Value of serum aluminium monitoring in dialysis patients: a multicentre study

The clinical relevance of regular serum aluminium monitoring in dialysis patients was investigated in a multicentre study by 6-monthly determination of the serum aluminium during 4 consecutive years. In a group totalling 1193 patients, a striking decrease of mean serum aluminium was observed the last 2 years of the study. This phenomenon was accompanied by a substantial reduction of the prescribed dose of aluminium hydroxide (Al(OH)3) and its partial replacement by calcium carbonate (CaCO3) and/or magnesium hydroxide (Mg(OH)2). Under this policy serum phosphate control remained satisfactory. In all the centres, water treatment was found to be adequate, yielding dialysate aluminium around 2 micrograms/l. Dialysis patients with clinically overt liver disease showed a significantly greater median serum aluminium concentration than that observed in a control dialysis population. Compared to the latter group, the median serum aluminium concentration of dialysis patients with diabetes mellitus did not differ significantly. Results further indicated that patients with biopsy-proven osteomalacia presented a significantly greater median serum aluminium compared to that of patients without osteomalacia. We demonstrated that a serum aluminium of 60 micrograms/l provides a relatively sensitive (82%) and specific (86%) index for the detection of aluminium-related bone disease (ARBD). Provided the aluminium determinations are performed by a qualified laboratory, serum monitoring in dialysis patients (a) allows the safer use of aluminium-containing phosphate binders, and (b) is of value in the diagnosis of overload/toxicity.     

Dialysate calcium reduction in CAPD patients treated with calcium carbonate and alfacalcidol.

The use of oral calcium carbonate as a phosphate binder is often complicated by hypercalcaemia, particularly with concomitant use of vitamin D analogues. We previously found that stepwise reduction of dialysate calcium effectively countered this complication in haemodialysis patients, and have now assessed the strategy in CAPD patients. Seventeen patients underwent conversion from aluminium hydroxide to calcium carbonate and were followed for 5 months, with subsequent addition of alfacalcidol for a further 5 months. Standard CAPD dialysate (1.75 mM calcium) was used, reducing to 1.45 mM and, if necessary, to 1.00 mM in patients who became hypercalcaemic. While receiving calcium carbonate alone, 12 of the 17 patients became hypercalcaemic, this responding in four to dialysate calcium reduction to 1.45 mM. In the remaining eight patients, further reduction to 1.00 mM was required and in two patients even this failed to control hypercalcaemia adequately, necessitating reversion to aluminium hydroxide. Phosphate control remained unchanged, as did calcium x phosphorus product. There were transient increases of blood ionised calcium, and decreases of parathyroid hormone, with progressive reduction of serum aluminium and alkaline phosphatase. The addition of alfacalcidol (0.25 microgram/day) led to hypercalcaemia in six subjects, successfully countered by dialysate calcium reduction in four. The results show that standard CAPD dialysate calcium at 1.75 mM is too high for the majority of calcium carbonate treated patients and that substantial reductions of the dialysate calcium concentration are required if calcium carbonate is to be used effectively.     

Low-calcium dialysis fluid and oral calcium carbonate in CAPD. A method of controlling hyperphosphataemia whilst minimizing aluminium exposure and hypercalcaemia.

Oral calcium carbonate is an effective phosphate binder in dialysis patients. Its use minimizes aluminium intake, and by maintaining a high-normal serum ionized calcium, suppresses serum parathyroid hormone levels. However, the dose required to control hyperphosphataemia may cause hypercalcaemia. We performed prospective studies in 50 previously undialysed patients starting CAPD (28 study group, 22 control group). Calcium carbonate was the only phosphate binder used in the study group which utilized a low calcium PD fluid (calcium 1.25 mmol/l), whilst the control group used standard PD solution (calcium 1.75 mmol/l) with calcium carbonate plus aluminium hydroxide phosphate binders as clinically indicated. The study group was able to take larger doses of oral calcium carbonate with no increase in episodes of hypercalcaemia compared to the control group. There were no instances of hypocalcaemia in any patient using the low-calcium dialysis fluid. Phosphate control was better in the study group, despite the additional use of aluminium-containing phosphate binders by some patients in the control group. Serum aluminium levels in the study group were maintained at < 11.5 mumol/l, but increased significantly in the control group from 3 months onward. Mean serum parathyroid hormone in the study group declined significantly from baseline values over the first 6 months, and remained at the lower level. Bone histology showed a tendency towards improvement over the 12 months, in terms of osteoclast numbers and activity. We conclude that using dialysis fluid with a reduced calcium concentration in compliant, well-monitored patients is safe.(ABSTRACT TRUNCATED AT 250 WORDS)     

