Chapter

• Chronic
74 Chronic Kidney Disease

kidney disease (CKD) is defined as abnormalities in kidney structure or

function, present for 3 months or longer, with implications for health. Structural
abnormalities include albuminuria of more than 30 mg/day, presence of hematuria
or red cell casts in urine sediment, electrolyte and other abnormalities due to tubular
disorders, abnormalities detected by histology, structural abnormalities detected by
imaging, or history of kidney transplant.
• CKD is classified by cause of kidney disease, glomerular filtration rate (GFR) cat-
egory, and albuminuria level based on new recommendations from the Kidney
Disease: Improving Global Outcomes (KDIGO) guidelines, referred to as CGA stag-
ing (cause, GFR, albuminuria) (Table 74–1).
• CKD stage 5, previously referred to as end-stage renal disease (ESRD), occurs when
the GFR falls below 15 mL/min/1.73 m2 (<0.14 mL/s/m2) or in patients receiving
renal replacement therapy (RRT). In this chapter, ESRD refers specifically to patients
who receive chronic dialysis.
• Prognosis depends on cause of kidney disease, GFR at time of diagnosis, degree of
albuminuria, and presence of other comorbid conditions.

PATHOPHYSIOLOGY
• Susceptibility factors increase the risk for kidney disease but do not directly cause
kidney damage. They include advanced age, reduced kidney mass and low birth
weight, racial or ethnic minority, family history, low income or education, systemic
inflammation, and dyslipidemia.
• Initiation factors directly result in kidney damage and are modifiable by drug therapy.
They include diabetes mellitus, hypertension, glomerulonephritis, polycystic kidney
disease, Wegener granulomatosis, vascular diseases, and human immunodeficiency
virus (HIV) nephropathy.
• Progression factors hasten the decline in kidney function after initiation of kidney
damage. They include glycemia in diabetics, hypertension, proteinuria, hyperlipid-
emia, obesity, and smoking.
• Most progressive nephropathies share a final common pathway to irreversible renal
parenchymal damage and ESRD (Fig. 74–1). Key pathway elements include loss of
nephron mass, glomerular capillary hypertension, and proteinuria.

CLINICAL PRESENTATION
• CKD development and progression are insidious. Patients with stage 1 or 2 CKD
usually do not have symptoms or metabolic derangements seen with stages 3 to 5,
such as anemia, secondary hyperparathyroidism, cardiovascular disease (CVD), mal-
nutrition, and fluid and electrolyte abnormalities that are more common as kidney
function deteriorates.
• Uremic symptoms (fatigue, weakness, shortness of breath, mental confusion, nausea,
vomiting, bleeding, and anorexia) are generally absent in stages 1 and 2, minimal
during stages 3 and 4, and common in patients with stage 5 CKD who may also expe-
rience itching, cold intolerance, weight gain, and peripheral neuropathies.
• Signs and symptoms of uremia are foundational to the decision to implement RRT.
TREATMENT
GENERAL APPROACH
• Goal of Treatment: The goal is to delay the progression of CKD, minimizing the
development or severity of complications.

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TABLE 74–1 GFR Categories

KDIGO GFR (mL/min/1.73 m2 Terms Corresponding KDOQI
Category [mL/s/m2]) Category
G1 >90 (>0.87) Normal or high Stage 1 CKD
G2 60–89 (0.58–0.86) Mildly decreased Stage 2 CKD
G3a 45–59 (0.43–0.57) Mildly to Stage 3 CKD
moderately
decreased
G3b 30–44 (0.29–0.42) Moderately Stage 3 CKD
to severely
decreased
G4 15–29 (0.14–0.28) Severely Stage 4 CKD
decreased
G5 <15 (<0.14) Kidney failure Stage 5 CKD (ESRD
if requiring dialysis)

ESRD, end-stage renal disease; GFR, glomerular filtration rate.

