Low vs standard calcium dialysate in peritoneal dialysis: differences in treatment, biochemistry and bone histomorphometry. A randomized multicentre study

Carmen Sánchez1, Fernando López-Barea2, Jesús Sánchez-Cabezudo3, Auxiliadora Bajo1, Alberto Mate2, Eugenia Martínez3 and Rafael Selgas4 for the Collaborators of the Multicentre Study Group

1Department of Nephrology, 2Department of Pathology and 3Biochemical Division of University Hospital ‘La Paz’ and 4Nephrology Division of University Hospital ‘La Princesa’, Madrid, Spain

Correspondence and offprint requests to: M. Carmen Sánchez, MD, Servicio de Nefrología, Hospital Universitario la Paz, Paseo Castellana 261, E-28046 Madrid, Spain. Email: csanchez.hulp{at}salud.madrid.org. Collaborators of the Multicentre Study Group include Ma Teresa González, MD PhD, University Hospital, Bellvitge (Barcelona); Josep Teixidó, MD PhD, University Hospital Germans Trias i Pujol (Badalona); Antonio Molina, MD PhD, University Hospital ‘Rio Hortega’ (Valladolid); Mercè Borràs Sans, MD, Hospital ‘Arnau de Vilanova’ (Lleida); César García, MD, ‘Hospital Insular’ Las Palmas de Gran Canaria; Rafael García, MD, Hospital ‘Clínico Universitario’ (Valencia); Aniana Oliet, MD PhD, Hospital ‘Severo Ochoa’ (Leganés).



   Abstract
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. In patients undergoing peritoneal dialysis (PD), low-calcium dialysate (LCD) has been proposed as the first choice for a better control of renal osteodystrophy. Our aim was to compare the effects on bone metabolism of LCD (calcium: 1.25 mmol/l) with that of a standard calcium dialysate (SCD; calcium: 1.75 mmol/l).

Methods. Forty-four PD patients were randomized to receive LCD or continue on SCD for a period of 12 months. Bone biopsies were taken at baseline and at 12 months. Biochemical data and treatment were evaluated every 3 months.

Results. Twenty-four patients completed the study. In the SCD group (n = 10), nine out of the 10 patients were initially diagnosed with adynamic bone lesion (ABL). After 1 year, six continued having ABL and three patients moved to high-turnover bone lesion (HTBL). The other patient, initially diagnosed with HTBL, changed to ABL. In the LCD group (n = 14), 10 patients were initially diagnosed with ABL. At 1 year, six of them continued having ABL and four patients changed to HTBL. Four patients were initially diagnosed with HTBL and did not change. Comparison between LCD and SCD groups showed an increase in serum parathyroid hormone (PTH) levels starting at month 3 and a higher intake of calcium salts in the former group (P<0.01). Serum calcium, phosphate levels and bone histological outcome did not differ between the two groups.

Conclusions. LCD use for 1 year was associated with an increase in PTH levels, but did not lead to histological changes different from those observed in SCD group. The LCD solution allowed a higher oral intake of calcium salts with a satisfactory control of the serum Calcium–Phosphorus product.

Keywords: bone biopsy; bone histomorphometry; low-calcium dialysate; peritoneal dialysis; renal osteodystrophy; standard calcium dialysate



   Introduction
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Phosphate retention plays a critical role in the development of secondary hyperparathyroidism and metastatic calcifications [1]. For many years, aluminium hydroxide has been prescribed as a phosphate binder in end-stage renal disease patients. However, in recent years, as a consequence of aluminium side effects, alternative methods have been developed to control serum phosphate [13]. Among them, the use of calcium-containing phosphate binders has become a favourite in clinical practice. Unfortunately, hypercalcaemia is a frequent serious side effect of this treatment, especially when associated with vitamin D analogues in patients dialysed with standard calcium dialysate (SCD; calcium concentration: 1.75 mmol/l) [25]. On the other hand, this standard calcium concentration has been associated with a tendency towards parathyroid hormone (PTH) inhibition and adynamic bone disease [2,4], the most frequent bone lesion described in peritoneal dialysis (PD) patients [6]. Reduced skeletal buffer capacity for ingested calcium seems to be an important contributor to an increase in the potential for metastatic and vascular calcification in some PD patients with low-bone turnover [2,7].

