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## Complete Summary

#### GUIDELINE TITLE

Clinical practice guidelines for bone metabolism and disease in chronic
kidney disease.

#### BIBLIOGRAPHIC SOURCE(S)

National Kidney Foundation. K/DOQI clinical practice guidelines for bone
metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003
Oct;42(4 Suppl 3):S1-201. \[664 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14520607)

#### GUIDELINE STATUS

This is the current release of the guideline.

### COMPLETE SUMMARY CONTENT

 SCOPE\
 METHODOLOGY - including Rating Scheme and Cost Analysis\
 RECOMMENDATIONS\
 EVIDENCE SUPPORTING THE RECOMMENDATIONS\
 BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS\
 QUALIFYING STATEMENTS\
 IMPLEMENTATION OF THE GUIDELINE\
 INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT
CATEGORIES\
 IDENTIFYING INFORMATION AND AVAILABILITY\
 DISCLAIMER

### SCOPE

#### DISEASE/CONDITION(S)

-   Mineral and bone metabolism and disease

-   Chronic kidney disease

#### GUIDELINE CATEGORY

Diagnosis\
Management\
Treatment

#### CLINICAL SPECIALTY

Family Practice\
Internal Medicine\
Nephrology

#### INTENDED USERS

Advanced Practice Nurses\
Allied Health Personnel\
Health Care Providers\
Nurses\
Physician Assistants\
Physicians

#### GUIDELINE OBJECTIVE(S)

To develop a set of clinical practice guidelines that would improve
diagnoses and treatment of bone disease in chronic kidney disease and
serve as a clinical action plan for the health care practitioner

#### TARGET POPULATION

Adults (18 years and older) with chronic kidney disease

#### INTERVENTIONS AND PRACTICES CONSIDERED

**Evaluation**

1.  Measurement of serum levels of calcium, phosphorus, and intact
    plasma parathyroid hormone (PTH)

2.  Assessment of bone disease, including:

    -   Iliac crest bone biopsy with tetracycline labeling and bone
        histomorphometric analysis

    -   Bone radiographs

    -   Bone mineral density (BMD) by dual energy x-ray (DEXA)

3.  Deferoxamine (DF0) testing

4.  Measurement of serum 25-hydroxyvitamin D and serum levels for carbon
    dioxide

**Treatment/Management**

1.  Maintain target plasma levels of intact PTH

2.  Maintenance/monitoring of serum phosphorus levels

3.  Dietary phosphorus restriction

4.  Use of phosphate binders

    -   Calcium-based binders, noncalcium-, nonaluminum-, and
        nonmagnesium-containing binders

    -   Combination calcium-based and non-calcium based phosphate
        binders

5.  Maintain corrected calcium levels within \"normal\" range

    -   Calcium salts and/or oral vitamin D sterols

6.  Vitamin D~2~ therapy

7.  Active vitamin D sterol therapy for patients on dialysis

    -   Monitor serum levels of calcium and phosphorus and serum PTH

8.  Maintain dialysate calcium at 2.5 mEq/L

9.  Kidney transplant

10. High-flux dialyzers

11. Treatment of bone disease

    -   Therapeutic management based on specific type of bone disease
        (hyperparathyroid and mixed bone disease, osteomalacia, and
        adynamic bone disease) as outlined in the guideline

12. Parathyroidectomy in patients with chronic kidney disease

    -   Supplemental alkali salts for metabolic acidosis

13. Immunosuppressive therapy for kidney transplant recipients

#### MAJOR OUTCOMES CONSIDERED

The Work Group Chair and Vice Chair initially formulated a working list
of \"key questions\" that should be addressed in the evidence report and
then converted into hypothetical guideline statements. Each key question
typically had several outcomes of interest, from long-term,
patient-oriented outcomes, such as quality of life and mortality, to
short-term intermediate outcomes such as serum calcium and phosphate
levels.

### METHODOLOGY

#### METHODS USED TO COLLECT/SELECT EVIDENCE

Hand-searches of Published Literature (Primary Sources)\
Searches of Electronic Databases

#### DESCRIPTION OF METHODS USED TO COLLECT/SELECT THE EVIDENCE

The Work Group and Evidence Review Team agreed on a systematic process
to review literature based on the key questions and hypothetical
guideline statements. Based on these key questions, information
specialists on the Evidence Review Team performed database literature
searches to identify the relevant published medical literature. A list
of terms pertaining to specific kidney and bone diseases was developed.
Major databases searched included: Medline, Embase, PsychLit, Cochrane
Library, and CINAHL. In total, 10 major data-bases were searched.

A priori criteria were established for determining whether an article
identified by the literature searches should be retrieved before the
searches were performed to reduce bias in selecting articles and
establish minimum standards of relevance and quality of the retrieved
articles. The cutoff date for all literature considered as evidence was
January 1, 2001.

Abstracts of each article identified in the electronic searches were
reviewed and articles were requested if they appeared to meet the
criteria. The resulting articles were then evaluated to determine
whether they met criteria for inclusion in this evidence report.

#### NUMBER OF SOURCE DOCUMENTS

467

#### METHODS USED TO ASSESS THE QUALITY AND STRENGTH OF THE EVIDENCE

Weighting According to a Rating Scheme (Scheme Given)

#### RATING SCHEME FOR THE STRENGTH OF THE EVIDENCE

**Strength of Evidence**

Each rationale statement was graded according to the level of evidence
on which it was based. The overall guideline was then graded according
to the strength of evidence supporting the rationale statements.

**Rationale Statements**

1.  Analysis of controlled trials, generalizable studies of high
    methodological quality

2.  Analysis of lower quality studies

3.  Vote count analysis of evidence tables

4.  Review of reviews and selected original articles

5.  Opinion

#### METHODS USED TO ANALYZE THE EVIDENCE

Meta-Analysis\
Systematic Review with Evidence Tables

#### DESCRIPTION OF THE METHODS USED TO ANALYZE THE EVIDENCE

**Evidence Tables**

Five types of evidence tables were prepared included in the Evidence
Reports prepared by the Evidence Review Team.