• Use the most current consensus guidelines and the best clinical practices for manage-
ment of CKD.
NONPHARMACOLOGIC THERAPY
• Restrict protein to 0.8 g/kg/day if GFR is less than 30 mL/min/1.73 m2.
• Encourage smoking cessation to slow progression of CKD and reduce the risk of
CVD.
• Encourage exercise at least 30 minutes five times per week and achievement of a body
mass index (BMI) of 20 to 25 kg/m2.
PHARMACOLOGIC THERAPY
Diabetes and Hypertension With CKD
• Progression of CKD can be limited by optimal control of hyperglycemia and hyper-
tension. Figure 74–2 provides an algorithm for management of diabetes in CKD.
• For more information on diabetes, see Chap. 19.
• Adequate blood pressure (BP) control (Fig. 74–3) can reduce the rate of decline in
GFR and albuminuria in patients without diabetes. KDIGO guidelines recommend a
target blood pressure of 140/90 mm Hg or less if urine albumin excretion or equiva-
lent is less than 30 mg/24 h.
• If urine albumin excretion is greater than 30 mg/24 h or equivalent, the target blood
pressure is 130/80 mm Hg or less and initiate first-line therapy with an angiotensin-
converting enzyme inhibitor (ACEI) or an angiotensin II receptor blocker (ARB).
Add a thiazide diuretic in combination with an ARB if additional reduction in
proteinuria is needed. Nondihydropyridine calcium channel blockers are generally
used as second-line antiproteinuric drugs when ACEIs or ARBs are contraindicated
or not tolerated.
• ACEI clearance is reduced in CKD; therefore, treatment should begin with the lowest
possible dose followed by gradual titration to achieve target BP and, secondarily, to
minimize proteinuria. No individual ACEI is superior to another.
• For more information on hypertension, see Chap. 10.
Anemia of CKD
• KDIGO definition of anemia: Hemoglobin (Hb) less than 13 g/dL (130 g/L; 8.07
mmol/L) for adult males and less than 12 g/dL (120 g/L; 7.45 mmol/L) for adult
females.
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 Initial pathogenic injury

Glomerular injury

Diabetes mellitus Reduced filtration area Arteriosclerosis

Adaptive hemodynamic
Formation of advanced Hyperlipidemia
changes
glycation end products

Increased glomerular Increased glomerular

Systemic hypertension
blood flow capillary pressure

Glomerular hypertrophy Epithelial injury Endothelial injury Mesangial injury

Chronic Kidney Disease   |   CHAPTER 74

Focal detachment of Proteinuria
epithelial foot processes

Glomerular Microthrombi occluding

hyaline deposition glomerular capillaries Mesangial expansion

Glomerulosclerosis Microaneurysm formation

Progression of
kidney disease

FIGURE 74–1.  Proposed mechanisms for progression of renal disease.

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SECTION 14   |   Renal Disorders

Targets:
BP:
≤140/90 mm Hg if urine albumin
excretion <30 mg/24 h
or Screen annually for diabetes with CKD in Metformin:
≤130/80 mm Hg if urine albumin patients 5 years from diagnosis of type 1
excretion >30 mg/24 h Continue in people with eGFR ≥45 mL/min/1.73 m2;
diabetes or from diagnosis of type 2 DM review in those with eGFR 30–44 mL/min/1.73 m2, and
HgbA1C: Measure ACR , sCR & eGFR discontinue in people with eGFR <30 mL/min/1.73 m2
~7% (~0.07; ~53 mmol/mol Hb)
but consider >7% (>0.07; >53 mmol/
mol Hb) if risk of hypoglycemia or limited
life expectancy

Guidelines for using ACEI or ARB:

• Contraindicated in pregnancy (ensure
premenopausal females on appropriate
contraception if sexually active), in
patients with bilateral renal artery
stenosis or patients with a history of
angioedema with ACEI or ARB.
• Check eGFR & K+ as outlined in
Table 29–6
• Hold if patient has severe vomiting,
diarrhea, or intravascular volume
depletion as risk of AKI (prerenal)
If urine albumin excretion >30 mg/24 h, then
start ACEI or ARB (use caution if
eGFR <30 mL/min/1.73 m2 or BP <110/70 mm Hg)
Repeat ACR in 4–6 weeks
Is urine albumin
excretion <30 mg/24 h or
reduced >30%–50%?
No
Increase dose of ACEI or ARB
Check BP every 3 months
Yes Yes
Is BP at target? Repeat blood and urine tests
as outlined in Table 29–7
No
Increase dose of ACEI or ARB
and/or add thiazide diuretic
(loop diuretic if edema) Yes

Add dihydropyridine CCB

If BP still not in target, then If required, add other
No BP at target 4–6
add clonidine, hydralazine, antihypertensives such as
or minoxidil β-blocker or α-blocker weeks later?
to achieve BP target

FIGURE 74–2.  Diabetes with chronic kidney disease (CKD) algorithm. Strategy for screening and treatment of diabetes with CKD based on urine albumin excre-
tion, target blood pressure, and estimated GFR (eGFR). (Data from National Kidney Foundation, KDOQI clinical practice guidelines and clinical practice recommenda-
tions for diabetes and chronic kidney disease. Am J Kidney Dis 2007;49(Suppl 2):S1–S180; reference 1.)
 No
Refer to Figure 29–4
BP target ≤130/80 mm Hg
Combination of ACEI plus
ARB is not recommended
FIGURE 74–3.  Treatment of hypertension in chronic kidney disease (CKD) patients, nondialysis CKD (ND-CKD) without diabetes mellitus. Strategy for treatment
of hypertension based on urine albumin excretion and target blood pressure. (Data from Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group.
KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 2013;3:1–150.)
791
ND-CKD without
diabetes mellitus?
Yes
No Choose agents based on
Urine albumin excretion current hypertension guidelines. BP target ≤140/90 mm Hg
>30 mg/24 h? See Chap. 10
Alternatives to decrease proteinuria if ACEI or ARB contraindicated*:
Yes
• Nondihydropyridine CCB (diltiazem, verapamil). Not recommended if
patient on β-blocker. May be used in pregnancy.
ACEI or ARB • Aldosterone antagonists (spironolactone, eplerenone). Associated with
Begin at low doses and increase increased risk of hyperkalemia.
the dose at 4-week intervals • Direct renin inhibitor (aliskiren). Not recommended in combination with
Chronic Kidney Disease   |   CHAPTER 74
ACEI or ARB if eGFR <60 mL/min/1.73 m2.
*Contraindications include pregnancy, bilateral renal artery stenosis,
angioedema with ACEI or ARB, intravascular fluid depletion.
BP at Yes
Continue present management
target?
No
Add thiazide diuretic (loop
diuretic if edema present),
CCB, or β-blocker
SECTION 14   |   Renal Disorders

• Initiate erythropoietic-stimulating agent (ESA) therapy in all CKD patients with