Although controversy exists, numerous investigators have suggested that using low-calcium dialysate (LCD) might benefit PD patients [35,8]. This PD solution (1.25 mmol/l) would permit a larger dose of calcium to control hyperphosphataemia with a lesser risk of hypercalcaemia [3] and also avoid excessive PTH suppression [2,3,8].

In general, the information about the effects of low-calcium solutions on bone histology outcome is scanty [3]. Most studies have been limited to densitometry and found no differences using these fluids [4,9]. Our objectives were to prospectively study the effects of a 1.25 mmol/l calcium dialysate vs a 1.75 mmol/l calcium dialysate over a 12 month period on (a) bone histology, (b) evolution of serum PTH, phosphorus and calcium and (c) dose of vitamin D analogues, calcium salts and requirements of aluminium-containing phosphate binders to maintain serum PTH, calcium and phosphorous levels within a target range.



   Subjects and methods
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Patients
All eligible patients were Caucasian, >=18 years old and with end-stage renal failure treated with continuous ambulatory peritoneal dialysis (CAPD) for >=6 months. Exclusion criteria were malignancy or metabolic bone disease other than renal osteodystrophy (ROD), severe hyperparathyroidism resistant to calcitriol therapy, hypercalcaemia [total serum calcium (TCa) >12 mg/dl or ionized Ca >1.45 mmol/l], presence of elevated basal aluminium levels (>100 µg/l), previous treatment with steroids or immunosuppressive agents, prior chronic haemodialysis of >9 months and/or transplantation. The ethics committee of each centre approved the study protocol. All included patients gave informed consent. Initially, we included 44 stable patients who were randomized to receive 1.25 mmol/l (LCD; n = 22) or to continue on a 1.75 mmol/l calcium solution (SCD; n = 22) for a period of 12 months. Magnesium concentration was 0.5 mEq/l in the LCD solution and 1.5 mEq/l in the SCD solution. Two iliac crest bone biopsy (BB) specimens were obtained, one at baseline and the other at the end of the follow-up period.

Study design
This was a multicentre study in which all patients were on CAPD using three or four 2-l exchanges per day of SCD. The following data were recorded: primary renal disease, previous haemodialysis, presence of diabetes mellitus, nephrectomy and parathyroidectomy.

The prescription (basal and months 3, 6, 9 and 12) and annual accumulated dose of calcium (g), calcitriol (µg) and aluminium salts (g) were recorded during the study period. The aim was to maintain serum TCa between 9.5 and 10.8 mg/dl, ionized calcium between 1.25 and 1.30 mmol/l and serum phosphate <5.5 mg/dl. Either calcium carbonate or calcium acetate was prescribed as the primary phosphate binder. Aluminium hydroxide salts was prescribed to replace calcium salts if risk of hypercalcaemia arose. Episodes of significant hyperphosphataemia (serum phosphate >6 mg/dl) and hypercalcaemia (serum TCa >10.8 mg/dl) were also recorded. None of the patients had been treated with vitamin D pulses at the baseline period. Vitamin D analogues used were always calcitriol, with the aim of maintaining serum PTH between 100 and 250 pg/ml.

Clinical evaluation and biochemical parameters included residual renal function (RRF), serum TCa and ionized plasma calcium, serum phosphate, magnesium, osteocalcin (OC), alkaline phosphatase (ALP) and intact PTH, which were all determined at the start of the study and every 3 months. Samples for serum determinations were taken simultaneously. The peritoneal ultrafiltration (UF) capacity was measured as net effluent collected with an overnight exchange using 2.27 g/dl dextrose.

Methods
Ionized calcium was assayed in total blood under anaerobic conditions by a selective electrode (Ciba Corning, Medfield, MA, USA). Autoanalysers were used to measure serum calcium and phosphate. Intact PTH was measured in plasma by an immunoradiometric assay (Nichols Institute, San Juan Capistrano, CA, USA). The normal range for this assay is 10–65 pg/ml. Serum OC was determined by radioimmunoassay (INCSTAR Corporation, Stillwater, MN, USA). The sensitivity of these assays was 1 pg/ml and 50 pg/ml, respectively, and their interassay variation coefficients were <10%.