Magnesium, calcium and PTH relationships in dialysis patients after magnesium repletion

Sixteen end-stage renal disease patients who received hemodialysis for 2.9 years with no magnesium in the dialysate were evaluated for serum calcium, magnesium and parathyroid hormone (PTH) status. Eleven of these patients became hypomagnesemic with subnormal total and ultrafiltrable serum Mg concentrations (low-Mg group). The five remaining patients had consistently normal serum Mg concentrations (normal-Mg group). All had normal total and ionized serum Ca. However, the total and ionized serum Ca levels in the low-Mg group were significantly lower than those of the normal-Mg group. Within 2 weeks of Mg repletion (by dialysis against 0.25 mM of Mg), the N-terminal PTH, total and ultrafiltrable serum Mg, and the total and ionized serum Ca increased in the low-Mg group. There was a strong negative correlation between initial serum Mg and the percent change in N-terminal PTH (r = 0.833) at 2 weeks for all patients. There was also a strong positive correlation between initial ionized Ca and total serum Mg for all patients (r = 0.774). Mg repletion decreased the incidence of cramps experienced during dialysis by all patients. These data suggest that Mg-free dialysis in some patients can cause Mg depletion, which is symptomatic and which may suppress the parathyroid gland.     

High-dose calcium carbonate with stepwise reduction in dialysate calcium concentration: effective phosphate control and aluminium avoidance in haemodialysis patients

To reduce potentially toxic aluminium exposure, the phosphate binding agent aluminium hydroxide was replaced by high-dose oral calcium carbonate in 15 haemodialysis patients. Stepwise reduction in dialysate calcium concentration (from 1.75 to 1.35 mmol/l and then to 1.05 mmol/l) was made when necessitated by hypercalcaemia. After 6 months, the mean daily dose of calcium carbonate was 62 mmol (range 25-150 mmol). This dose maintained good control of plasma phosphate (baseline, 1.34 +/- 0.32 mmol/l (mean +/- SD); 12 weeks, 1.30 +/- 0.22 mmol/l; 24 weeks, 1.51 +/- 0.31 mmol/l). Calcium x phosphate product did not rise significantly (baseline, 3.41; 12 weeks, 3.44; 24 weeks, 4.02). Apart from a transient early increase, ionised calcium did not change significantly (baseline, 1.23 +/- 0.10 mmol/l; 12 weeks, 1.24 +/- 0.10 mmol/l). Intact (1-84) parathyroid hormone concentration decreased from 241 pg/ml to 116 pg/ml (median values, P less than 0.05) after 12 weeks. This simple and well-tolerated regimen almost completely eliminated oral aluminium exposure, effectively controlled plasma phosphate and calcium concentrations, and reduced hyperparathyroidism.     

Use of magnesium hydroxide and low magnesium dialysate does not permit reduction of aluminum hydroxide during continuous ambulatory peritoneal dialysis

In an effort to reduce the ingestion of aluminum in phosphate-binding antacids, we treated seven patients on continuous ambulatory peritoneal dialysis (CAPD) with low magnesium dialysate and phosphate binders containing both aluminum and magnesium hydroxide. The total amount of phosphate binders prescribed was adjusted to maintain the serum phosphorus at normal levels. The dose of magnesium hydroxide was limited by intolerable gastrointestinal side effects in six of the seven patients. One patient also developed symptomatic hypermagnesemia. When magnesium hydroxide was prescribed in tolerable doses, the mean aluminum dose was not significantly decreased compared with the dose when taking aluminum hydroxide alone. We conclude that substitution of magnesium hydroxide for aluminum hydroxide as a phosphate binder fails to reduce the dose of aluminum in most patients on CAPD.     