Hb is between 9 and 10 g/dL (90 and 100 g/L; 5.59 and 6.21 mmol/L). Target Hb is
controversial.
• Iron deficiency is the primary cause of resistance to treatment of anemia with
ESAs. Iron supplementation is required by most CKD patients to replete iron stores
depleted by ongoing blood loss and increased iron demands.
• Parenteral iron therapy improves response to ESA therapy and reduces the dose
required to achieve and maintain target indices. In contrast, oral therapy is limited
by poor absorption and nonadherence with therapy primarily due to adverse effects
(Fig. 74–4).
• IV iron preparations have different pharmacokinetic profiles, which do not correlate
with pharmacodynamic effect.
• Adverse effects of IV iron include allergic reactions, hypotension, dizziness, dyspnea,
headaches, lower back pain, arthralgia, syncope, and arthritis. Some of these reac-
tions can be minimized by decreasing the dose or rate of infusion. Sodium ferric
gluconate, iron sucrose, and ferumoxytol have a better safety record than iron dextran
products.
• Subcutaneous (SC) administration of epoetin alfa is preferred because IV access is
not required, and the SC dose that maintains target indices is 15% to 30% lower than
the IV dose.
• Darbepoetin alfa has a longer half-life than epoetin alfa and prolonged biologic
activity. Doses are administered less frequently, starting at once a week when admin-
istered IV or SC.
• ESAs are well tolerated. Hypertension is the most common adverse event.
Evaluation of Anemia Therapeutic Outcomes
• Iron indices (transferrin saturation [TSat]; ferritin) should be evaluated before
initiating an ESA. Iron status should be reassessed every month during initial ESA
treatment and every 3 months for those on a stable ESA regimen.
• Hemoglobin should be monitored at least monthly, although more frequent moni-
toring (eg, every 1–2 weeks) is warranted after initiation of an ESA or after a dose
change until hemoglobin is stable.
• Patients should be monitored for potential complications, such as hypertension,
which should be treated before starting an ESA.
• For more information on anemia, see Chap. 33.
CKD-Related Mineral and Bone Disorder
• Disorders of mineral and bone metabolism (CKD-MBD) are common in the CKD
population and include abnormalities in parathyroid hormone (PTH), calcium,
phosphorus, the calcium-phosphorus product, vitamin D, and bone turnover, as well
as soft tissue calcifications.
• Calcium-phosphorus balance is mediated through a complex interplay of hormones
and their effects on bone, the gastrointestinal (GI) tract, kidneys, and the parathyroid
gland. As kidney disease progresses, renal activation of vitamin D is impaired, which
reduces gut absorption of calcium. Low blood calcium concentration stimulates
secretion of PTH. As renal function declines, serum calcium balance can be main-
tained only at the expense of increased bone resorption, ultimately resulting in renal
osteodystrophy (ROD).
• Secondary hyperparathyroidism is associated with increased morbidity and mortality
and sudden death in hemodialysis patients.
Treatment
• Dietary phosphorus restriction, dialysis, and parathyroidectomy are nonpharmaco-
logic approaches to management of hyperphosphatemia and CKD-MBD.
• The KDOQI guidelines provide desired ranges of calcium, phosphorus, calcium-
phosphorus product, and intact PTH based on the stage of CKD (see Table 74–2).

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 Diagnosis of Anemia of CKD

Evaluate Iron Indices

TSat and Serum Ferritin

If Ferritin <100 ng/mL (<100 µg/L; If Ferritin 100–500 ng/mL(100–500 µg/L; If Ferritin >500 ng/mL (>500 µg/L;
<225 pmol/L) in ND-CKD or <200 ng/mL 225–1,100 pmol/L) in ND-CKD or CKD-PD or >1,100 pmol/L) or TSat >30%
(<200 µg/L; <450 pmol/L) in CKD-HD and 200–500 (200–500 µg/L; 450–1,100 pmol/L) (>0.30), do not give additional iron
TSat <20% (<0.20), give IV iron (total of in CKD-HD and TSat 20–30% (0.20–0.30),
1 g in divided doses). In ND-CKD patients consider a trial of IV iron. In ND-CKD patients
a 1- to 3-month trial of oral iron is an alternativea a 1- to 3-month trial of oral iron is an alternativea

Reevaluate iron indices following a course of iron If Hb >10 g/dL (>100 g/L;
If Hb <10 g/dL (<100 g/L;
supplementation and proceed based on criteria above >6.21 mmol/L) ESA may be
<6.21 mmol/L), initiate ESA; choice
considered if improvements in
of ESA based on CKD stage and
quality of life are expected and the
treatment setting (eg, dialysis
patient is aware of and accepts
setting versus clinic, etc)b.
risks of ESA therapy

c
If Hb 10–11 g/dL (100–110 g/L; Assess Hb weekly until stable, and
6.21–6.83 mmol/L) in CKD-D or then at least monthly in CKD-D and
maintained as desired below every 3 months in ND-CKD

Chronic Kidney Disease   |   CHAPTER 74

10 g/dL in ND-CKD, continue Continue to monitor iron status at
current ESA regimen least every 3 months