Bone biopsy
Transiliac BBs were obtained using a Bordier trephine with a 7 mm internal diameter after in vivo double tetracycline labelling. Each patient received a tetracycline double label in two 3-day courses at an interval of 10 days. The bone specimen was obtained 5 days after the last tetracycline dose. BBs were treated as previously reported [6]. Histological staining for aluminium was performed with the aurin tricarboxylic acid method. Aluminium intoxication was defined as aluminium staining in >25% of the bone surface. All bone samples were examined and diagnosed by two pathologists who were unaware of biochemical data or the calcium concentration solutions used. Parameters for bone formation and resorption were determined [10] using a semiautomatic image analysis system (Videoplan II; Kontron, Munich, Germany). Quantitative measurements for static and dynamic parameters were made on the trabecular bone area [6] for the following static parameters: total bone volume (BV/TV%), Osteoid volume (OV/BV%), Osteoid surface (OS/BS%), Osteoid seam thickness (OTH, NM), Osteoblast surface (Ob.S/BS%), Osteoclast number per mm2 tissue section (N.Oc/TA, mm2), fibrosis volume (fb.V/TV%), fibrosis surface (fb.S/BS%), and surface stained with aluminium (Al.S/BS%). The dynamic parameters of bone formation included mineral opposition rate (MAR, µm/day) and bone formation rate (BFR/BS, µm3/µm2/day), obtained by multiplying the MAR by the total labeled mineralizing surface (double-labeled plus one-half of the single label surface). Histological criteria to define adynamic bone lesion (ABL) and high-turnover bone lesion (HTBL) were used following the classic recommendations [11,12]. HTBL included severe hyperparathyroidism (OV/BV% <15%, BFRS/BS >0.031 µm3/µm2/day and Fb.V/TV% >0.5%) as well as mild hyperparathyroidism (OV/BV% <15%, BFS/BS >0.031 µm3/µm2/day and Fb.V/TV% <0.5%). All parameters were calculated following the recommendations of the Histomorphometry Nomenclature Committee of the American Society of Bone and Mineral Research [10]. BBs from six Caucasian and normal individuals who were cadaveric kidney donors provided control values for the static bone parameters.

Statistical analysis
Results are expressed as means±SD. In the case of serum PTH, OC and magnesium, data are also expressed as median, 25th and 75th quartile box plots, since the values were not normally distributed. For continuous variables, data analysis was performed by Mann–Whitney U-tests (patients treated with LCD or SCD) and Wilcoxon rank-sum test (paired data). Fisher's exact and McNemar's paired comparison tests were used to assess differences between categorical variables. Values of <0.05 were considered statistically significant. Serial biochemical measurements and intake of vitamin D, calcium and aluminium salts were analysed using a P<0.01 level with a Bonferroni correction of alpha error (risk type 1), since multiple comparisons were made for five repeated measurements during the study.

An increase in percentage index from baseline to final PTH ({triangleup}PTH) [(month 12 PTH–baseline PTH/baseline PTH) x 100] for the SCD and LCD groups was calculated to investigate the variability of PTH during the course of the study.

To identify factors associated with changes in the final diagnosis of bone histology, receiver operating curves (ROC) also were calculated. The possible values range from 1.0 (perfect separation of test values into two groups) to 0.5 (no distributional difference). An area under the curve (AUC) greater than 0.7 indicates a discriminating strength of statistical significance; an AUC greater than 0.8 indicates excellent discriminating power for the test. Multivariate analysis was not possible due to the low number of patients in the study.



   Results
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
After randomized allocation to either SCD or LCD, 44 patients initiated the study. As a consequence of the enormous difficulty of obtaining double BBs, it was impossible to obtain a higher number of cases even though this was a multicentre study. Six bone samples were excluded at baseline, five for inadequate bone sample and one for presenting a ROD mixed lesion. Another 14 patients dropped out subsequently from the study due to transplantation (n = 6), death (n = 2), transfer to haemodialysis (n = 2), refused the second BB (n = 3) and final inadequately-sized bone samples (n = 1). Twenty-four patients completed the study with two biopsies (13 men, 11 women). Mean patient age was 56±11 years and they had received PD for a mean period of 14±5 months (range: 6–26 months). Ten patients had received SCD and 14 patients LCD. The SCD and LCD groups did not differ significantly in terms of age (SCD: 58±8 years vs LCD: 54±12 years), time on PD (SCD: 14±4 months vs LCD: 13.8±5 months) or RRF at baseline and after 12 months of treatment. Seven patients had type 2 diabetes mellitus (SCD: n = 4; LCD: n = 3). Figure 1 shows the follow-up of the 24 final patients.