Alkalosis and hypomagnesaemia: unwanted effects of a low-calcium CAPD solution

We studied 43 CAPD patients for 4 months during the change froma high-calcium dialysis fluid (Baxter PD1) to a low-calciumfluid (Baxter PD4), which also contained low magnesium (0.25mmol/l) and high lactate concentrations (40 mmol/l). Serum calciumfell significantly as did the incidence of hyper-calcaemia,whilst the proportion of patients taking calcium-containingphosphate binders increased. There was a non-significant increasein serum i-PTH levels but the proportion with i-PTH > 150pg/ml (normal range 10–65 pg/ml) increased significantly.There was a significant fall in serum magnesium level and sevenpatients developed hypomagnesaemia. Serum bicarbonate increasedsignificantly and progressively and 17 patients were alkaloticat 4 months, five severely (bicarbonate 35–40 mmol/l).One patient developed recurrent episodes of painful subcutaneousand periarticular calcification, which may have been relatedto the alkalosis. Initial serum bicarbonate levels correlatedsignificantly with dialysis adequacy assessed by daily Kt/V(r=0.458, P=0.002). The relationship to adequacy was abolishedduring the period of use of the high-lactate dialysis fluid.Use of low-magnesium CAPD fluids must be supported by regularmonitoring of serum magnesium levels. The high lactate concentrationin such fluids may not be appropriate and is potentially hazardouswhen individualization of dialysis dose demands the use of relativelyhigh exchange volumes. Low serum bicarbonate levels in CAPDpatients reflect inadequate dialysis, which use of these fluidsserves to mask.     

Effect of treatment with 1.25 and 1.75 mmol/l calcium dialysate on bone mineral density in haemodialysis patients

The effect of two different dialysate solutions with a calciumconcentration of 1.25 and 1.75 mmol/l was evaluated in 14 patients,using a cross-over design. Patients were treated with each solutionduring a period of 6 months. Treatment with calcium supplements,vitamin D and aluminium hydroxide was adapted weekly, accordingto the results of blood chemistry. PTH, SAP, and ionized calciumwere determined monthly, bone density with DXA and QCT beforeand after 6 months of treatment. During treatment with both1.25 and 1.75 calcium dialysate (cad), the control of serumcalcium and phosphate was similar. PTH did not change duringeither treatment. SAP decreased during treatment with 1.75,but remained stable with 1.25 mmol/1 cad. Bone density evaluatedwith DXA remained unchanged during both treatments. QCT measuredbone density increased from 101.29± 13.50 to 106.79±13.14mg/ml in the 1.75 cad group, while it did not vary in the 1.25cad group, (107.75 ±13.48 versus 108.97 ±13.40mg/ml). It is concluded that lowering the calcium content ofthe dialysate does not negatively influence the control of serumcalcium and phosphate, nor does it aggravate hyper-parathyroidismwhen vitamin D is administered simultaneously. Under the presentconditions, osteopenia and possibly bone mineralization improveonly in the group dialysed with 1.75 Ca.     

Inverse correlation between serum magnesium and parathyroid hormone in peritoneal dialysis patients: a contributing factor to adynamic bone disease?

Background Secondary hyperparathyroidism (SHPTH) is present in many patients with end-stage renal disease (ESRD) and has been linked to uremic bone disease. Parathyroid hormone (PTH) levels are affected by calcium, vitamin D, and phosphorus. Recent data suggests that serum magnesium may also modulate PTH levels. Objective The aim of this retrospective study was to investigate the impact of different calcium (Ca) and magnesium (Mg) concentrations of dialysis solutions on serum Mg and serum PTH levels in peritoneal dialysis (PD) patients. Patients and methods Two groups of PD patients-group A (n = 17) on “standard” Ca and Mg dialysis solution (SCa–MgD) (Ca: 1.62 mmol/l, Mg: 0.75 mmol/l and Lactate 35 mmol/l), and group B (n = 29) on “low” Ca and Mg dialysis solution (LCa–MgD) (Ca: 1.25 mmol/l, Mg: 0.25 mmol/l and Lactate 40 mmol/l), on PD for more than 6 months, were studied. Calcium carbonate (CaCO₃) was used as the phosphate (P) binder in 87% (40/46) of the patients. Biochemical parameters were evaluated every 1–2 months over 6 months and the mean values were computed. Results No significant differences were found between the two groups in all parameters except for serum Mg and PTH. Serum Mg was higher in SCa–MgD group compared to those in the LCa–MgD group (1.05 ± 0.19 vs 0.90 ± 0.23 mmol/l, respectively) and serum PTH was higher in LCa–MgD group compared to those in SCa–MgD group (72.3 ± 64.2 vs 31.1 ± 39.0 pmol/l, respectively) even though serum Ca was not different. There was a statistically significant inverse correlation between serum Mg and PTH levels (r = −0.357, p < 0.05). Conclusion Serum Mg is lower and serum PTH higher in patients dialyzed with lower Mg concentration dialysis solution compared to those with higher Mg concentration dialysis solution. Our study confirms previous reports that serum Mg may have a suppressive role on PTH synthesis and/or secretion, and thus may play a role in pathogenesis of adynamic bone disease that often develops in patients on chronic PD with high calcium and high magnesium concentrations.     

