Maintaining a normal serum phosphate level is vital in preventing and treating secondary hyperparathyroidism or the abnormal increase in parathyroid (PTH) hormone level. Elevated phosphate levels and the calcium-phosphate product can lead to extraosseous calcifications (excessive calcium deposits in blood vessels and other soft tissues) and increase mortality in hemodialysis patients.
End-stage renal disease (ESRD) patients should ingest phosphate-binding agents combined with phosphate restriction to keep serum phosphate levels under control. Additionally, dialysis should be used to remove any excess phosphate from the blood.
Hemodialysis filters blood outside the body through a machine by removing waste and extra fluid. Phosphate binders are drugs taken with meals to help remove phosphate from the blood. Aluminum and calcium salts and non-aluminum and non-calcium agents are all effective, but they also have disadvantages. Magnesium-containing agents are an excellent option for aluminum- and calcium-free binders and are inexpensive. While not widely used, magnesium carbonate (MgCO3) and magnesium hydroxide (Mg(OH)2) have been administered with good results in small studies involving hemodialysis patients. ESRD patients are not often prescribed magnesium supplements because there is a fear of hypermagnesemia (too much magnesium in the blood) and the belief that these supplements often cause gastrointestinal disorders.
This study aimed to evaluate the safety and efficacy of MgCO3 as a phosphate-binder in hemodialysis patients. The control of serum phosphate was the primary outcome, while secondary outcomes were changes in serum calcium, magnesium, calcium-phosphate product, parathyroid hormone levels, and changes in bowel movements.
43 patients on maintenance hemodialysis completed the study. They were randomly allocated into two groups: 23 received 250-milligram (mg) MgCO3, 20 had 420-mg calcium carbonate (CaCO3), ingested in tablet form for six months. Both groups continued with their four-hour, thrice-a-week hemodialysis sessions. The concentration of Mg in the dialysate bath was 0.30 millimoles per liter (mmol/l) in the MgCO3 group and 0.48 mmol/l in the CaCO3 group.
The starting dose of both phosphate-binders was three tablets of MgCO3 or CaCO3 daily, adjusted after that depending on the serum phosphate, magnesium and calcium values, weekly for the first month and then monthly. The study drug dosage was increased to one or two tablets per meal to achieve the maximum target serum phosphate level of 5.5 mg per deciliter (dl).
Complete biochemical profiles were obtained at baseline, then weekly during the first month, and monthly thereafter. PTH hormone level was measured at baseline and then at monthly intervals. No patient received vitamin D or a calcimimetic agent during the study.
At month 6, phosphate levels in the MgCO3 and CaCO3 groups were comparable at 5.12 vs. 5.28 mg/dl. 17 of 23 (74%) patients in the MgCO3 and 13 of 20 (65%) of the CaCO3 group had serum phosphate values within the range recommended by the Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines with an upper limit of 5.5 mg/dl. These values were lower than in any of the earlier studies made.
More patients in the MgCO3 group (17/23, 73.91%) than in the CaCO3 group (5/20, 25%) had serum calcium levels that fell within the K/DOQI guidelines, with a significant difference.
Our study shows that magnesium carbonate administered for six months is an effective and inexpensive agent to manage serum phosphate levels in hemodialysis patients. It has a good phosphate-binding ability, is well tolerated by most patients, and is accompanied by a low incidence of side effects. The administration of magnesium carbonate in combination with a low dialysate magnesium concentration avoids the risk of severe hypermagnesemia.