View larger version (16K):
[in this window]
[in a new window]
 
Fig. 1. ROD distribution after SCD (1.75 mmol/l) and LCD (1.25 mmol/l) treatment in the 24 patients who completed the study.

 
Serum PTH and OC increased more in the LCD group than the SCD group during the follow-up (Figures 2A and 2B). Moreover, we observed a higher increase in PTH at month 12 with respect to baseline PTH in the LCD group than in the SCD group ({triangleup}PTH: 174.4±254.2 vs 21.3±88.1 pg/ml, respectively; P<0.05). Serum magnesium decreased more in the LCD group than in the SCD group (Figure 2C), as a consequence of lower magnesium levels in the LCD. Serum phosphate and calcium values were similar in both groups (Figure 3). No differences were found between groups in the number of episodes of hypercalcaemia, hyperphosphataemia and Ca–P product. In respect of treatment, patients on LCD received a higher total calcium intake than the SCD group (Table 1).



View larger version (21K):
[in this window]
[in a new window]
 
Fig. 2. Box plots based on the median, 25th and 75th quartiles and extreme values: baseline and at months 3, 6, 9 and 12 in patients treated with SCD (1.75 mmol/l) and LCD (1.25 mmol/l). The box represents the interquartile range, which contains 50% of values. The whiskers are lines extending from the box to the highest and lowest values, excluding outliers ({circ}) (cases with values between 1.5 and 3 box lengths from the upper or lower edge of the box) and extreme values (*) (cases with values >3 box lengths from the upper or lower edge of the box). The line crossing the box indicates the median. Differences between the 1.75 and 1.25 mmol/l calcium groups: (A) serum PTH (month 6, P = 0.003; month 9, P = 0.007; month 12, P = 0.0004); (B) serum OC (month 6, P = 0.005; month 12, P = 0.005); and (C) serum magnesium (month 6, P = 0.009; month 12, P = 0.005). Bonferroni correction was applied.

 


View larger version (46K):
[in this window]
[in a new window]
 
Fig. 3. Biochemical values in the SCD (1.75 mmol/l) and LCD (1.25 mmol/l) groups. (A) Serum total calcium levels, (B) ionized plasma calcium and (C) serum phosphate levels. There were no significant differences between groups.

 

View this table:
[in this window]
[in a new window]
 
Table 1. Treatment in SCD (1.75 mm/l) and LCD (1.25 mmol/l) groups

 
Evolution of histomorphometric (HMF) data is shown in Table 2. The UF capacity was greater in the LCD than the SCD group (627.78±447.99 vs 247.14±176.04 cc; P<0.05).


View this table:
[in this window]
[in a new window]
 
Table 2. HMF parameters in SCD (1.75 mm/l) or LCD (1.25 mmol/l) groups, at baseline and after 12 months follow-up

 
Changes induced by the LCD, evaluated as differences between baseline and final data in that group, occurred in serum PTH (from 226±228 to 332±188 pg/ml; P = 0.01), serum ALP (from 133±69 to 182±123 UI/l; P = 0.04) and a number of patients treated with aluminium hydroxide (from 2/14 to 6/14; P = 0.04) and vitamin D (from 5/14 to 11/14; P = 0.03). No differences were observed in the SCD group between baseline and final data.

In order to investigate differences between patients receiving the same dialysate whose bone diagnosis changed in the course of the study, we compared patients dialysed with LCD with a final ABL (n = 6) to patients dialysed with LCD who had a final HTBL (n = 8). We found that patients with a final diagnosis of ABL were older (63.0±8.1 years) than those with a final HTBL (48.0±12 years; P = 0.019). Using ROC curve analysis, age was confirmed as a predictive factor for final ABL (AUC: 0.875; 95% confidence interval: 0.683–1; P = 0.02). In fact, when we took into account the baseline bone histological diagnosis, we also found that patients who retained the ABL diagnosis (n = 6) were older than the other four patients who had converted to HTBL (63.0±8.1 vs 50.5±6.5 years; P<0.019). In the SCD group (n = 10), the only patient with HTBL at baseline had moved to ABL at the end. This patient was the only one in this group to have been treated with vitamin D (Table 1).