Detailed tables contain data from each field of the components of the
data abstraction forms. These tables are contained in the Appendix of
each Evidence Report.

In-text study detail tables summarized the most salient aspects of study
design, in particular those aspects that were used to determine the
methodology quality rating. In-text patient characteristics tables
summarized the most salient aspects of the patients included in each
study. In-text evidence tables were produced for each outcome measure
within each key question. The evidence tables reported the evidence as
it was used by the Evidence Review Team to perform quantitative
analyses, not the evidence as it was reported by the authors of a study.
Whenever possible, the results from each study were recalculated and
standardized into a common, metric, Hedges´ d.

Study Quality Overview tables, also included in the body of the evidence
reports, were produced for those key questions that addressed a
treatment issue for which controlled trials were available. The rating
scheme used was applied only to controlled trials. No rating scheme was
developed for diagnostic studies, as there is no widely accepted
hierarchy of evidence in the technology assessment community. These
tables described the strength of evidence according to 3 dimensions:
size of the study, applicability, and methodological quality.

**Quantitative Analysis of Studies**

To analyze diagnostic trials, a method called the \"summary receiver
operator characteristics (ROC) curve\" was used. This is the most widely
accepted analytical method for combining results from different
diagnostic trials. It combines and plots the sensitivity (true positive
rate) against specificity (inverse of the false positive rate) of a
particular diagnostic test from several trials. The summary ROC includes
95% confidence intervals for complete evaluation of the statistical
significance of the efficacy of the test compared to flipping a coin
(chance). In this way, all the available evidence about a test\'s
tradeoffs between false positives and false negatives can be considered.

#### METHODS USED TO FORMULATE THE RECOMMENDATIONS

Expert Consensus

#### DESCRIPTION OF METHODS USED TO FORMULATE THE RECOMMENDATIONS

**Overview of Process**

Three Work Group meetings and a series of conference calls were carried
out to develop an evidence model, assess the literature, evaluate the
evidence base, review the evidence report, and draft guideline
statements. Prior to the development of the evidence base, a set of
hypothetical guideline statements (leaving a blank where values from the
evidence were to be inserted following development of the final evidence
report) were developed by the Work Group in order to define the
parameters of the literature review. This evidence base consisted of an
evidence report prepared by the Evidence Review Team that included 26
meta-analyses of the available scientific literature and numerous
summaries of data.

The steps used to develop the guidelines and evidence base are listed in
Table 7 of the original guideline document.

**Development of Guideline Statements**

A working list of \"key questions\" that should be addressed in the
evidence report and then converted into hypothetical guideline
statements was formulated. At an initial Work Group meeting in April
2000, these questions and resulting statements were refined through
discussions between the Work Group and the Evidence Review Team. Work
Group members were given two additional opportunities to refine the key
questions, which were finalized in May 2000. Each key question typically
had several outcomes of interest, from long-term, patient-oriented
outcomes, such as quality of life and mortality, to short-term
intermediate outcomes, such as serum calcium and phosphate levels. The
key questions were divided into 9 sections.

Hypothetical guideline statements were then prepared from the key
questions and these statements were used to formulate and refine the
final guideline statements. The Work Group voted on the final wording of
each guideline statement in relationship to the final evidence report
presented. As the hypothetical guideline statements were formulated,
these questions were redivided into 16 different Guideline areas
corresponding to the guidelines set forth in this document.

**Voting Procedures**

Final voting was used to arrive at a Work Group consensus on final
guideline statements and supporting rationale, graded according the
level of evidence on which it was based. The overall guidelines were
then graded according to the strength of evidence supporting the line of
logic of the rationale statements.

The following voting method was used: A tally was taken to determine
whether consensus among Work Group members existed for each Guideline
statement. Consensus among Work Group members was defined by at least a
75% majority approval of a Guideline statement (e.g., with 12 Work Group
members present, a vote of 9 was necessary to consider the statement
approved). Guidelines that did not receive approval were re-drafted and
re-submitted to Work Group members for final voting.

#### RATING SCHEME FOR THE STRENGTH OF THE RECOMMENDATIONS

In formulating the guidelines, the rationale and evidentiary basis of
each recommendation was made explicit.

-   When all components of the rationale for a guideline were based on
    published evidence, the guidelines were labeled **\"Evidence.\"**

-   When no definite evidence existed or the evidence was considered
    inconclusive, and either the guideline or steps in its rationale
    were based on judgment they were labeled **\"Opinion.\"**

As such, it is the available literature that determined the labeling of
each guideline.

#### COST ANALYSIS

A formal cost analysis was not performed and published cost analyses
were not reviewed.

#### METHOD OF GUIDELINE VALIDATION

External Peer Review\
Internal Peer Review

#### DESCRIPTION OF METHOD OF GUIDELINE VALIDATION

Prior to their publication, a final draft of the guidelines was
subjected to a broad-based review by experts, organizations, and the
public. Thus, the chain of reasoning and recommendation of each opinion
based guideline was exposed to open debate, with the final published
product reflecting a wide consensus of healthcare professionals,
providers, managers, organizations, associations, and patients.

### RECOMMENDATIONS

#### MAJOR RECOMMENDATIONS

**Evidentiary Basis for Recommendations**

-   When all components of the rationale for a guideline were based on
    published evidence, the guidelines were labeled **\"Evidence.\"**

-   When no definite evidence existed or the evidence was considered
    inconclusive, and either the guideline or steps in its rationale
    were based on judgment they were labeled **\"Opinion.\"**

**Guideline 1. Evaluation of Calcium and Phosphorus Metabolism**

1.1 Serum levels of calcium, phosphorus, and intact plasma parathyroid
hormone (PTH) should be measured in all patients with chronic kidney
disease (CKD) and glomerular filtration rate (GFR) \<60 mL/min/1.73
m^2^. (**Evidence**) The frequency of these measurements should be based
on the stage of chronic kidney disease (see Table 14 in the original
guideline document). (**Opinion**)

1.2 These measurements should be made more frequently if the patient is
receiving concomitant therapy for the abnormalities in the serum levels
of calcium, phosphorus, or PTH, as detailed in Guidelines 4, 5, 7, and
8, and in transplant recipient, Guideline 16.

