panacea, they provide researchers with the tools to begin to examine the complex interplay between calcium, phosphate, vitamin D, and PTH, such that further progress is fortunately inevitable.     

The pivotal role of sodium balance in control of blood pressure in dialysis patients

In hemodialysis patients, as in patients with normal kidney function, sodium balance is the major determinant of changes in extracellular volume, and extracellular volume is an important determinant of blood pressure. The osmotic thresholds for thirst and ADH release are normal in kidney failure; pre‐dialysis serum sodium concentration shows a high index of individuality in oliguric hemodialysis patients. Non‐osmotic storage of sodium in vascular walls may also amplify the volume‐sensitivity of blood pressure. The variable relationship between volume removal and change in blood pressure described in clinical studies reflects a state of permanent volume expansion in those whose blood pressure does not fall, or rises, during dialysis, whereas those whose blood pressure falls during dialysis are those who approach normovolemia. Rigorous control of extracellular volume often results in perfect blood pressure control, but may be difficult to achieve safely other than with long, slow dialysis combined with dietary salt restriction.     

Clinical Experiences Calcium and phosphate balance in children on home nocturnal hemodialysis (NHD)

Objective: To evaluate and describe biochemical indices of bone metabolism in 4 children on NHD. Method: The children, aged 12, 13, 14, and 16 yrs, have been treated exclusively on NHD for 6, 9, 9, and 15 mos. Subsequently, Pt 1 converted to a hybrid program of 4 nights on home nocturnal plus 1 session of in center conventional HD per week. Biochemical indices of bone metabolism have been collected prospectively. Results: All baseline pre‐dialysis calcium levels were within normal ranges and each patient was started on a dialysis calcium concentration of 3.0 mEq/L. However, over time the number of asymptomatic biochemical hypocalcaemic episodes increased. The dialysate calcium concentration was increased to 3.5 mEq/L in one and decreased to 2.0 mEq/L in another who was hypercalcemic and receiving concurrent calcitonin for bone pain related to osteoporosis. In Pt 1, the dialysate calcium was increased to 3.5 mEq/L during nocturnal and continued on hybrid therapy. Including an evaluation of dietary intake, all 4 patients had a net positive calcium balance, ranging between 9.8 to 23.5 mmol (393–942 mg). A significant reduction in the predialysis phosphate level was observed in all 4 patients, and none required dietary restrictions or the use of phosphate binders within 2 months or vitamin D within 6 months of HND. In addition, phosphate was added to provide a dialysate concentration of 2.4–6.1 mEq/L to prevent hypophosphatemia. This is reflected by significant reductions in intact PTH levels to the desired range (twice the normal range) in all 4, but the level continued to drop to the normal range and below in 2. In Pt 1, after introduction of hybrid therapy, both levels of phosphate and PTH rose, necessitating recommencement of phosphate binders and vitamin D. Likewise, the (Ca × PO₄) dropped and remained <55 in all 4 patients exclusively on NHD, but started to climb in Pt 1 during hybrid therapy. Conclusion: In our cohort of patients, NHD rapidly lowered plasma phosphate and PTH levels. With NHD, additional dialysate phosphate and possibly calcium may be necessary to prevent chronic losses and development of renal osteodystrophy, and caution is required to prevent either oversuppression of PTH and extraskeletal calcification.     

Modifications to bicarbonate conductivity: A way to increase phosphate removal during hemodialysis? Proof of concept

Introduction Hyperphosphatemia and cardiovascular mortality are associated particularly with end‐stage renal disease. Available therapeutic strategies (i.e., diet restriction, calcium [or not]‐based phosphate binders, calcimimetics) are associated with extrarenal blood purification. Compartmentalization of phosphate limits its depuration during hemodialysis. Several studies suggest that plasmatic pH is involved in the mobilization of phosphate from intracellular to extracellular compartments. Consequently, the efficiency of modified bicarbonate conductivity to purify blood phosphate was tested. Methods Ten hemodialysis patients with chronic hyperphosphatemia (>2.1 mmol/L) were included in the two three–sessions‐per week periods. Bicarbonate concentration was fixed at 40 mmol/L and 30 mmol/L in the first and second periods, respectively. Phosphate depuration was evaluated by phosphate mobilization clearance (K_M). Findings Although bicarbonatemia was lower during the second period (21.0 ± 2.7 vs. 24.4 ± 3.1 mmol/L, P < 0.01), no difference was observed in phosphatemia (2.4 ± 0.5 vs. 2.3 ± 0.4 mmol/L, P = NS). The in‐session variation of phosphate was lower (?1.45 ± 0.42 vs. ?1.58 ± 0.44 mmol/L, P < 0.05) and K_M was higher during the second period (82.94 ± 38.00 vs. 69.74 ± 24.48 mL/min, P < 0.05). Discussion The decrease of in‐session phosphate and the increase in K_M reflect phosphate refilling during hemodialysis. Thus, modulation of serum bicarbonate may play a role in controlling the phosphate pool. Even though correcting metabolic acidosis during hemodialysis remains important, alkaline excess can impair phosphate mobilization clearance. Clinical trials are needed to test the efficiency and relevance of a strategy where bicarbonatemia is corrected less at the beginning of sessions.     