In conclusion, in 11 patients with a final HTBL, we observed that the cumulative doses of aluminium salt and vitamin D during the study were greater in those dialysed with LCD (n = 8) than in those treated with SCD (n = 3) (537.66±169.7 vs 172.50±96.23 mg, P = 0.02; 78.94 ± 61.30 vs 0.00±00 µg, P = 0.0013, respectively). Among patients with a final ABL diagnosis (n = 13), those receiving LCD (n = 6) showed higher serum PTH and higher serum OC levels at month 12 than those receiving SCD (n = 7) (205±97 vs 67.2±39 pg/ml, P<0.01; 18.8±8 vs 8.8±3 ng/ml, P<0.01, respectively).



   Discussion
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 
In this randomized study on the effects of two different calcium contents in PD solutions, we found that the low-calcium solution showed a clear tendency to increase PTH levels. However, both levels of calcium concentration seemed to induce a similar proportion of HTBL after 1 year of follow-up, whereas older age was an important factor for ABL presence. The low-calcium solution allowed higher doses of oral calcium and vitamin D to be administered without hypercalcaemia development.

Biochemical outcome
While some previous studies have reported no significant changes after using LCD [4] or even a decrease in the median serum PTH [1,3], the most widely acknowledged opinion is that LCD will induce a clinically significant increase in PTH levels [5,9,13,14]. Our findings are consistent with the latter results. We observed higher {triangleup}PTH and serum PTH levels during the study in the group of patients treated with LCD than in the SCD group, although the median serum calcium levels remained within the normal range in both groups. Furthermore, at the time of the second BB, patients dialysed with LCD showed higher serum PTH levels than did SCD patients, despite showing the same final histological diagnosis. Taken together, these findings suggest that LCD might be responsible for increased PTH secretion [4,13]. Studies have demonstrated that mass calcium transfer is negative with the 1.25 mmol/l calcium dialysate, that is, there is a movement of calcium from patient to the dialysate [8]. In contrast, the mass calcium transfer with the 1.75 mmol/l calcium dialysate is positive for the patient. Therefore, at any particular level of UF, dialysing with 1.25 mmol/l calcium might result in a considerably more negative mass calcium transfer than using 1.75 mmol/l calcium [8]. In our study, the higher UF capacity observed in the LCD group could agree with this hypothesis of a stimulation of PTH being a consequence of a higher calcium efflux. In addition, and similar to another study [3], the mean serum magnesium in the LCD group declined from hypermagnesaemic values on starting dialysis to reach the normal range (1.7±0.5 mg/dl) after the third month. Hypermagnesaemia has been reported to suppress PTH synthesis and/or secretion [15]. It is tempting to think that ‘normalizing’ the serum Mg levels might contribute to the lack of PTH inhibition in the LCD group.

Bone histology findings
Most reports, limited to densitometry studies, did not observe any influence of the calcium dialysate on bone mineral density [4,9]. Hutchison et al. [3] studied BBs from 16 PD patients treated with 1.25 Ca dialysate. They found a non-significant tendency towards improved bone histology. In our study, the rise in dynamic parameters (mineral apposition rate and bone formation rate) in patients dialysed with this 1.25 mmol/l calcium fluid almost reached statistical significance and, again, serum magnesium might have played a role. The reduced level of magnesium in the 1.25 mmol/l calcium fluid may have a beneficial effect on bone morphology [16] and this would make it beneficial for patients with low-turnover bone disease [4,12]. On the other hand, it has been reported [16] that, after 1 year with 1.25 mmol/l calcium dialysate, PD patients with an adynamic lesion can develop hyperparathyroidic changes. We also observed a tendency in patients initially manifesting a low-turnover lesion to evolve towards hyperparathyroidism bone disease, but, surprisingly, this occurred in both groups. As can be observed in Table 2, both groups showed a tendency to improve osteoblast surfaces over time and, in these cases, the disorder can be reversible [17]. In addition, all our patients had been receiving a 1.75 mmol/l calcium concentration before starting the study and the change to LCD might be another cause for reversibility in ABL [17,18]. In consequence, and under some circumstances, ABL seems to be more a status than a permanent lesion. In any case, the long-term consequences of this status are still unclear. We could not find a correlation between the higher PTH levels observed in the patients on LCD with a higher expected frequency of conversion to HTBL in this group. One possibility is that with LCD, bone turnover might be suppressed due to a high intake of calcitriol and higher serum PTH levels (>300 pg/ml) would be necessary to suffer a HTBL (Tables 3 and 4). The relatively small number of patients and/or short period of observation might also have provoked this result.