1.3 Measurement of plasma PTH levels may be done less frequently for
those with levels within the low end of the target levels (see Table 15
in the original guideline document). (**Opinion**)

1.4 The target range of plasma levels of intact PTH in the various
stages of CKD are denoted in Table 15 in the original guideline document

**Guideline 2. Assessment of Bone Disease Associated with CKD**

2.1 The most accurate diagnostic test for determining the type of bone
disease associated with CKD is iliac crest bone biopsy with double
tetracycline labeling and bone histomorphometric analysis.
(**Evidence**)

2.2 It is not necessary to perform bone biopsy for most situations in
clinical practice. However, a bone biopsy should be considered in
patients with kidney failure (Stage 5) who have:

2.2a Fractures with minimal or no trauma (pathological fractures)
(**Opinion**)

2.2b Intact plasma PTH levels between 100 and 500 pg/mL (11.0 to 55.0
pmol/L) (in CKD Stage 5) with coexisting conditions such as unexplained
hypercalcemia, severe bone pain, or unexplained increases in bone
alkaline phosphatase activity **(Opinion**)

2.2c Suspected aluminum bone disease, based upon clinical symptoms or
history of aluminum exposure (**Opinion**) (See Guideline 11)

2.3 Bone radiographs are not indicated for the assessment of bone
disease of CKD, (**Evidence**) but they are useful in detecting severe
peripheral vascular calcification (**Opinion**) and bone disease due to
beta~2~ microglobulin amyloidosis. (See Guideline 10) (**Evidence**)

2.4 Bone mineral density (BMD) should be measured by dual energy x-ray
absorptiometry (DEXA) in patients with fractures and in those with known
risk factors for osteoporosis. (**Opinion**).

**Guideline 3. Evaluation of Serum Phosphorus Levels**

3.1 In CKD patients (Stages 3 and 4), the serum level of phosphorus
should be maintained at or above 2.7 mg/dL (0.87 mmol/L) (**Evidence**)
and no higher than 4.6 mg/dL (1.49 mmol/L). (**Opinion**)

3.2 In CKD patients with kidney failure (Stage 5) and those treated with
hemodialysis or peritoneal dialysis, the serum levels of phosphorus
should be maintained between 3.5 to 5.5 mg/dL (1.13 to 1.78 mmol/L).
(**Evidence**)

**Guideline 4. Restriction of Dietary Phosphorus in Patients with CKD**

4.1 Dietary phosphorus should be restricted to 800 to 1,000 mg/day
(adjusted for dietary protein needs) when the serum phosphorus levels
are elevated \>4.6 mg/dL (1.49 mmol/L) at Stages 3 and 4 of CKD,
(**Opinion**) and \>5.5 mg/dL (1.78 mmol/L) in those with kidney failure
(Stage 5). (**Evidence**)

4.2 Dietary phosphorus should be restricted to 800 to 1,000 mg/day
(adjusted to dietary protein needs) when the plasma levels of intact PTH
are elevated above target range of the CKD Stage (see Table 15 in
Guideline 1). (**Evidence**)

4.3 The serum phosphorus levels should be monitored every month
following the initiation of dietary phosphorus restriction.
(**Opinion**)

**Guideline 5. Use of Phosphate Binders in CKD**

*In CKD Patients (Stages 3 and 4)*:

5.1 If phosphorus or intact PTH levels cannot be controlled within the
target range (see Guidelines 1, 3), despite dietary phosphorus
restriction (see Guideline 4), phosphate binders should be prescribed.
(**Opinion**)

5.2 Calcium-based phosphate binders are effective in lowering serum
phosphorus levels (**Evidence**) and may be used as the initial binder
therapy. (**Opinion**)

*In CKD Patients with Kidney Failure (Stage 5)*:

5.3 Both calcium-based phosphate binders and other noncalcium-,
nonaluminum-, and nonmagnesium-containing phosphate-binding agents (such
as sevelamer hydrochloride \[HCl\]) are effective in lowering serum
phosphorus levels (**Evidence**) and either may be used as the primary
therapy. (**Opinion**)

5.4 In dialysis patients who remain hyperphosphatemic (serum phosphorus
\>5.5 mg/dL \[1.78 mmol/L\]) despite the use of either of calcium-based
phosphate binders or other noncalcium-, nonaluminum-,
nonmagnesium-containing phosphate-binding agents, a combination of both
should be used. (**Opinion**)

5.5 The total dose of elemental calcium provided by the calcium-based
phosphate binders should not exceed 1,500 mg/day (**Opinion**), and the
total intake of elemental calcium (including dietary calcium) should not
exceed 2,000 mg/day. (**Opinion**)

5.6 Calcium-based phosphate binders should not be used in dialysis
patients who are hypercalcemic (corrected serum calcium of \>10.2 mg/dL
\[2.54 mmol/L\]), or whose plasma PTH levels are \<150 pg/mL (16.5
pmol/L) on 2 consecutive measurements. (**Evidence**)

5.7 Noncalcium-containing phosphate binders are preferred in dialysis
patients with severe vascular and/or other soft-tissue calcifications.
(**Opinion**)

5.8 In patients with serum phosphorus levels \>7.0 mg/dL (2.26 mmol/L),
aluminum-based phosphate binders may be used as a short-term therapy (4
weeks), and for one course only, to be replaced thereafter by other
phosphate binders. (**Opinion**) In such patients, more frequent
dialysis should also be considered. (**Evidence**)

**Guideline 6. Serum Calcium and Calcium-Phosphorus Product**

*In CKD Patients (Stages 3 and 4)*:

6.1 The serum levels of corrected total calcium should be maintained
within the \"normal\" range for the laboratory used. (**Evidence**)

*In CKD Patients With Kidney Failure (Stage 5)*:

6.2 Serum levels of corrected total calcium should be maintained within
the normal range for the laboratory used, preferably toward the lower
end (8.4 to 9.5 mg/dL \[2.10 to 2.37 mmol/L\]). (**Opinion**)

6.3 In the event corrected total serum calcium level 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 phosphate binders, the dose should
be reduced or therapy switched to a noncalcium-, nonaluminum-,
nonmagnesium-containing phosphate binder. (**Opinion**) See Guideline 5.

