KDOQI (Kidney Disease Outcomes Quality Initiative)

NKF KDOQI GUIDELINES

Executive Summaries | Anemia | Hemodialysis | Peritoneal Dialysis
Vascular Access | Nutrition | CKD 2002 | Dyslipidemias | Bone Metabolism
History of KDOQI



KDOQI Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease


CLINICAL PRACTICE GUIDELINES

GUIDELINE 13. TREATMENT OF BONE DISEASE IN CKD

The therapeutic approach to bone disease in CKD is based on its specific type. As such, this Guideline encompasses 3 parts: Guideline 13A deals with high-turnover and mixed bone disease; Guideline 13B with osteomalacia; and Guideline 13C with adynamic bone disease.

GUIDELINE 13A. HYPERPARATHYROID (HIGH-TURNOVER) AND MIXED (HIGH-TURNOVER WITH MINERALIZATION DEFECT) BONE DISEASE

13A.1 In CKD patients (Stages 3 and 4) who have plasma levels of intact PTH >70 pg/mL (7.7 pmol/L) (Stage 3) or >110 pg/mL (12.1 pmol/L) (Stage 4) on more than 2 consecutive measurements, dietary phosphate intake should be restricted. If this is ineffective in lowering plasma PTH levels, calcitriol, (EVIDENCE) or 1 of its analogs [alfacalcidol (EVIDENCE) or doxercalciferol (OPINION)] should be given to prevent or ameliorate bone disease. (See Guideline 8A.)

13A.2 In CKD patients (Stage 5) who have elevated plasma levels of intact PTH (>300 pg/mL [33.0 pmol/L]), calcitriol (EVIDENCE) or 1 of its analogs (doxercalciferol, alfacalcidol, or paricalcitol) (OPINION) should be used to reverse the bone features of PTH overactivity (ie, high-turnover bone disease), and to treat defective mineralization. (See Guideline 8B.)

Background

Numerous studies have shown that high-turnover bone (encompassing both osteitis fibrosa and mixed uremic osteodystrophy) is often associated with serum levels of intact PTH of over 400 pg/mL (44.0 pmol/L), though high-turnover lesions may be seen at lower intact PTH levels and low-turnover bone disease may occur at serum levels of intact PTH above 400 pg/mL (44.0 pmol/L).

Rationale

The understanding of bone disease in CKD has evolved dramatically over the years. The recognition that hyperparathyroidism is a complication of kidney failure actually predated, by many years, the initiation of dialysis treatment. Early studies of osteodystrophy focused largely on understanding the pathophysiology and the prevention of hyperparathyroidism. The development of increasingly more precise and specific PTH assays permitted more careful studies of the calcium and PTH interaction and the importance of phosphate in this interaction.

Strength of Evidence

Because of the difficulty and expense of obtaining bone biopsies, most clinical studies of osteodystrophy have utilized the levels of PTH, particularly intact PTH, as a marker for bone turnover. Thus, the newer vitamin D analogs have largely obtained FDA approval for use in the control of intact PTH and do not have adequate data to document their effect on bone histology. Limited data do exist to show that features of hyperparathyroid bone disease (osteitis fibrosa) are improved by both oral and parenteral calcitriol. Since intact PTH levels correlate with bone turnover, it was assumed that avoidance of very high or very low intact PTH levels would prevent either the hyperactive osteitis fibrosa or the hypoactive adynamic disorder, though no convincing outcome studies proved this. Indeed, it has been shown recently that the intact PTH assays measure not only PTH-(1-84) but also large C-terminal fragments, some of which antagonize the effects of PTH-(1-84) on bone.

Limitations

See the corresponding section in Guidelines 8A and 8B.

Recommendations for Research

Studies are needed to evaluate the changes in bone histology, PTH, and its fragments with the available vitamin D analogs and other therapeutic approaches.

 


2003 National Kidney Foundation, Inc.