View this table:
[in this window]
[in a new window]
 
Table 3. ROD and serum PTH outcome in patients treated with SCD (1.75 mmol/l, n = 10)

 

View this table:
[in this window]
[in a new window]
 
Table 4. ROD and serum PTH outcome in patients treated with LCD (1.25 mmol/l, n = 14)

 
Another interesting finding in our study was the relationship between age and the presence of ABL. That was confirmed by the ROC analysis. This association is a well-known phenomenon in the dialysis population [2,6,12,17].

Treatment outcome
Most reports have demonstrated that high-normal plasma calcium could be achieved with LCD treatment with a minimal risk of incidental hypercalcaemia [1,35,8,9,13]. In our study, serum calcium did not differ between the two groups, although calcium salts and calcitriol doses were higher in the LCD group. Unlike other authors [1,3,4], we did not observe a reduction of aluminium-containing phosphate binders with LCD use; these results coincide with those of other investigators [2,9,14,19]. Indeed, a further analysis of subgroups showed that the overall intake of phosphate-binding drugs tended to be higher in patients in the LCD group. This might be the consequence of a concomitant treatment with higher doses of calcitriol. Calcitriol, by increasing oral phosphate absorption, could increase the total dose of phosphate binder required to maintain satisfactory serum phosphate control [9,14]. As a result, this manoeuvre helped maintain the Calcium–phosphorus product within the target range.

In view of our results, we believe that a 1.25 mmol/l calcium dialysate can be used effectively and safely in PD patients who comply with their calcium treatment, since the observed increase in PTH did not concur with an aggravation of bone histology, at least at 1 year of observation, and with serum PTH levels of ~300 pg/ml. The 1.25 mmol/l calcium dialysate avoids hypercalcaemia and although it does not always offer advantages in terms of reducing the aluminium hydroxide intake, a new calcium-plus aluminium-free phosphate binder may be useful for phosphate control [20]. Nevertheless, it is essential that the dialysate concentration be individualized and the low-calcium solution not be used as a standard solution. Also, some patients still require ‘tailored’ dialysis fluids to maintain good serum Calcium–phosphorus control.

Conflict of interest statement. None declared.