6.3b In patients taking active vitamin D sterols, the dose should be
reduced or therapy discontinued until the serum levels of corrected
total calcium return to the target range (8.4 to 9.5 mg/dL \[2.10 to
2.37 mmol/L\]). (**Opinion**) See Guideline 8B.

6.3c If hypercalcemia (serum levels 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 phosphate binders,
dialysis using low dialysate calcium (1.5 to 2.0 mEq/L) may be used for
3 to 4 weeks. (**Opinion**) See Guideline 9.

*In CKD Patients (Stages 3 to 5)*:

6.4 Total elemental calcium intake (including both dietary calcium
intake and calcium-based phosphate binders) should not exceed 2,000
mg/day. (**Opinion**) See Guideline 5.

6.5 The serum calcium-phosphorus product should be maintained at \<55
mg^2^/dL^2^. (**Evidence**) This is best achieved by controlling serum
levels of phosphorus within the target range. (**Opinion**) See
Guidelines 3, 4, and 5.

6.6 Patients whose serum levels 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 levels if:

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

6.6b The plasma intact PTH level is above the target range for the CKD
Stage. (See Table 15 in Guideline 1.) (**Opinion**)

6.7 Therapy for hypocalcemia should include calcium salts such as
calcium carbonate (**Evidence**) and/or oral vitamin D sterols.
(**Evidence**) See Guideline 8B.

**Guideline 7. Prevention and Treatment of Vitamin D Insufficiency and
Vitamin D Deficiency in CKD Patients (Algorithm 1)**

*In CKD Patients (Stages 3 and 4)*:

7.1 If plasma intact PTH is above the target range for the stage of CKD
(Table 15, Guideline 1) serum 25-hydroxyvitamin D should be measured at
first encounter. If it is normal, repeat annually. (**Evidence**)

7.2 If the serum level of 25-hydroxyvitamin D is \<30 ng/mL,
supplementation with vitamin D~2~ (ergocalciferol) should be initiated
(see Table 26 in the original guideline document). (**Opinion**)

7.3 Following initiation of vitamin D therapy:

7.3a The use of ergocalciferol therapy should be integrated with the
serum calcium and phosphorus (see Algorithm 1 in the original guideline
document).

7.3b The serum levels of corrected total calcium and phosphorus should
be measured at least every 3 months. (**Opinion**)

7.3c If the serum levels of corrected total calcium exceeds 10.2 mg/dL
(2.54 mmol/L), discontinue ergocalciferol therapy and all forms of
vitamin D therapy. (**Opinion**)

7.3d If the serum phosphorus exceeds 4.6 mg/dL, add or increase the dose
of phosphate binder. (See Guidelines 4 and 5.) If hyperphosphatemia
persists, discontinue vitamin D therapy. (**Opinion**)

7.3e Once patients are replete with vitamin D, continued supplementation
with a vitamin-D--containing multi-vitamin preparation should be used
with annual reassessment of serum levels of 25-hydroxyvitamin D, and the
continued assessment of corrected total calcium and phosphorus every 3
months. (**Opinion**)

*In CKD Patients With Kidney Failure (Stage 5)*:

7.4 Therapy with an active vitamin D sterol (calcitriol, alfacalcidol,
paricalcitol, or doxercalciferol) should be provided if the plasma
levels of intact PTH are \>300 pg/mL. (**Opinion**) See Guideline 8B.

**Guideline 8. Vitamin D Therapy in CKD Patients**

This Guideline encompasses 2 parts: Guideline 8A, which deals with
active vitamin D sterol therapy in CKD Stages 3 and 4, and Guideline 8B,
which deals with CKD Stage 5.

**Guideline 8A. Active Vitamin D Therapy in Patients with Stages 3 and 4
CKD (Algorithm 2)**

8A.1 In patients with CKD Stages 3 and 4, therapy with an active oral
vitamin D sterol (calcitriol, alfacalcidol, or doxercalciferol) is
indicated when serum levels of 25(OH)-vitamin D are \>30 ng/mL (75
nmol/L) and plasma levels of intact PTH are above the target range for
the CKD stage (see Table 15, Guideline 1). (**Evidence**) The initial
doses are provided in Table 27 in the original guideline document.

8A.1a Treatment with an active vitamin D sterol should be undertaken
only in patients with serum levels of corrected total calcium \<9.5
mg/dL (2.37 mmol/L) and serum phosphorus \<4.6 mg/dL (1.49 mmol/L).
(**Opinion**)

8A.1b Vitamin D sterols should not be prescribed for patients with
rapidly worsening kidney function or those who are noncompliant with
medications or follow-up. (**Opinion**)

8A.2 During therapy with vitamin D sterols, serum levels of calcium and
phosphorus should be monitored at least every month after initiation of
therapy for the first 3 months, then every 3 months thereafter. Plasma
PTH levels should be measured at least every 3 months for 6 months, and
every 3 months thereafter. (**Opinion**)

8A.3 Dosage adjustments for patients receiving active vitamin D sterol
therapy should be made as follows:

8A.3a If plasma levels of intact PTH fall below the target range for the
CKD stage (see Table 15 in the original guideline document, Guideline
1), hold active vitamin D sterol therapy until plasma levels of intact
PTH rise to above the target range, then resume treatment with the dose
of active vitamin D sterol reduced by half. If the lowest daily dose of
the active vitamin D sterol is being used, reduce to alternate-day
dosing. (**Opinion**)

8A.3b If serum levels of corrected total calcium exceed 9.5 mg/dL (2.37
mmol/L), hold active vitamin D sterol therapy until serum calcium
returns to \<9.5 mg/dL (2.37 mmol/L), then resume treatment at half the
previous dose. If the lowest daily dose of the active vitamin D sterol
is being used, reduce to alternate-day dosing. (**Opinion**)