Intensive weight loss combining flexible dialysis with a personalized,ad libitum,coach‐assisted diet program. A “pilot” case series

Obesity is a growing problem on dialysis. The best approach to weight loss has not been established. The risks of malnutrition may offset the advantages of weight loss. Personalized hemodialysis schedules, with an incremental approach, are gaining interest; to date, no studies have explored its potential in allowing weight loss. This case series reports on combining flexible, incremental hemodialysis, and intensive weight loss. Setting: a small Dialysis Unit, following incremental personalized schedules (2–6 sessions/week, depending on residual function), tailored to an equivalent renal clearance >12 mL/min. Four obese and two overweigh patients (5 male, 1 female; age: 40–63 years; body mass index [BMI] 31.1 kg/m²) were enrolled in a coach‐assisted weight loss program, with an “ad libitum” approach (3–6 foods/day chosen on the basis of their glycemic index and glycemic load). The diet consists of 8 weeks of rapid weight loss followed by 8–12 weeks of maintenance; both phases can be repeated. This study measures weight loss, side effects, and patients' opinions. Over 12–30 months, all patients lost weight (median ?10.3 kg [5.7–20], median ΔBMI–3.2). Serum albumin (pre‐diet 3.78; post‐diet 3.83 g/dL), hemoglobin (pre‐diet 11; post‐diet 11.2 g/dL), and acid–base balance (HCO₃ pre‐diet: 23.3; post‐diet: 23.4 mmol/L) remained stable, with decreasing needs for erythropoietin and citrate or bicarbonate supplements. Calcium‐phosphate‐parathyroid hormone (PTH) balance improved (PTH‐pre 576; post 286 pg/mL). Three out of 4 hypertensive patients discontinued, 1 decreased antihypertensives. None experienced severe side effects. Patient satisfaction was high (9 on a 0–10 analog scale). Personalized, incremental hemodialysis schedules allow patient enrollment in intensive personalized weight loss programs, with promising results.     

Citrate vs. acetate dialysate on intradialytic heparin dose: A double blind randomized crossover study

Introduction Citrate containing dialysate has a calcium‐binding anticoagulant effect compared to standard acetic acid containing dialysate. We performed a randomized, double‐blind, crossover trial in maintenance HD patients to determine if citrate dialysate (“citrate”) safely allows for a lower cumulative heparin dose (“heparin dose”). Methods Intradialytic heparin was adjusted to the minimum during a 2‐week run‐in phase. Patients remaining on heparin at the end of the run‐in phase were then randomized to two weeks of HD with acetate dialysate (“acetate”) followed by two weeks of citrate (sequence 1) or two weeks of citrate followed by two weeks of acetate (sequence 2). We estimated a minimum of 14 patients are required to show a 30% reduction in heparin dose per HD session with citrate compared with acetate. Twenty‐five patients entered the run‐in phase, 20 were randomized, and 19 completed the study. Findings The mean heparin dose was reduced by 19% (656 units, 95% CI ?174 to ?1139 units, P = 0.011) in the acetate group, and 30% (1046 units 95% CI ?498 to 1594 units, P < 0.001) in the citrate group. There was no difference in the mean heparin dose reduction between the two dialysates (P > 0.05). The intradialytic ionized calcium in the citrate group was lowered by 0.10 mmol/L (95% CI 0.07 to 0.14 mmol/L, P < 0.001), and remained unchanged in the acetate group. Discussion Although citrate is a safe alternative to acetate, it does not result in additional heparin dose reduction.     