Risk of Aluminium Intoxication in Long-term Acetate Redy Dialysis

Closed-circuit dialysis using the Redy sorbent cartridge toregenerate the dialysate has been incriminated in previous reportsas a cause of severe fracturing osteomalacia and fatal encephalopathyin several patients treated with this procedure for 15–36months. In a retrospective study, we compared 15 unselectedpatients who had received Redy dialysis for 66±14 monthswith 15 control patients dialysed with single passage of dialysate. Redy and control patients were matched for age, sex, and durationof dialysis. They belonged to two dialysis centres, situatedin the same geographical area and having a common water supply.Mean serum and bone aluminium concentrations were slightly greaterin the Redy group but the differences were not significant.Pathological fractures had occurred in two Redy patients andin one control, but could not be attributed to aluminium-inducedbone disease. Although the histochemical staining for aluminiumin bone was positive in six patients, diagnosis of aluminium-inducedbone disease was made in one case only. The results of bonehistomorphometry did not differ significantly between the twogroups. Our findings may be explained by the strict applicationof the measures required to avoid aluminium contamination ofthe Redy dialysate, i.e. sufficient rinsing before dialysis,use of almost aluminium-free water, and of acetate-buffereddialysate.     

Minimising changes in plasma calcium and magnesium concentrations during plasmapheresis

Hypocalcaemic tetany is a known complication of plasmapheresis. It has two causes. Intravenously administered 4.5% human albumin solution (HAS) has no calcium or magnesium, so the replacement of plasma with this fluid depletes these ions. The citrate in fresh frozen plasma (FFP) chelates divalent cations, so the exchange with this at the end reduces the proportion of calcium and magnesium that is ionised. We studied the effect of supplementing HAS with 2 mmol/l calcium chloride and 0.8 mmol/l magnesium sulphate on the changes in ionised and total calcium and magnesium concentrations throughout plasmapheresis. The supplements prevented the falls in these concentrations that is otherwise seen during the HAS infusion, and, thus, the transient fall in ionised calcium concentration induced by the citrate in the FFP was not so profound, reaching 0.92 instead of 0.78 mmol/l (P = 0.002). Supplementation with calcium and magnesium during HAS maintains their balance and prevents tetany during the FFP infusion.     

Ranitidine reduces phosphate binding in dialysis patients receiving calcium carbonate

BACKGROUND: In a previous controlled study we showed that ranitidine significantlyreduced the phosphate binding of aluminium hydroxide in patientswith renal failure, probably by increasing intragastric pH. METHODS: In this study we have investigated the effect of ranitidineon the phosphate binding of calcium carbonate in fifteen dialysispatients. Ranitidine 300 mg or a placebo tablet was taken beforebreakfast for two 4-week periods in a double-blind crossovertrial with no washout period. The mean daily dose of calciumcarbonate was 2 g and neither the dose nor the patient's dietwas changed during the study period. Blood was taken at 2-weeklyintervals for serum phosphate, calcium, albumin, and alkalinephosphatase measurements, and at the end of each treatment periodfor parathyroid hormone (PTH) level. RESULTS: Serum phosphate concentrations were significantly higher duringthe ranitidine than the placebo phase, 1.78 (±0.43 SD)versus 1.59 (±0.49 SD) mmol/1 (P<0.001). Serum calcium,albumin, PTH, and alkaline phosphatase concentrations did notdiffer between the two treatment periods. CONCLUSION: This study shows that ranitidine has a significant adverse effecton the phosphate binding of calcium carbonate in patients withrenal failure.     