8A.3c If serum levels of phosphorus rise to \>4.6 mg/dL (1.49 mmol/L),
hold active vitamin D therapy, initiate or increase dose of phosphate
binder until the levels of serum phosphorus fall to [\<]{.underline}4.6
mg/dL (1.49 mmol/L); then resume the prior dose of active vitamin D
sterol. (**Opinion**)

**Guideline 8B. Vitamin D Therapy in Patients on Dialysis (CKD Stage
5)**

8B.1 Patients treated with hemodialysis or peritoneal dialysis with
serum levels of intact PTH levels \>300 pg/mL should receive an active
vitamin D sterol (such as calcitriol, alfacalcidol, paricalcitol, or
doxercalciferol; see Table 28 of the guidelines) to reduce the serum
levels of PTH to a target range of 150 to 300 pg/mL. (**Evidence**)

8B.1a The intermittent, intravenous administration of calcitriol is more
effective than daily oral calcitriol in lowering serum PTH levels.
(**Evidence**)

8B.1b In patients with corrected serum calcium and/or phosphorus levels
above the target range (see Guidelines 3 and 6, respectively), a trial
of alternative vitamin D analogs, such as paricalcitol or
doxercalciferol may be warranted. (**Opinion**)

8B.2 When therapy with vitamin D sterols is initiated or the dose is
increased, serum levels of calcium and phosphorus should be monitored at
least every 2 weeks for 1 month and then monthly thereafter. The plasma
PTH should be measured monthly for at least 3 months and then every 3
months once target levels of PTH are achieved. (**Opinion**)

8B.3 For patients treated with peritoneal dialysis, oral doses of
calcitriol (0.5 to 1.0 micrograms) or doxercalciferol (2.5 to 5.0
micrograms) can be given 2 or 3 times weekly. Alternatively, a lower
dose of calcitriol (0.25 micrograms) can be administered daily.
(**Opinion**)

8B.4 When either hemodialysis or peritoneal dialysis patients are
treated with active vitamin D sterols, management should integrate the
changes in serum calcium, serum phosphorus, and plasma PTH. Each of
these 3 variables is considered separately with suggested interventions
based on the various values obtained in Algorithm 3, Algorithm 4, and
Algorithm 5 in the original guideline document. (**Opinion**)

**Guideline 9. Dialysate Calcium Concentrations**

9.1 The dialysate calcium concentration in hemodialysis or peritoneal
dialysis should be 2.5 mEq/L (1.25 mmol/L). (**Opinion**)

9.2 Higher or lower dialysate calcium levels are indicated in selected
patients. (See Clinical Applications section in the original guideline
document) (**Opinion**)

**Guideline 10. Beta~2~-Microglobulin Amyloidosis**

10.1 Screening for beta~2~-microglobulin amyloidosis, including
measurement of serum levels of beta~2~-microglobulin, is not
recommended. (**Opinion**)

10.1a No currently available therapy (except kidney transplantation) can
stop disease progression of beta~2~-microglobulin amyloidosis or provide
symptomatic relief. (**Evidence**)

10.1b Kidney transplant should be considered to stop disease progression
or provide symptomatic relief in patients with beta~2~-microglobulin
amyloidosis. (**Evidence**)

10.1c In patients with evidence of, or at risk for,
beta~2~-microglobulin amyloidosis noncuprophane (**Evidence**),
high-flux dialyzers (**Opinion**) should be used.

**Guideline 11. Aluminum Overload and toxicity in CKD**

11.1 To prevent aluminum toxicity, the regular administration of
aluminum should be avoided and the dialysate concentration of aluminum
should be maintained at \<10 micrograms/L. (**Evidence**)

11.1a CKD patients ingesting aluminum should not receive citrate salts
simultaneously. (**Evidence**)

11.2 To assess aluminum exposure and the risk of aluminum toxicity,
serum aluminum levels should be measured at least yearly and every 3
months in those receiving aluminum-containing medications. (**Opinion**)

11.2a Baseline levels of serum aluminum should be \<20 micrograms/L.
(**Opinion**)

11.3 A deferoxamine (DFO) test should be performed if there are elevated
serum aluminum levels (60 to 200 micrograms/L); clinical signs and
symptoms of aluminum toxicity (see Table 31 in the original guideline
document); or prior to parathyroid surgery if the patient has had
aluminum exposure. (**Evidence**) (see Algorithms 6 and 7 in the
original guideline document).

11.3a The test is done by infusing 5 mg/kg of DFO during the last hour
of the dialysis session with a serum aluminum measured before DFO
infusion and 2 days later, before the next dialysis session.
(**Opinion**)

11.3b The test is considered positive if the increment of serum aluminum
is [\>]{.underline}50 micrograms/L. (**Opinion**)

11.3c A DFO test should not be performed if the serum levels of aluminum
are \>200 micrograms/L to avoid DFO-induced neurotoxicity. (**Opinion**)

11.4 The presence of aluminum bone disease can be predicted by a rise in
serum aluminum of [\>]{.underline}50 micrograms/L following DFO
challenge combined with plasma levels of intact PTH of \<150 pg/mL (16.5
pmol/L). (**Opinion**) However, the gold standard for the diagnosis of
aluminum bone disease is a bone biopsy showing increased aluminum
staining of the bone surface ([\>]{.underline}15% to 25%) using aluminum
stain and often adynamic bone or osteomalacia. (**Evidence**).

**Guideline 12. Treatment of Aluminum Toxicity (See Algorithm 8 and
Algorithm 9 in the original guideline document)**

12.1 In all patients with baseline serum aluminum levels \>60
micrograms/L, a positive DFO test, or clinical symptoms consistent with
aluminum toxicity (Guideline 11, see Table 31 in the original guideline
document), the source of aluminum should be identified and eliminated.
(**Opinion**)

12.2 In symptomatic patients with serum aluminum levels \>60
micrograms/L but \<200 micrograms /L or a rise in aluminum after DFO
\>50 micrograms /L, DFO should be given to treat the aluminum overload.
(See Algorithm 8 and Algorithm 9 in the original guideline document).
(**Opinion**)

12.3 To avoid DFO-induced neurotoxicity in patients with serum aluminum
\>200 micrograms /L, DFO should not be given until intensive dialysis (6
days per week) with high-flux dialysis membrane and a dialysate aluminum
level of \<5 micrograms /L and until the pre-dialysis serum aluminum
level has been reduced to \<200 micrograms/L. (**Opinion**)

**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 one 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
one of its analogs (doxercalciferol, alfacalcidol, or paricalcitol)
(**Opinion**) should be used to reverse the bone features of PTH
overactivity (i.e., high-turnover bone disease) and to treat defective
mineralization. (See Guideline 8B.)

