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1.
Int Urol Nephrol ; 40(1): 193-201, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18193489

RESUMO

BACKGROUND: Magnesium salts bind dietary phosphorus, but their use in renal patients is limited due to their potential for causing side effects. The aim of this study was to evaluate the efficacy and safety of magnesium carbonate (MgCO(3)) as a phosphate-binder in hemodialysis patients. METHODS: Forty-six stable hemodialysis patients were randomly allocated to receive either MgCO(3) (n=25) or calcium carbonate (CaCO(3)), (n=21) for 6 months. The concentration of Mg in the dialysate bath was 0.30 mmol/l in the MgCO(3) group and 0.48 mmol/l in the CaCO(3) group. RESULTS: Only two of 25 patients (8%) discontinued ingestion of MgCO(3) due to complications: one (4%) because of persistent diarrhea, and the other (4%) because of recurrent hypermagnesemia. In the MgCO(3) and CaCO(3) groups, respectively, time-averaged (months 1-6) serum concentrations were: phosphate (P), 5.47 vs. 5.29 mg/dl, P=ns; Ca, 9.13 vs. 9.60 mg/dl, P<0.001; Ca x P product, 50.35 vs. 50.70 (mg/dl)(2), P=ns; Mg, 2.57 vs. 2.41 mg/dl, P=ns; intact parathyroid hormone (iPTH), 285 vs. 235 pg/ml, P<0.01. At month 6, iPTH levels did not differ between groups: 251 vs. 212 pg/ml, P=ns. At month 6 the percentages of patients with serum levels of phosphate, Ca x P product and iPTH that fell within the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines were similar in both groups, whereas more patients in the MgCO(3) group (17/23; 73.91%) than in the CaCO(3) group (5/20, 25%) had serum Ca levels that fell within these guidelines, with the difference being significant at P<0.01. CONCLUSION: Our study shows that MgCO(3) administered for a period of 6 months is an effective and inexpensive agent to control serum phosphate levels in hemodialysis patients. The administration of MgCO(3) in combination with a low dialysate Mg concentration avoids the risk of severe hypermagnesemia.


Assuntos
Falência Renal Crônica/terapia , Magnésio/uso terapêutico , Fosfatos/metabolismo , Fósforo/sangue , Diálise Renal , Fosfatase Alcalina/sangue , Cálcio/sangue , Carbonato de Cálcio/uso terapêutico , Seguimentos , Humanos , Falência Renal Crônica/sangue , Magnésio/efeitos adversos , Magnésio/sangue , Pessoa de Meia-Idade , Hormônio Paratireóideo/sangue , Valores de Referência , Resultado do Tratamento
2.
Int Urol Nephrol ; 46(11): 2199-205, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25118610

RESUMO

BACKGROUND: The aim of the study was to evaluate the impact of magnesium (Mg) on the evolution of arterial calcifications in hemodialysis patients. PATIENTS AND METHODS: Seventy-two stable hemodialysis patients were randomly allocated to two groups: 36 administered a regimen containing magnesium carbonate plus calcium acetate as a phosphate binder (Mg group), while the rest 36 received calcium acetate alone (Ca group). The presence and the progression of arterial calcifications were evaluated in plain X-rays using a simple vascular calcification score. The duration of the follow-up period was 12 months. RESULTS: Thirty-two patients of the Mg group and 27 of the Ca group completed the study. The mean time average values of the biochemical laboratories did not differ between the two groups, except serum Mg: 2.83 + 0.38 in the Mg group versus 2.52 + 0.27 mg/dl in the Ca group, p = 0.001. In 9/32 (28.12 %) patients of the Mg group and in 12/27 (44.44 %) patients of the Ca group, the arterial calcifications were worsened, p = 0.276. Moreover, in 4/32 (15.6 %) patients of the Mg group and in 0/27 (0 %) patients of the Ca group, they were improved, p = 0.040. The multivariate logistic regression analysis revealed that serum magnesium was an independent predictor for no progression of the arterial calcifications, p = 0.047. CONCLUSIONS: Magnesium probably retards the arterial calcifications in hemodialysis patients. Further clinical studies are needed to clarify whether magnesium provides cardiovascular protection to this group of patients.


Assuntos
Falência Renal Crônica/terapia , Magnésio/administração & dosagem , Doença Arterial Periférica/prevenção & controle , Diálise Renal/efeitos adversos , Calcificação Vascular/prevenção & controle , Administração Oral , Idoso , Relação Dose-Resposta a Droga , Método Duplo-Cego , Feminino , Seguimentos , Humanos , Masculino , Doença Arterial Periférica/diagnóstico , Doença Arterial Periférica/etiologia , Projetos Piloto , Estudos Prospectivos , Resultado do Tratamento , Calcificação Vascular/diagnóstico , Calcificação Vascular/etiologia
3.
Int Urol Nephrol ; 41(2): 363-71, 2009.
Artigo em Inglês | MEDLINE | ID: mdl-19115076

RESUMO

Magnesium plays a critical role in cellular physiology in humans, regulating many fundamental functions. In the general population its deficiency is associated with many disorders, the most significant being cardiovascular diseases. The role of magnesium in many aspects of end-stage renal disease (ESRD) may be also very important, although this has not been explored in depth. The most significant of these roles are use of magnesium salts as phosphate binders and its ability to inhibit the development or progression of vascular calcification. Moreover, serum magnesium suppresses parathyroid hormone excretion, whereas high magnesium dialysate may result in intradialytic hemodynamic stability. Data provided by recent studies on these issues have promoted promising renewed interest in the role of magnesium in ESRD and its possible favorable therapeutic application in these patients. Further large studies are needed to establish its efficacy and safety, and, probably, to re-evaluate its appropriate concentration in hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) fluids.


Assuntos
Falência Renal Crônica/terapia , Compostos de Magnésio/uso terapêutico , Magnésio/farmacologia , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/prevenção & controle , Humanos , Falência Renal Crônica/complicações , Falência Renal Crônica/metabolismo , Deficiência de Magnésio/sangue , Deficiência de Magnésio/complicações , Deficiência de Magnésio/terapia , Hormônio Paratireóideo/sangue , Diálise Renal
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