Magnesium homeostasis in patients undergoing continuous ambulatory peritoneal dialysis: role of the dialysate magnesium concentration

We carried out this retrospective study to examine the magnesium status of our chronic ambulatory peritoneal dialysis (CAPD) patients dialyzed with 0.75 mmol/L (group I) or 0.50 mmol/L (group II) magnesium peritoneal dialysis solution. A total of 34 anuric patients on CAPD (age:31-72 years; duration of CAPD:7-74 months) were studied. None of them received magnesium-containing phosphate binders or vitamin D. Biochemical parameters including magnesium, calcium, phosphate, parathormone, and albumin were measured in all patients. The corrected for hypoalbuminemia serum magnesium concentration in group I was significantly higher compared to that found in group II. However, there were no significant differences in the other measured parameters between the two groups of CAPD patients, though iPTH levels were somewhat increased in group II patients. Serum magnesium levels were weakly correlated with serum prealbumin levels in both groups of CAPD patients (r=0.16, P=0.08 and r=0.17, P=0.07). The incidence of hypermagnesemia was significantly higher in group I patients versus those in group II (13/19 68.4%] vs. 2/15 13.3%], P<0.01). On the other hand, no patient developed hypomagnesemia (corrected total magnesium <0.65 mmol/L), despite the trend toward decreased magnesium levels in group II patients. Our results point out that serum iPTH levels and nutritional parameters, such as prealbumin levels, should be taken into account in the choice of the magnesium concentration of the peritoneal dialysis fluid.     

The Renin-Angiotensin-Aldosterone System During Haemodialysis With Acetate or Bicarbonate at Different Dialysate Sodium Concentrations

The hormones of the renin–angiotensin–aldosteronesystem were measured during regular haemodialysis with acetateor bicarbonate at dialysate sodium concentrations of 135, 140,145, and 150 mmol/l. Plasma renin activity and aldosterone concentrationwere higher during acetate haemodialysis than during bicarbonatehaemodialysis. At lower dialysate sodium concentrations, plasmarenin activity (acetate dialysis and bicarbonate dialysis) andaldosterone concentration (only acetate dialysis) were higherthan they were at higher dialysate sodium concentrations. Plasmarenin activity increased during acetate dialysis, but did notchange during bicarbonate dialysis. Aldosterone and potassiumconcentrations were positively correlated. Aldosterone decreasedduring haemodialysis (increase to predialysis values at theend of haemodialysis (4 h) at lower dialysate sodium concentrations).It is concluded that the renin-angiotensin-aldosterone systemis activated more during acetate dialysis than during bicarbonatedialysis. Aldosterone concentrations seem to be related moreclosely to serum potassium than to renin–angiotensin–aldosteronesystem and to serum sodium intradialytically.     

Reduced calcium dialysate in CAPD patients: efficacy and limitations

Background. The increasing use of 'reduced calcium' dialysate in CAPD patients treated with calcium-based phosphate binders has raised concerns that this could lead to negative calcium balance, worsening hyperparathyroidism, and osteopenia. Methods. The present study was conducted to examine the possibilities (a) that 1.25 mM calcium dialysate leads to negative calcium balance and worsening hyperparathyroidism, and (b) that conversely 1.25 mM calcium dialysate is still too high for some patients. We studied 22 patients who, after a 2-month run in using 1.75 mM calcium dialysate and aluminium hydroxide binders, entered a 3-month phase of 1.25 mM calcium dialysate with continuation of aluminium hydroxide as the sole phosphate binder. The patients then entered a final 9-month phase in which dialysate calcium remained at 1.25 mM and calcium carbonate was substituted for aluminium hydroxide and progressively titrated to achieve optimum phosphate control. Results. During the initial 3-month period, parathyroid hormone increased from 259, range 11-1149 to 405, range 16-1318 pg/ml (P=0.0001) and ionized calcium decreased from 1.17±0.06 to 1.11±0.08 mM (P=0.0004). The subsequent 9-month phase was associated with return of parathyroid hormone to baseline levels. Further dialysate calcium reduction to 0.6 mM was implemented in the four patients, who became hypercalcaemic. Conclusion. This study has clearly shown that reduction of dialysate calcium to 1.25 mM can be harmful to CAPD patients if oral calcium availability is inadequate. It has also shown that dialysate calcium at 1.25 mM is a compromise, with increased risk of hyperparathyroidism if calcium intake is too low and, conversely, risk of hypercalcaemia and unacceptable increases of the Ca x Pi product in a minority of patients. At these extremes there is a need for a high-calcium dialysate (1.75 mM) and a very low-calcium dialysate (0.6 mM or less), to optimize management.     