**Guideline 13B. Osteomalacia**

13B.1 Osteomalacia due to aluminum toxicity should be prevented in
dialysis patients by maintaining aluminum concentration in dialysate
fluid at \<10 micrograms/L and avoiding the use of aluminum-containing
compounds (including sucralfate). (**Opinion**)

13B.2 Aluminum overload leading to aluminum bone disease should be
treated with deferoxamine (DFO). (See Guidelines 11 and 12.)
(**Opinion**)

13B.3 Osteomalacia due to vitamin D~2~ or D~3~ deficiency or phosphate
depletion, though uncommon, should be treated with vitamin D~2~ or D~3~
supplementation (see Guideline 7) and/or phosphate administration,
respectively. (**Opinion**)

13B.3a If osteomalacia due to vitamin D deficiency fails to respond to
ergocalciferol or cholecalciferol, particularly in patients with kidney
failure (Stage 5), treatment with an active vitamin D sterol may be
given. (**Opinion**) (See Guideline 8B.)

13B.3b Doses of phosphate supplementation should be adjusted upwards
until normal serum levels of phosphorus are achieved. (**Opinion**)

**Guideline 13C. Adynamic Bone Disease**

13C.1 Adynamic bone disease in Stage 5 CKD (as determined either by bone
biopsy or intact PTH \<100 pg/mL \[11.0 pmol/L\]) should be treated by
allowing plasma levels of intact PTH to rise in order to increase bone
turnover. (**Opinion**)

13C.1a This can be accomplished by decreasing doses of calcium-based
phosphate binders and vitamin D or eliminating such therapy.
(**Opinion**)

**Guideline 14. Parathyroidectomy in Patients with CKD**

14.1 Parathyroidectomy should be recommended in patients with severe
hyperparathyroidism (persistent serum levels of intact PTH \>800 pg/mL
\[88.0 pmol/L\]), associated with hypercalcemia and/or hyperphosphatemia
that are refractory to medical therapy. (**Opinion**)

14.2 Effective surgical therapy of severe hyperparathyroidism can be
accomplished by subtotal parathyroidectomy or total parathyroidectomy
with parathyroid tissue autotransplantation. (**Evidence**)

14.3 In patients who undergo parathyroidectomy the following should be
done:

14.3a The blood level of ionized calcium should be measured every 4 to 6
hours for the first 48 to 72 hours after surgery, and then twice daily
until stable. (**Opinion**)

14.3b If the blood levels of ionized or corrected total calcium fall
below normal (\<0.9 mmol/L or \<3.6 mg/dL corresponding to corrected
total calcium of 7.2 mg/dL \[1.80 mmol/L\]), a calcium gluconate
infusion should be initiated at a rate of 1 to 2 mg elemental calcium
per kilogram body weight per hour and adjusted to maintain an ionized
calcium in the normal range (1.15 to 1.36 mmol/L or 4.6 to 5.4 mg/dL).
(**Opinion**) *A 10-mL ampule of 10% calcium gluconate contains 90 mg of
elemental calcium.*

14.3c The calcium infusion should be gradually reduced when the level of
ionized calcium attains the normal range and remains stable.
(**Opinion**)

14.3d When oral intake is possible, the patient should receive calcium
carbonate 1 to 2 g 3 times a day, as well as calcitriol of up to 2
micrograms/day, and these therapies should be adjusted as necessary to
maintain the level of ionized calcium in the normal range. (**Opinion**)

14.3e If the patient was receiving phosphate binders prior to surgery,
this therapy may need to be discontinued or reduced as dictated by the
levels of serum phosphorus. (**Opinion**)

14.4 Imaging of parathyroid glands with ^99^Tc-Sestamibi scan,
ultrasound, computed tomography (CT) scan, or magnetic resonance imaging
(MRI) should be done prior to re-exploration parathyroid surgery.
(**Opinion**)

**Guideline 15. Metabolic Acidosis**

15.1 In CKD Stages 3, 4, and 5, the serum level of total CO~2~ should be
measured.

15.1a The frequency of these measurements should be based on the stage
of CKD as shown in Table 32 in the original guideline document.
(**Opinion**)

15.2 In these patients, serum levels of total CO~2~ should be maintained
at [\>]{.underline}22 mEq/L (22 mmol/L). (**Evidence**) If necessary,
supplemental alkali salts should be given to achieve this goal.
(**Opinion**)

**Guideline 16. Bone Disease in the Kidney Transplant Recipient**

16.1 Serum levels of calcium, phosphorus, total CO~2~ and plasma intact
PTH should be monitored following kidney transplantation. (**Opinion**)

16.1a The frequency of these measurements should be based on the time
following transplantation, as shown in Table 33 in the original
guideline document. (**Opinion**)

16.2 During the first week after kidney transplantation, serum levels of
phosphorus should be measured daily. Kidney transplant recipients who
develop persistently low levels of serum phosphate (\<2.5 mg/dL \[0.81
mmol/L\]) should be treated with phosphate supplementation.
(**Opinion**)

16.3 To minimize bone mass loss and osteonecrosis, the immunosuppressive
regimen should be adjusted to the lowest effective dose of
glucocorticoids. (**Evidence**)

16.4 Kidney transplant recipients should have bone mineral density (BMD)
measured by dual energy x-ray absorptiometry (DEXA) to assess the
presence or development of osteoporosis. (**Opinion**)

16.4a DEXA scans should be obtained at time of transplant and 1 year and
2 years post-transplant. (**Opinion**)

16.4b If bone mineral density t-score is equal to or less than --2 at
the time of the transplant, or at subsequent evaluations, therapy with
parenteral amino-bisphosphonates should be considered. (**Opinion**)

