Journal Information
Vol. 33. Issue. 6.November 2013
Pages 751-868
Vol. 33. Issue. 6.November 2013
Pages 751-868
DOI: 10.3265/Nefrologia.pre2013.Jul.12156
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Comment on 'Magnesium and chronic kidney disease'
Comentario a «Magnesio y enfermedad renal crónica»
Patricia Domínguez-Apiñaniza, José Portolés-Péreza, Darío Janeiro-Matína, Sofia Karstena, Paula López-Sáncheza
a Servicio de Nefrolog??a, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid,
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To the Editor:


We read with interest the abovementioned article and found little specific information on peritoneal dialysis (PD) patients.1 There are several reports in the 1990s on the use of calcium acetate/magnesium carbonate (CAMG) as a phosphorus binder. In one particular series on 32 patients, phosphate binders were compared with calcium and metal binders.2 However, this line of work was lost with the development of new binders (sevelamer and lanthanum). We have recently carried out studies that have renewed interest in CAMG in haemodialysis (HD), comparing its efficacy with that of other monotherapy binders. Nevertheless, we do not have similar clinical trials for PD. Studies that achieved the authorisation of CAMG included PD patients, but no specific subanalyses have been carried out on patients using this home technique. We already reported the need to carry out this type of study, since hyperparathyroidism (HPTH) management in PD is not identical to that of HD.3

As such, we wanted to contribute data on our preliminary experience with 10 patients on PD with moderate HPTH (mean baseline parathyroid hormone [PTH] 277pg/ml, range [150-606]), who we treated with CAMG (Osvaren®) for 6 months. Our main objective was to assess the tolerability and safety of the drug and obtain preliminary results on its efficacy in the control of serum phosphorus. The patients (54.8±9.4 years and 50% male) had a median time of 6.3 months on PD (7 on continuous ambulatory peritoneal dialysis, 3 on automated peritoneal dialysis) and achieved the dialysis efficacy objectives. The median treatment dose during follow-up was 2 pills per day (range 1-3). Treatment was well tolerated in all cases and it was not necessary to reduce the dose due to side effects. In two patients it was necessary to re-introduce another phosphorus binder at low doses (in one 750mg/24h of lanthanum carbonate and in another 1200mg/24h of sevelamer carbonate); 7 received Zemplar® and 3 Mimpara® from 3 months before the start of CAMG. At the start of treatment 7 patients displayed phosphorus within the range specified by the K/DOQI guidelines with the foregoing regimen and in just 4 months, all patients were well-controlled with CAMG. The number of patients who simultaneously achieved the objectives for phosphorus and PTH set by the K/DOQI guidelines increased from 4 to 8 in this time. Mean phosphorus had decreased from 4.8±0.6mg/dl to 4.6±1.0mg/dl at the end of the six-month follow-up.

We are aware of the limitations of our preliminary analysis, but we are interested in demonstrating the possibility of using CAMG in PD. It is striking that in the 30 laboratory tests we carried out during follow-up, we only found one high magnesium value (1.8mmol/l) and none for calcium above 10.5mg/dl. There was no clinical impact in any of these cases and it was easily corrected by adjusting the dialysate or diet. Four patients had cramp at the start and none at the end of follow-up. None of the patients displayed gastrointestinal intolerance and treatment allowed for a reduced use of laxatives.

The small amount of data available on the use of CAMG in PD may be due, on the one hand, to the fear of side effects (gastrointestinal intolerance and hypermagnesaemia), and on the other, to the difficulty of carrying out studies in PD units, which are still small in our country.

We have indirect evidence that hypomagnesaemia causes greater clinical problems than hypermagnesaemia in PD patients,4 similarly to that reported by De Francisco for HD patients.1 In fact, several observational studies have found that low magnesium is associated with worse control of HPTH, more calcifications, malnutrition and higher mortality.5,6

Furthermore, the laxative effect is interesting in PD, since the vast majority of patients require laxative drugs to achieve an adequate bowel pattern (one stool deposition per day). In conclusion, the cost of new non-calcium binders is 6 times the cost of CAMG, which is relevant for the sustainability of our health care system.7

Due to all of the above, we believe that CAMG may have a role to play as the first line of treatment in PD and that more PD-specific studies are necessary.


Conflicts of interest


The authors declare that they have no conflicts of interest related to the contents of this article.

De Francisco ALM, Rodr??guez M. Magnesio y enfermedad renal cr??nica. Nefrologia 2013;33(3):389-99. [Pubmed]
Parsons V, Baldwin D, Moniz C, Mardsen J, Ball E, Rifkin I. Successful control of HPTH in patients in CAPD using magnesium carbonate and calcium carbonate as phosphate binders. Nephron 1993;63:379-83. [Pubmed]
Portol??s J, L??pez-S??nchez P, Bajo MA, Castellano I, del Peso G, Rodr??guez JR, et al. Cinacalcet improves control of secondary hyperparathyroidism in peritoneal dialysis: a multicenter study. Perit Dial Int 2012;32(2):208-11. [Pubmed]
Tzanakis IP, Oreopoulos DG. Beneficial effects of magnesium in chronic renal failure: a foe no longer. Int Urol Nephrol 2009;41:363-71. [Pubmed]
Wei M, Esbaei K, Bargman J, Oreopoulos DG. Relationship between serum magnesium, parathyroid hormone, and vascular calcification in patients on dialysis: a literature review. Perit Dial Int 2006;26:366-73. [Pubmed]
Fein P, Suda V, Borawsky C, Kapupara H, Butikis A, Matza B, et al. Relationship of serum magnesium to body composition and inflammation in peritoneal dialysis patients. Adv Perit Dial 2010;26:112-5. [Pubmed]
De Francisco AL. Captores de f??sforo. ??El precio determina la elecci??n?: S??. Nefrologia 2012;32(2):235-9.
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