Comparison between different dialysate calcium concentrations in nocturnal hemodialysis

Benefits of dialysate with greater calcium (Ca) concentration are reported in nocturnal hemodialysis (NHD) to prevent Ca depletion and subsequent hyperparathyroidism. Studies with patients dialyzing against 1.25 mmol/L Ca baths demonstrate increases in alkaline phosphatase (ALP) and parathyroid hormone (PTH) and increasing dialysate Ca subsequently corrects this problem. However, whether 1.5 or 1.75 mmol/L dialysate Ca is most appropriate for NHD is yet to be determined, and differences in the effect on mineral metabolism of daily vs. alternate daily NHD have also not been well defined. We retrospectively analyzed mineral metabolism in 48 patients, from 2 institutions (30 at Monash and 18 at Geelong), undergoing home NHD (8 hr/night, 3.5-6 nights/week) for a minimum of 6 months. Thirty-seven patients were dialyzed against 1.5 mmol/L Ca bath and 11 patients against 1.75 mmol/L. We divided patients into 4 groups, based on dialysate Ca and also on the hours per week of dialysis, <40 (1.5 mmol/L, n=29 and 1.75 mmol/L, n=8) or > or =40 (n=4 and 7). We compared predialysis and postdialysis serum markers, time-averaged over a 6-month period, and the administration of calcitriol and Ca-based phosphate binders between 1.5 and 1.75 mmol/L Ca dialysate groups. Baseline characteristics between all groups were similar, with a slightly longer, but nonsignificant, duration of NHD in both 1.75 mmol/L dialysate groups compared with 1.5 mmol/L. The mean predialysis Ca, phosphate, and Ca x P were similar between the 1.5 and 1.75 mmol/L groups, regardless of NHD hr/week. Postdialysis Ca was significantly greater, with 1.75 vs. 1.5 mmol/L in those dialyzing <40 hr/week (2.64+/-0.19 vs. 2.50+/-0.12 mmol/L, p=0.046), but postdialysis Ca x P were similar (2.25+/-0.44 vs. 2.16+/-0.29 mmol(2)/L(2), p=0.60). Parathyroid hormone was also lower with 1.75 vs. 1.5 mmol/L baths in the <40 hr/week groups (31.99+/-26.99 vs. 14.47+/-16.36 pmol/L, p=0.03), although this difference was not seen in those undertaking NHD > or =40 hr/week. Hemoglobin, ALP, and albumin were all similar between groups. There was also no difference in vitamin D requirement when using 1.75 mmol/L compared with the 1.5 mmol/L dialysate. Multivariate analysis to determine independent predictors of postdialysis serum Ca showed a statistically significant positive association with predialysis Ca, dialysate Ca, and total NHD hr/week. An elevated dialysate Ca concentration is required in NHD to prevent osteopenia but differences in serum markers of mineral metabolism between 1.5 and 1.75 mmol/L Ca dialysate in NHD in our study were few. This was similar for patients undertaking NHD <40 or > or =40 hr/week, although differences in the frequency of NHD may also be as important as dialysate Ca with regard to serum Ca levels. With concerns that prolonged higher Ca levels contribute to increased cardiovascular mortality, the optimal Ca dialysate bath is still unknown and further studies addressing bone metabolism with larger NHD numbers are required.     

Regional citrate anticoagulation in CVVH: A new protocol combining citrate solution with a phosphate‐containing replacement fluid

Regional citrate anticoagulation (RCA) is a valid anticoagulation method in continuous renal replacement therapies (CRRT) and different combination of citrate and CRRT solutions can affect acid‐base balance. Regardless of the anticoagulation protocol, hypophosphatemia occurs frequently in CRRT. In this case report, we evaluated safety and effects on acid‐base balance of a new RCA‐ continuous veno‐venous hemofiltration (CVVH) protocol using an 18 mmol/L citrate solution combined with a phosphate‐containing replacement fluid. In our center, RCA‐CVVH is routinely performed with a 12 mmol/L citrate solution and a postdilution replacement fluid with bicarbonate (protocol A). In case of persistent acidosis, not related to citrate accumulation, bicarbonate infusion is scheduled. In order to optimize buffers balance, a new protocol has been designed using recently introduced solutions: 18 mmol/L citrate solution, phosphate‐containing postdilution replacement fluid with bicarbonate (protocol B). In a cardiac surgery patient with acute kidney injury, acid‐base status and electrolytes have been evaluated comparing protocol A (five circuits, 301 hours) vs. protocol B (two circuits, 97 hours): pH 7.39 ± 0.03 vs. 7.44 ± 0.03 (P < 0.0001), bicarbonate 22.3 ± 1.8 vs. 22.6 ± 1.4 mmol/L (NS), Base excess ?2.8 ± 2.1 vs. ?1.6 ± 1.2 (P = 0.007), phosphate 0.85 ± 0.2 vs. 1.3 ± 0.5 mmol/L (P = 0.027). Protocol A required bicarbonate and sodium phosphate infusion (8.9 ± 2.8 mmol/h and 5 g/day, respectively) while protocol B allowed to stop both supplementations. In comparison to protocol A, protocol B allowed to adequately control acid‐base status without additional bicarbonate infusion and in absence of alkalosis, despite the use of a standard bicarbonate concentration replacement solution. Furthermore, the combination of a phosphate‐containing replacement fluid appeared effective to prevent hypophosphatemia.     