16.5 Treatment of disturbances in bone and mineral metabolism is
determined by the level of kidney function in the transplant recipient
as provided in Guidelines 1 through 15 for CKD patients. (**Opinion**)

#### CLINICAL ALGORITHM(S)

The following algorithms are provided in the original guideline
document:

-   Algorithm 1: Vitamin D supplementation in chronic kidney disease
    (CKD) (Stages 3 and 4)

-   Algorithm 2: Management of chronic kidney disease (CKD) patients
    (Stages 3 and 4) with active Vitamin D sterols

-   Algorithm 3: Managing Vitamin D sterols based on serum calcium
    levels

-   Algorithm 4: Managing Vitamin D sterols based on serum phosphorus
    levels

-   Algorithm 5: Managing Vitamin D sterols based on intact parathyroid
    hormone (PTH) levels

-   Algorithm 6: Evaluation of aluminum neurotoxicity

-   Algorithm 7: Evaluation of aluminum-related disorders:
    considerations for deferoxamine (DFO) test and subsequent DFO
    treatment

-   Algorithm 8: DFO treatment after P~AI~ rise [\>]{.underline}300
    micrograms/L

-   Algorithm 9: DFO treatment after P~AI~ rise between 50 and 300
    micrograms/L

-   Algorithm 10: CKD Stages 3 and 4

-   Algorithm 11: CKD Stage 5 (on dialysis)

### EVIDENCE SUPPORTING THE RECOMMENDATIONS

#### TYPE OF EVIDENCE SUPPORTING THE RECOMMENDATIONS

In formulating the guidelines, the rationale and evidentiary basis of
each recommendation was made explicit. When all components of the
rationale for a guideline were based on published evidence, the
guidelines were labeled \"Evidence.\" When no definite evidence existed
or the evidence was considered inconclusive, and either the guideline or
steps in its rationale were based on judgment they were labeled
\"Opinion.\" As such, it is the available literature that determined the
labeling of each guideline.

### BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS

#### POTENTIAL BENEFITS

-   Prevention of the disturbances in mineral and bone metabolism and
    their management early in the course of chronic kidney disease are
    extremely important in improving patients´ quality of life and
    longevity.

-   Although much remains to be learned about these conditions, the
    recommendations made in these guidelines are intended to aid
    clinicians in developing an integrated approach to their diagnosis
    and management of this complicated area, based on the best available
    evidence.

#### POTENTIAL HARMS

A deferoxamine (DFO) test should not be performed if the serum levels of
aluminum are greater than 200 micrograms/L to avoid deferoxamine-induced
neurotoxicity.

**Subgroups Most Likely to Experience Harms**

-   Calcium-based phosphate binders should not be used in dialysis
    patients who are hypercalcemic or whose plasma parathyroid hormone
    (PTH) levels are \<150 pg/mL on 2 consecutive measurements.

-   Vitamin D sterols should not be prescribed for patients with rapidly
    worsening kidney function or those who are noncompliant with
    medications or follow-up.

### QUALIFYING STATEMENTS

#### QUALIFYING STATEMENTS

No clinical practice guidelines, irrespective of the rigor of their
development, can accomplish the intended improvement in outcomes without
an implementation plan. Since the majority of the recommendations made
in this set of guidelines are based on opinion, it is imperative that
evaluation of their clinical outcomes be made a component of their
implementation. In addition, the paucity of evidence-based information
in this field requires that a more integrated approach to research
efforts be planned and conducted to provide answers to the many issues
that remain to be elucidated.

### IMPLEMENTATION OF THE GUIDELINE

#### DESCRIPTION OF IMPLEMENTATION STRATEGY

An implementation strategy was not provided.

#### IMPLEMENTATION TOOLS

Clinical Algorithm

For information about
[availability](#identifying-information-and-availability), see the
\"Availability of Companion Documents\" and \"Patient Resources\" fields
below.

### INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT CATEGORIES

#### IOM CARE NEED

Living with Illness

#### IOM DOMAIN

Effectiveness

### IDENTIFYING INFORMATION AND AVAILABILITY

#### BIBLIOGRAPHIC SOURCE(S)

National Kidney Foundation. K/DOQI clinical practice guidelines for bone
metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003
Oct;42(4 Suppl 3):S1-201. \[664 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14520607)

#### ADAPTATION

Not applicable: The guideline was not adapted from another source.

#### DATE RELEASED

2003 Oct

#### GUIDELINE DEVELOPER(S)

National Kidney Foundation - Disease Specific Society

#### SOURCE(S) OF FUNDING

National Kidney Foundation (NKF)

#### GUIDELINE COMMITTEE

NKF-K/DOQI (National Kidney Foundation-Kidney Disease Outcomes Quality
Initiative) Chronic Kidney Disease Work Group

#### COMPOSITION OF GROUP THAT AUTHORED THE GUIDELINE

*Members*: Shaul G. Massry, MD (*Chair*), KECK School of Medicine,
University of Southern California, Los Angeles; Jack W. Coburn, MD
(*Vice-Chair*), VA Greater Los Angeles Healthcare System; Glenn M.
Chertow, MD, MPH, University of California San Francisco; Keith Hruska,
MD, Barnes Jewish Hospital, St. Louis, MO; Craig Langman, MD,
Children\'s Memorial Hospital, Chicago, IL; Hartmut Malluche, MD,
University of Kentucky, Lexington; Kevin Martin, MD, BCh, St. Louis
University, St. Louis, MO; Linda M. McCann, RD, CSR, LD, Satellite
Dialysis Centers, Rocklin, CA; James T. McCarthy, MD, Mayo Clinic,
Rochester, MN; Sharon Moe, MD, Indiana University, Wishard Memorial,
Indianapolis, IN; Isidro B. Salusky, MD, UCLA School of Medicine, Los
Angeles, CA; Donald J. Sherrard, MD, VA Puget Sound Healthcare System,
Seattle, WA; Miroslaw Smogorzewski, MD, University of Southern
California, Los Angeles; Kline Bolton, MD, RPA Liaison, University of
Virginia, Charlottesville