Serum concentrations of calcitriol and PTH in hemo-dialysis patients on treatment with calcium carbonate.

The effects of calcium carbonate and aluminium hydroxide as phosphate binders were investigated in nine patients on chronic hemodialysis. Aluminium hydroxide, 1 g X 3, was given during four weeks followed by a period of four weeks without any phosphate binders and after this calcium carbonate, 2.5 g X 3, was introduced for four weeks. Calcium carbonate resulted in lowering of bioactive PTH in serum from 22.4 to 16.4 pM and a rise of serum calcitriol from 8.0 to 11.5 pg/ml with maintained control of phosphate and without significant difference in the calcium-phosphate product. Calcium in serum rose from 2.27 to 2.57 mM and mild hypercalcemia (less than 3.0 mM) in five of the patients could be controlled by dose reduction of calcium carbonate without losing control of serum phosphate levels. We conclude that calcium carbonate offers advantages as a phosphate binder compared to aluminium hydroxide in that it offers equal control of serum phosphate and elevates serum calcium which helps to control the hyperparathyroidism secondary to uremia.     

The Use of Calcium Carbonate to Treat the Hyperphosphataemia of Chronic Renal Failure

This study evaluates the use of calcium carbonate in chronicrenal failure. Forty-eight patients (25 male, 23 female, meanage 54.3 years, six pre-dialysis, 12 CAPD, 30 haemodialysis)on phosphate restriction and requiring aluminium hydroxide (mean2.4±0.8 g/ day) to control serum phosphate, were convertedto an equivalent dose of calcium carbonate (2.5±0.6 g/day).None received vitamin D analogues. Three months post-conversionthere was a significant decrease in mean (±SEM) serumphosphate (1.86±0.08 versus 1.66±0.05 mmol/l,P<0.01) and serum aluminium (28.3±5.4 versus 13.2±3.0µg/l,P<0.0001); calcium/phosphate product was unchanged. Post-conversionthere was an increase in serum bicarbonate, (20.6±0.5versus 22.1±0.6 mmol/l, P<0.01) and serum calcium(2.32±0.02 versus 2.45±0.03 mmol/l, P<0.0001).No change in serum creatinine, alkaline phosphatase or parathormoneoccurred. No adverse effects were reported but nine (18%) patientsbecame hypercalcaemic (2.7 to 2.93 mmol/l), eight of whom respondedto dose reduction. Hypercalcaemia did not correlate with pre-conversionserum calcium, parathyroid hormone, alkaline phosphatase oraluminium. Calcium carbonate is an effective alternative toaluminium-based phosphate binders. It produces a beneficialincrease in serum calcium and bicarbonate and a significantdecrease in serum aluminium. Hypercalcaemia is unpredictablebut is easily reversible in the majority of patients.     

The role of magnesium binders in chronic kidney disease

Magnesium is predominantly an intracellular cation that plays a critical role in cellular physiology. Serum levels are often slightly elevated in patients on chronic hemodialysis and older reports suggests that total body stores may also be increased, based on bone biopsies in patients treated with higher dialysate magnesium levels than are currently in use today. Several studies have shown that magnesium, particularly in the form of magnesium carbonate, is an effective phosphate binder and can decrease patients' exposure to calcium. Retrospective studies suggest that magnesium may prevent vascular calcification in dialysis patients, although this remains controversial and has not been evaluated prospectively. Magnesium may reduce arrhythmias postoperatively and, while it may theoretically reduce arrhythmic death in dialysis patients, this hypothesis has never been tested. While short-term or adjuvant use of magnesium carbonate appears safe and effective as a phosphate binder, more studies are needed to evaluate the long-term effects on vascular calcification, bone histology, and mortality.     