Determination of free calcium and calcium-containing species in human plasma by capillary electrophoresis-inductively coupled plasma optical emission spectrometry

A new method for the determination of free calcium concentration in human plasma was developed by online coupling capillary electrophoresis (CE) with inductively coupled plasma optical emission spectrometry (ICP-OES). Baseline separation of calcium-containing species was achieved by CE-ICP-OES in a 120-cm-long capillary with 100-microm internal diameter, at 20 kV applied voltage, with a 30 mmol/L Tris-HCl buffer at pH 7.4. A total of eight calcium-containing species were found in human plasma; the concentration of free calcium ion was found to be 41.9 mg/L. The concentrations of calcium for other seven calcium species, estimated from the calibration against Ca(2+) standard, were 3.14-15.6 mg/L. The precision (RSD, n = 10) ranged from 1.2 to 2.7% for the migration time and 2.8 to 3.9% for the peak area. The developed method was also applied to analyze plasma samples with recovery ranged from 94.5 to 102% for samples spiked with 40 mg/L free Ca(2+) ion.     

Quotidian dialysis Survival in 221 patients treated by short daily hemodialysis for 315 patient years

Scanty data suggests that large solutes show a kinetic behavior that is different from urea. The question investigated in this study is whether other small water‐soluble solutes such as some guanidino compounds show a kinetic behavior comparable or dissimilar to that of urea. This study included 7 stable conventional hemodialysis patients without residual diuresis undergoing low flux polysulphone dialysis (F8 and F10HPS). Blood samples were collected from the inlet and outlet blood lines before the dialysis session, after 5, 15, 30, 120 minutes, and immediately after discontinuation of the session. Plasma concentrations of urea, creatinine (CTN), creatine (CT), guanidinosuccinic acid (GSA), guanidinoacetic acid (GAA), guanidine (G), and methylguanidine (MG) were used to calculate corresponding dialyzer clearances. A two‐pool kinetic model was fitted to the measured plasma concentration profiles, resulting in the calculation of the perfused volume (V₁), the total distribution volume (V_tot), and the inter‐compartmental clearance (K₁₂); solute generation and ultrafiltration were determined independently. No significant differences were observed between V₁ and K₁₂ for urea (6.4 ± 3.3 L and 822 ± 345 mL/min) and for the guanidino compounds. However, with respect to V_tot, GSA was distributed in a smaller volume (30.6 ± 4.2 L) compared to urea (42.7 ± 6.0 L ? P < 0.001), while CTN, CT, GAA, G, and MG showed significantly larger volumes (54.0 ± 5.9 L, 98.0 ± 52.3 L, 123.8 ± 66.9 L, 89.7 ± 21.4 L, and 102.6 ± 33.9 L, respectively). These differences resulted in markedly divergent effective solute removal: 67%(urea), 58%(CTN), 42%(CT), 76%(GSA), 37%(GAA), 43%(G), and 42%(MG). In conclusion, the kinetics of the guanidino compounds under study are different from that of urea; hence, urea kinetics are not representative for the removal of other uremic solutes, even if they are small and water‐soluble like urea.     

Modelling calcium leaching kinetics of cement asphalt paste

Calcium leaching is an important durability problem for cement asphalt (CA) mortar used in ballastless slab track which is under the coupled action of train-induced dynamic load and rainwater erosion. In this paper, a model based on the calcium mass conservation and the thermodynamic equilibrium of calcium was developed to describe the calcium leaching of CA paste in both deionized water and ammonium nitrate solution. In this model, the spatial–temporal distribution of solid calcium content in skeleton, porosity and diffusivity, which are directly or indirectly relevant to the calcium concentration in pore solution, were considered. Finite difference method was utilized to solve this model, and a three layer Crank–Nicolson differential scheme was applied to improve the stability. The model was experimentally verified using the Ca/Si molar ratio in solid and the calcium leaching rate characterized by SEM–EDX and potentiometric titration respectively. It was found that asphalt content does not change the spatial distribution of solid calcium in CA paste. Asphalt affects the leaching rate by reducing solid calcium concentration and changing the activation energy of micro-pore wall. Accelerating factors by ammonium nitrate solution were experimentally determined and predicted by the model.     