*Evidence Review Team Members*: Charles Turkelson, PhD, Chief Research
Analyst; Karyn Tappe, MS, Lead Research Analyst; Stephen Tregear, PhD,
Research Analyst; James Reston, PhD, Research Analyst; Wendy Bruening,
PhD, Research Analyst; Mark Monteforte, MD, Research Analyst; Janice
Kaczmarek, Project Coordinator; Vivian Coates, MBA, Vice President

*Advisory Board Members*: Garabed Eknoyan, MD (*Co-Chair*); Adeera
Levin, MD, FRCPC (*Co-Chair*); Nathan Levin, MD, FACP (*Co-Chair
Emeritus*); George Bailie, PharmD, PhD; Bryan Becker, MD; Gavin Becker,
MD, MBBs; Jerrilynn Burrowes, PhD, RD; Fernando Carrera, MD; David
Churchill, MD, FACP; Allan Collins, MD, FACP; Peter W. Crooks, MD; Dick
DeZeeuw, MD, PhD; Thomas Golper, MD; Frank Gotch, MD; Antonio Gotto, MD;
Roger Greenwood, MSc, MD, FRCP; Joel W. Greer, PhD; Richard Grimm, Jr.,
MD; William E. Haley, MD; Ronald Hogg, MD; Alan R. Hull, MD; Lawrence
Hunsicker, MD; Cynda Ann Johnson, MD, MBA; Michael Klag, MD, MPH; Saulo
Klahr, MD; Norbert Lameire, MD; Francesco Locatelli, MD; Sally
McCulloch, MSN, RN, CNN; Maureen Michael, BSN, MBA; Joseph V. Nally, MD;
John M. Newmann, PhD, MPH; Allen Nissenson, MD; Keith Norris, MD;
Gregorio Obrador, MD, MPH; William Owen, Jr., MD; Thakor G. Patel, MD,
MACP; Glenda Payne, MS, RN, CNN; Claudio Ronco, MD; Rosa A.
Rivera-Mizzoni, MSW, LCSW; Anton C. Schoolwerth, MD; Robert Star, MD;
Michael Steffes, MD, PhD; Theodore Steinman, MD; John-Pierre Wauters,
MD; Nanette Wenger, MD

*Ex-Officio*: Josephine Briggs, MD; Thomas Hostetter, MD

*Support Group*: Garabed Eknoyan, MD (*Co-Chair*); Aderra Levin, MD,
FRCPC (*Co-Chair*); Nathan Levin, MD, FACP (*Co-Chair Emeritus*); Sharon
P. Andreoli, MD; Sally Burrows-Hudson, RN; Derrick Latos, MD; Donna
Mapes, DNSc, RN; Edith Oberley, MA; Brian J. G. Pereira, MD, DM, MBA;
Kerry Willis, PhD

*Guideline Development NKF Staff*: Nadine Ferguson; Donna Fingerhut;
Anthony Gucciardo; Margaret Klette; Doreen Mallard; Kerry Willis, PhD

#### FINANCIAL DISCLOSURES/CONFLICTS OF INTEREST

Jack W. Coburn, MD, FACP, is on the Medical Advisory Boards of Bone Care
International, R & D Laboratories, and Amgen, Inc., and has also
consulted with Genzyme Corporation.

Glenn M. Chertow, MD, MPH, has received research support from and has
served as an advisor to Amgen, Inc., Genzyme, Inc., and GelTex
Pharmaceuticals, Inc.

Keith A. Hruska, MD, is on the Medical Advisory Board of Bone Care
International and has received funding or compensation from it as well
as Allo-Source, Creative BioMolecules, Inc., and Monsanto/Pharmacia.

Craig B. Langman, MD, is on the Academic Advisory Board of Total Renal
Care, Inc, and has been a consultant for many pharmaceutical
laboratories, health-care companies, and health-care-related
foundations, including Merck USA, Roche Pharmaceuticals, Abbott
Laboratories, and the Oxalosis and Hyperoxaluria Foundation.

Hartmut Malluche, MD, has received several grants from the NIH and other
organizations including the Veterans Administration.

Kevin J. Martin, MB, BCh, FACP, has been a consultant to Amgen, Inc.,
and Abbott Laboratories and has also received funding from Genzyme
Corporation.

Shaul G. Massry, MD, is a consultant to Genzyme Corporation and has
participated in Advisory Board Meetings of Abbott Laboratories and
Amgen, Inc.

Linda McCann, RD, CSR, LD, has consulted for Abbott Laboratories.

James T. McCarthy, MD, is a member of the Scientific Advisory Boards of
MinnTech Corporation and Nx-Stage, and has received research grants from
Schein Pharmaceuticals, GelTex Pharmaceuticals, Bayer Corporation,
Amgen, and Luitpoldt Pharmaceutical.

Sharon M. Moe, MD, has been a consultant for Genzyme Corporation, Amgen,
Inc., and Bone Care International and has received grants from Genzyme,
Amgen, and Abbott Laboratories.

Isidro B. Salusky, MD, FAAP, is a consultant for Genzyme Corporation,
Bone Care International, and Abbott Laboratories.

Donald J. Sherrard, MD, has received funding from and consulted with
Amgen, Inc., Abbott Laboratories, and Geltex Pharmaceuticals.

#### GUIDELINE STATUS

This is the current release of the guideline.

#### GUIDELINE AVAILABILITY

Electronic copies: Available from the [National Kidney Foundation (NKF)
Web
site](http://www.kidney.org/professionals/kdoqi/guidelines_bone/index.htm).

Print copies: Available from the National Kidney Foundation (NKF), 30
East 33rd St., New York, NY 10016. These guidelines are also available
on CD-ROM.

#### AVAILABILITY OF COMPANION DOCUMENTS

None available

#### PATIENT RESOURCES

None available

#### NGC STATUS

This NGC summary was completed by ECRI on April 8, 2004.

#### COPYRIGHT STATEMENT

This NGC summary is based on the original guideline, which is
copyrighted by the National Kidney Foundation (NKF).

### DISCLAIMER

#### NGC DISCLAIMER

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Date Modified: 11/3/2008