Calcium balance and intact PTH variations during haemodiafiltration

BACKGROUND.: Recent approaches to prevent and treat secondary hyperparathyroidismin dialysis patients include decreasing dialysate Ca contentfrom 1.75 to 1.5 mM or lower. We have recently observed thatby decreasing dialysate Ca to 1.25 mM a rise in intact parathormoneserum levels occurs despite adequately controlled predialysisCa and phosphate serum levels. In that study complementary treatmentwith high-dose 1(OH) vitamin D3 was required to suppress theparathormone. In the present study we aimed to assess the totalCa balance as well as the modifications in parathormone inducedby the dialysis session in order to understand the reasons forwhich the rise in parathormone was induced. METHODS.: Fourteen HD patients treated with haemodi-afiltration threetimes/week gave their informed consent for the study. They weredistributed in two groups with identical treatment but for thedialysate Ca content which was 1.5 and 1.25 mM respectivelyand for the amount of oral CaCO₃ received. Total and ionizedCa, phosphate, pH, and albumin as well as parathormone weremeasured in serum before and after dialysis and in the spentdialysate during two dialysis sessions. RESULTS.: Serum ionized Ca (normalized to pH 7.4) did not change during1.25 mM dialysate Ca and significantly increased with 1.5mM(P<0.001). The end-dialysis values being 1.25±0.02and 1.38±0.02 mM respectively. Total Ca significantlydecreased with 1.25mM dialysate Ca (P<0.04) and increasedwith 1.5mM (P<0.003), the end-dialysis values being 2.51±0.03and 2.75±0.04mM respectively. In the dialysate the differencein ionized Ca concentrations, fresh minus spent dialysate was–1.78±1.12 mmol/l (NS) and 4.26±1.47 mmol/l(P<0.02) respectively for 1.25 and 1.5 mM dialysate Ca. Thedifference in total Ca concentrations, fresh minus spent dialysatewas –0.1±0.01 mmol/l (P<0.005 and –0.002±0.01 mmol/l (NS) respectively. Phosphate removal was higherin 1.25 mM dialysate-Ca-treated patients (40.4±1.75 mmol/sessionversus 34±1.3 mmol/session respectively, P<0.015).The use of 1.25 mM dialysate Ca did not result in a change inserum parathormone, while the use of 1.5 mM resulted in a decreaseof 43±15% (P<0.02) in patients with marked hyperparathyroidism. CONCLUSIONS.: Our data remind us of the difficulty in assessing Ca balancesand identifies the phosphate content as one of the factors influencingthe amount of ionized Ca in the dialysate. Although the long-termparathormone increase we observed using 1.25 mM dialysate Camay well not be explained only by the acute intradialytic modifications,the negative Ca balance identified here (which was missed withthe analysis of ionized Ca alone), and the lack of parathormoneinhibition may participate in the relapse of hyperparathyroidism.     

Magnesium Hydroxide as a Complementary Aluminium-free Phosphate Binder to Moderate Doses of Oral Calcium in Uraemic Patients on Chronic Haemodialysis: Lack of Deleterious Effect on Bone Mineralisation

To control hyperphosphataemia without hyperaluminaemia. Al (OH)₃which was given in addition to high doses of oral calcium, wasreplaced by Mg(OH)₂ for 6 months in 20 haemodialysed patientsand for 20 months in 12. The treatment during the control periodwas 110±91 mmol/day of oral calcium element given asCaCO₃ and/or Calcium Sorbisterit and 1.05±1.47 g/dayof Al(OH)₃ Haemodialysis treatment was 4 h, thrice weekly. Toprevent hypermagnesaemia, dialysate magnesium was decreasedfrom 0.75 mmol/1 to 0.375 mmo/1. After a control period of 3months, Mg(OH)₂ was given at a mean dose of 2.6±2g/dayand oral calcium supplements were decreased to 76 mmol/day.Two subsequent bone histomorphometry studies were performedat 8 month intervals in four patients and at 20 month intervalsin seven patients. The results show a good control of plasmacalcium (mean±SD: 2.43±0.1 µmol/1); phosphate(1.76±0.4 to 1.66±0.3 mmol/1); aluminium (1.3±0.1µmol/1 to 0.6±0.1µmol/1); alkaline phosphatase(135±65 to 125±40 IU); and PTH fragments (PTHCterminal decreased from 260±214 to 185±l82pg/ml,PTH medium from 4185±5113 to 2270±4880 pg/ml).Plasma magnesium increased from 0.96±0.2 to 1.54±0.2mmol/1. Bone histomorphometry shows no change in mineralisation,and a borderline decrease of resorption parameters. The mainside-effects are (1) diarrhoea, which was well controlled bytransieni treatment with karaya gum, and (2) an increased needfor potassium binders. It is concluded (I) that Mg(OH)₂ canreplace Al(OH)₃ in the control of hyperphosphataemia in dialysedpatients taking simultaneous moderate doses of CaCO₃ providedthe dialysate magnesium is decreased, and (2) that mild hypermagnesaemiahas no long-term deleterious effect on bone mineralisation after20 months.