Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease: An Overview

George R. Bailie, PharmD, PhD, FCCP; Shaul G. Massry, MD

Disclosures

Pharmacotherapy. 2005;25(12):1687-1707. 

In This Article

Guideline 6: Serum Calcium and Calcium-Phosphorus Product

Guideline Statements

In Stages 3 and 4

6.1 - The serum concentrations of corrected total calcium should be maintained within the normal range for the laboratory used (E).

In Stage 5

6.2 - Serum concentrations of corrected total calcium should be maintained within the normal range for the laboratory used, preferably toward the lower end (8.4-9.5 mg/dl [2.10-2.37 mmol/L]) (O).

6.3 - In the event corrected total serum calcium concentration exceeds 10.2 mg/dl (2.54 mmol/L), therapies that cause serum calcium to rise should be adjusted as follows:

 

6.3a - In patients taking calcium-based phosphorus binders, the dosage should be reduced or therapy switched to a non-calcium-, non-aluminum-, non-magnesium-containing phosphorus binder (O).

 

 

6.3b - In patients taking active vitamin D sterols, the dosage should be reduced or therapy discontinued until the serum concentrations of corrected total calcium return to the target range (8.4-9.5 mg/dl [2.10-2.37 mmol/L]) (O).

 

 

6.3c - If hypercalcemia (serum concentrations of corrected total calcium > 10.2 mg/dl [2.54 mmol/L]) persists despite modification of therapy with vitamin D and/or discontinuation of calcium-based phosphorus binders, dialysis using low dialysate calcium (1.5-2.0 mEq/L) may be used for 3-4 weeks (O).

 

In Stages 3-5

6.4 - Total elemental calcium intake (including both dietary calcium intake and calcium-based phosphorus binders) should not exceed 2000 mg/day (O).

6.5 - The serum calcium-phosphorus product should be maintained at less than 55 mg2/dl2 (E). This is best achieved by controlling serum concentrations of phosphorus within the target range (O).

6.6 - Patients whose serum concentrations of corrected total calcium are below the lower limit for the laboratory used (< 8.4 mg/dl [2.10 mmol/L]) should receive therapy to increase serum calcium concentrations if one of the following is present:

 

6.6a - There are clinical symptoms of hypocalcemia such as paresthesia, Chvostek's and Trousseau's signs, bronchospasm, laryngospasm, tetany, and/or seizures (O); or

 

 

6.6b - The plasma iPTH concentration is above the target range for the CKD stage (O).

 

6.7 - Therapy for hypocalcemia should include calcium salts such as calcium carbonate (E) and/or oral vitamin D sterols (E).

Patients with CKD who are treated with vitamin D analogs or calcium supplementation are prone to develop hypercalcemia. This may also occur in patients who are concomitantly treated with vitamin D analogs and calcium-containing phosphorus binders. This complication occurs especially in those with low-turnover bone disease. The clinical manifestation of acute hypercalcemia varies from a mild, asymptomatic, biochemical abnormality detected during routine screening to a life-threatening emergency. Hypercalcemia and hyperphosphatemia, individually or together, can result in an increased blood calcium-phosphorus product. High calcium-phosphorus product in blood increases the risk of soft-tissue calcification.

Corrected Serum Calcium Concentrations

Total calcium concentrations should be adjusted for the concentration of albumin to better reflect the free calcium concentration. The recommended equation that most closely approximates corrected total calcium concentration in patients with CKD is as follows:

 

Corrected serum calcium (mg/dl) = total serum calcium (mg/dl) + 0.0704 · (34 · serum albumin [g/L]).

 

Hypocalcemia is a risk for bone disease and for development of secondary hyperparathyroidism and/or increased risk of mortality. Thus, the detection of true hypocalcemia and its appropriate treatment is important for the treatment of patients with CKD. When to begin calcium supplementation during the course of CKD is unclear. In the presence of overt hypocalcemia, calcium supplementation is clearly indicated. In earlier stages of CKD, calcium supplementation should be considered when plasma PTH concentrations begin to rise (usually when GFR decreases to < 60 ml/min/1.73 m2 [stage 3 CKD]).

Both increased mortality and extraskeletal calcification are related to calcium-phosphorus product. If the product exceeds 55 mg2/dl2, there is increased risk for development of calcification and possibly increased risk for a lower rate of patient survival. Thus, the goal is to maintain the calcium-phosphorus product at less than 55 mg2/dl2.

The implications for active involvement of pharmacists in the selection of appropriate phosphorus binder therapies are clear. Those involved in formulary controls should ensure that both calcium-containing agents and sevelamer (and eventually, presumably, lanthanum) are available, particularly in light of the increasing frequency of adynamic bone disease, which requires a judicious approach to calcium influx from all sources. Furthermore, pharmacists could play a pivotal educational role, particularly for primary care providers who may be less familiar with the nuances of the complications of bone disease.

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