Treating mineral metabolism disorders in patients undergoing long hemodialysis: A search for an optimal strategy

In hemodialysis (HD) patients, mineral metabolism (MM) disorders have been associated with an increased mortality rate. We report the evolution of MM parameters in a stable HD population undergoing long hemodialysis by performing an annual cross-sectional analysis for every year from 1994 to 2008. The therapeutic strategy has changed: the dialysate calcium concentration has decreased from a mean of 1.7 ± 0.1 to 1.5 ± 0.07 mmol/L and has been adapted to parathyroid hormone serum levels (from 1 to 1.75 mmol/L). The use of calcium-based and aluminum-based phosphate binders has decreased and they have been replaced by sevelamer; alfacalcidol has partly been replaced by native vitamin D. The percentage of patients with a parathyroid hormone serum level between 150 and 300 pg/mL has increased from 9% to 67% (P<0.001); the percentage of patients with phosphataemia between 1.15 and 1.78 mmol/L has increased from 39% to 84% (P<0.001). The percentage of those with albumin-corrected calcemia between 2.1 and 2.37 mmol/L has increased from 29% to 61% (P<0.001), and that of patients with a calcium-phosphorous product (Ca × P) level >4.4 mmol/L decreased from 8.8% to 2% (P=0.02). Although patients undergo long and intensive HD treatment, MM disorders are common. However, an appropriate strategy, mostly consisting of native vitamin D supplementation, progressive replacement of calcium-based phosphate binders with non–calcium-based ones, and individualization of dialysis session duration and dialysate calcium concentration, would result in a drastic improvement.     

Regional Anticoagulation with Sodium Citrate in Pediatric Patients on Intermittent Hemodialysis Therapy with Bleeding Risks

Heparin‐free anticoagulation in hemodialysis (HD) is advocated for patients with clotting abnormalities and risk of bleeding. Objective: First publication on regional citrate anticoagulation (RCA) in children. RCA is free from systemic effects, guarantees excellent dialyzer life, but requires careful monitoring. Methods: We report on 3 patients treated by intermittent RCA HD (4 h each, high‐flux dialyzer F40, Fresenius): (1) 17‐year‐old boy (renal transplant failure, access via cubital Cimino fistula) after hypertensive intra‐cerebral hemorrhage (2 sessions); (2) 13‐year‐old girl (hemolytic uremic syndrome, access via jugular vein Shaldon catheter) after abdominal surgery and bleeding (8 sessions); and (3) 7‐year‐old boy (hyperoxaluria, access via PermCath^® jugular vein catheter) after renal transplant biopsy (3 sessions). Sodium citrate 30% was infused into the extra corporeal circuit (blood flow 150 mL/min) before dialyzer (initial flow 30 mL/min) and calcium gluconate 10% for antidote into venous line near of catheter or fistula (initial flow 40 mL/min). Post‐dialyzer extracorporeal serum Ca⁺⁺ (aim < 0.3 mmol/L) and pre‐dialyzer intra‐corporeal Ca⁺⁺ (aim > 0.9) were measured for every 30 min. Serum Na⁺, K⁺, base excess (BE), blood flow, blood pressure, heart rate, and blood out‐flow and in‐flow pressure were also monitored. Results: For adequate RCA (mean extracorporeal serum Ca⁺⁺ 0.24 ± 0.04 mmol/L), a mean citrate flow of 36.1 ± 5.9 mL/h and a mean calcium substitution rate of 40.8 ± 3.4 mL/h were needed. Intra‐corporeal Ca⁺⁺ was kept at 1.10 ± 0.07 mmol/L. Extracorporeal activated clotting time (ACT) was 194 ± 41 and intra‐corporeal ACT 90 ± 12 sec. Serum Na⁺, K⁺, and BE during HD were 138 ± 2, 3.5 ± 0.3, and ?0.6 ± 1.1 mmol/L, respectively. Mean arterial blood pressures of patients 1–3 were 117 ± 5, 103 ± 5, and 102 ± 6 mmHg. All patients were stable and without any bleeding during HD. The only adverse event was 1 episode of hypocalcemia (Ca⁺⁺ < 0.6 mmol/L) cured by stopping dialysis. Conclusions: Local anticoagulation with sodium citrate during intermittent HD can be applied safely in children and adolescents.