   References
 Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. Slatopolsky E, Weerts C, Norwood K et al. Long-term effects of calcium carbonate and 2.5 mEq/liter calcium dialysate on mineral metabolism. Kidney Int 1989; 36: 897–903[ISI][Medline]
  2. Hruska K. New concepts in renal osteodystrophy. Nephrol Dial Transpl 1998; 13: 2755–2760[Free Full Text]
  3. Hutchison AJ, Freemont AJ, Boulton HF, Gokal R. Low-calcium dialysis fluid and oral calcium carbonate in CAPD. A method of controlling hyperphosphataemia whilst minimizing aluminium exposure and hypercalcaemia. Nephrol Dial Transplant 1992; 7: 1219–1225[Abstract]
  4. Weinreich T, Passlick-Deetjen J, Ritz E, for the Collaborators of the Peritoneal Dialysis Multicenter Study Group. Low dialysate calcium in continuous ambulatory peritoneal dialysis: a randomized controlled multicenter trial. Am J Kidney Dis 1995; 25: 452–460[ISI][Medline]
  5. Armstrong A, Beer J, Noonan K, Cunningham J. Reduced calcium dialysate in CAPD patients: efficacy and limitations. Nephrol Dial Transpl 1997; 12: 1223–1228[Abstract]
  6. Sanchez MC, Bajo M.A, Selgas R et al. Parathormone secretion in peritoneal dialysis patients with adynamic bone disease. Am J Kidney Dis 2000; 36: 953–961[ISI][Medline]
  7. Kurz P, Monier-Faugere MC, Bognar B et al. Evidence for abnormal calcium homeostasis in patients with adynamic bone disease. Kidney Int 1994; 46: 855–861[ISI][Medline]
  8. Bender F, Piraino B, Bernardini J. Calcium mass transfer with dialysate containing 1.25 and 1.75 mmol/l calcium in peritoneal dialysis patients. Am J Kidney Dis 1992; 20: 367–371[ISI][Medline]
  9. Johnson DW, Rigby RJ, McIntyre HD, Brown A, Freeman J. A randomized trial comparing 1.25 mmol/l calcium dialysate to 1.75 mmol/l calcium dialysate in CAPD patients. Nephrol Dial Transpl 1996; 11: 88–93[Abstract]
  10. Parfitt AM, Drezner MK, Glorieux FH et al. Bone histomorphometry: standardization of nomenclature, symbols and units. J Bone Miner Res 1987; 2: 595–610[ISI][Medline]
  11. García-Carrasco N, Gauson M, de Vernejoul MC, Denne MA, Miravet L. Osteocalcin and bone morphometric parameters in adults without bone disease. Calcified Tissue Int 1988; 42: 13–17[ISI][Medline]
  12. Sherrard DJ, Hercz G, Pei Y et al. The spectrum of bone disease in end-stage renal failure: an evolving disorder. Kidney Int 1993; 43: 436–442[ISI][Medline]
  13. Argilés A, Mourad G. How do we have to use the calcium in the dialysate to optimize the management of secondary hyperparathyroidism? Nephrol Dial Transpl 1998; 13 [Suppl 3]: 62–64[Medline]
  14. Banalagay E, Bernardini J, Holley J, Chen T, Piraino B. A randomized trial comparing 2.5 mEq/l calcium dialysate and calcitriol to 3.5 mEq/l calcium dialysate in patients on peritoneal dialysis. Adv Perit Dial 1993; 9: 280–283[Medline]
  15. Navarro JF, Mora C, García J. Serum magnesium and parathyroid hormone levels in dialysis patients. Kidney Int 2000; 57: 2654–2656
  16. Hutchison J, Gokal R. Towards tailored dialysis fluids in CAPD. The role of reduced calcium and magnesium in dialysis fluids. Perit Dial Int 1992; 12: 299–303
  17. Hercz G, Pei Y, Greewood C et al. Aplastic osteodystrophy without aluminum: the role of ‘suppressed’ parathyroid function. Kidney Int 1993; 44: 860–866[ISI][Medline]
  18. Salusky I, Goodman WG. Adynamic renal osteodystrophy: is there a problem? J Am Soc Nephrol 2001; 12: 1978–1985[Free Full Text]
  19. Wadhwa NK, Howell N, Suh H, Cabralda T. Low calcium (2.5 mEq/l) and high calcium (3.5 mEq/l) dialysate in peritoneal dialysis patients. Adv Perit Dial 1992; 8: 385–388[Medline]
  20. Chertow GM, Burke SB, Dillon MA, Slatopolsky E, for the Renal Gel Study Group. Long-term effects of sevelamer hydrochloride on the calcium x phosphate product and lipid profile of haemodialysis patients. Nephrol Dial Transplant 1999; 14: 2907–2914[Abstract/Free Full Text]
Received for publication: 28.10.03
Accepted in revised form: 13. 2.04





This Article
Abstract
FREE Full Text (PDF)
All Versions of this Article:
19/6/1587    most recent
gfh214v1
Alert me when this article is cited
Alert me if a correction is posted
Services
Email this article to a friend
Similar articles in this journal
Similar articles in ISI Web of Science
Similar articles in PubMed
Alert me to new issues of the journal
Add to My Personal Archive
Download to citation manager
Disclaimer
Request Permissions
Google Scholar
Articles by Sánchez, C.
Articles by Selgas, R.
PubMed
PubMed Citation
Articles by Sánchez, C.
Articles by Selgas, R.