- Click here for explanation of classification scheme.

To review the consequences and treatment of hyperphosphatemia in patients with chronic renal disease.

Article inclusion criteria not specifically mentioned.

Article exclusion criteria not specifically mentioned.

Recruitment:  article selection methods not described.

Design:  Narrative Review

Blinding Used (if applicable):  not applicable

Intervention (if applicable):  not applicable

Statistical Analysis:  statistical analysis not completed

 

Timing of Measurements:  not applicable

Dependent Variables:  not applicable

Independent Variables:  not applicable

Control Variables:  not applicable

Initial N:  122 references

Attrition (final N):  122

Age:  not mentioned

Ethnicity:  not mentioned

Other relevant demographics:

Anthropometrics:

Location:  worldwide studies

Phosphorus Metabolism Normal Renal Function

1. Studies show that an acute load of oral phosphate leads to an increase in serum phosphorus, a decrease in serum ionized calcium levels and an increase in PTH in normal subjects.

2. Feeding studies in animals show that long-term administration of a high-phosphorus diet causes parathyroid hyperplasia and increased PTH.

Mild and Moderate Renal Failure

1. As GFR decreases, renal excretion of phosphorus/unit of glomerular filtration increases in response to increased secretion of PTH. Therefore, serum phosphorus levels are usually normal until GFR decreases to 30 ml/min.

2. When GFR is decreased 30 ml/min, dietary phosphorus restriction results in an increase in calcitriol and a decrease in PTH values; this is probably due to enhanced intestinal absorption of calcium and a direct suppressive effect of calcitriol on PTH synthesis.

Severe Renal Failure and End-Stage Renal Disease

1. The magnitude of PTH excess and calcitriol deficiency is evident as is calcium malabsorption; dietary phosphorus restriction has little effect on calcitriol probably because of lack of functioning kidney tissue for converting 25(OH) D to 1,25(OH)2D.

2. Phosphorus restriction however is important to prevent 2° hyperparathyroidism which results in decreased serum calcium that is a potent stimulator for PTH secretion as well as metastatic calcification of soft tissue.

Strategies to Prevent Phosphorus Accumulation

Diet: 1. A 40 g protein diet would provide 25.5±1.4 mmol (790±43mg) phosphorus/d; 1.0 g protein/kg/d provides 32 mmol (~990 mg)/d; 1.4 g protein/kg/d results in a positive phosphorus balance.

Removal (Dialysis): 1. Hemodialysis removes ~32.5 mmol (1,006 mg) phosphorus/d.

2. CAPD removes 9.9 mmol (300 mg)/d

Phosphorus Binders: 1. Calcium; The dose of elemental calcium needed for phosphorus control was 10 to 15 mmol (400 to 600 mg)/meal. One study showed that the average daily dose of elemental calcium as calcium acetate was 25.4±8.2 mmol and 46.9±23.9 mmol as calcium carbonate. However, calcium acetate ? the absorption of aluminum and therefore is not recommended.

2. Magnesium: 38 mmol of magnesium acetate results in absorption of only 28% of dietary phosphorus. Doses as high as 21 to 63 mmol/d provided control of phosphorus without the development of hypermagnesemia. However, diarrhea may be a side affect with this amount of magnesium.

Reasons for Failure to Prevent Hyperphosphatemia Compliance

 

1. Compliance: can be improved with frequent RD counseling, positive reinforcement by nursing staff, appropriate intervention by social workers and support by the nephrologist.

2. Prescription errors: A careful dietary history is mandatory to successfully match the quantity of binders ordered to the amount of phosphorus ingested with each meal.

3. Dissolution problems: There is variability in dissolution rates of calcium carbonate with more problems with generic brands.

4. Severe 2° hyperparathyroidism: Often the cause is long-standing renal failure and noncompliance with medicines and diet. Frequently the only recourse is to advise a subtotal parathyroidectomy.

Phosphorus Control in Perspective

1. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.

2. In a study of over 12,000 hemodialysis patients, low levels of phosphorus, potassium, albumin, cholesterol, urea and creatinine were all associated with a high risk of death. These data suggest that poor nutrition is associated with subsequent mortality.

3. Dietary protein intake of hemodialysis patients is affected by the amount of dialysis delivered and can be increased with more intensive dialysis.

 

 

Restriction of dietary phosphorus within the constraints of an adequate protein intake is critical in the control of phosphorus. Phosphorus binders containing calcium are the binders of choice. Calcium carbonate, because of its high content of calcium and relative inexpensiveness, remains the most popular calcium-containing phosphorus binder. It should be prescribed in amounts proportional to the phosphorus content of each meal.

 

Government:	NIDDK,
University/Hospital:	Washington University School of Medicine

Excellent review of hyperphosphatemia and treatment. The authors stress the importance of a good diet history in order to prescribe the appropriate amount of calcium binder with meals. Also, reviewing the type of calcium supplement is important—some brands do not dissolve adequately to be effective. OsCal and Tums are two brands that dissolve adequately for treatment.

The role of the RD is emphasized in this review.