If Hb has not increased by 1 g/dL

If Hb increases by >1 g/dL
(>10 g/L; 0.62 mmol/L), after
(>10 g/L; 0.62 mmol/L), in a 2-week
4 weeks, consider a 25% increase
period or exceeds 11 g/dL
in ESA dose. (If hyporesponsive to
(110 g/L; 6.83 mmol/L) in CKD-D
ESAd, avoid repeat escalations in
or 10 g/d L in ND-CKD, reduce the
ESA dose beyond double the initial
dose by 25% or interrupt the dose
weight-based dose)
a
Route should be selected based on severity of iron deficiency, IV access, prior response to oral therapy, adverse effects with previous exposure to IV or po iron, and cost.
b
Decision of whether to initiate ESA therapy should be individualized based on the rate of fall in Hb, risk of needing a blood transfusion, risks of ESA therapy, and presence
of symptoms of anemia.
c
Use the lowest ESA dose to reduce the need for blood transfusion.
d
Hyporesponsiveness is defined as having no increase in Hb from baseline after the first month of ESA therapy using appropriate weight-based dosing.

FIGURE 74–4.  Algorithm for management of anemia using iron and erythropoiesis-stimulating agent (ESA) therapy. (From Kidney Disease: Improving Global
Outcomes (KDIGO) Anemia Work Group. KDIGO clinical practice guideline for anemia in chronic kidney disease. Kidney Int Suppl 2012;2:279–335.)
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TABLE 74–2 G uidelines for Calcium, Phosphorus, Calcium-Phosphorus Product,

and Intact Parathyroid Hormone
Chronic Kidney Diseasea
Parameter Stage 3 Stage 4 Stage 5
Corrected calcium “Normal range” “Normal range” 8.4–9.5 mg/dLb (2.10–2.38
mmol/L)
Phosphorus 2.7–4.6 mg/dLc 2.7–4.6 mg/dLc 3.5–5.5 mg/dLd
Ca × P product <55 mg2/dL2 e <55 mg2/dL2 e <55 mg2/dL2 e
Intact parathyroid 35–70 pg/mLf 70–110 pg/mLg 150–300 pg/mLh
hormone
a
Differences with Kidney Disease: Improving Global Outcomes (KDIGO) described in test (see Desired
Outcome Under CKD-Related Mineral and Bone Disorder in test).
b
Recommend normal range for laboratory used, but keep target at lower end of range.
c
SI units: 0.87–1.49 mmol/L.
d
SI units: 1.13–1.78 mmol/L.
e
SI units: 4.4 mmol2/L2.
f
SI units: in ng/L or 3.7–7.5 pmol/L.
g
SI units: in ng/L or 7.5–11.8 pmol/L.
h
SI units: in ng/L or 16–32 pmol/L.
From Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice
guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral
and bone disorder (CKD-MBD). Kidney Int 2009;113(Supp):S1–S130; and Eknoyan G, Levin A, Levin NW.
Bone metabolism and disease in chronic kidney disease. Am J Kidney Dis 2003;42:1–201.

PHOSPHATE-BINDING AGENTS
• Phosphate-binding agents decrease phosphorus absorption from the gut and are
first-line agents for controlling both serum phosphorus and calcium concentrations
(Table 74–3).
• KDOQI guidelines recommend that elemental calcium from calcium-containing
binders should not exceed 1500 mg/day, and the total daily intake from all sources
should not exceed 2000 mg. This may necessitate a combination of calcium- and
non–calcium-containing products (eg, sevelamer HCL and lanthanum carbonate).
• Adverse effects of all phosphate binders are generally limited to GI effects, including
constipation, diarrhea, nausea, vomiting, and abdominal pain. Risk of hypercalcemia
may necessitate restriction of calcium-containing binder use and/or reduction in
dietary intake. Aluminum and magnesium binders are not recommended for regular
use in CKD because aluminum binders have been associated with CNS toxicity and
the worsening of anemia, whereas magnesium binders may lead to hypermagnesemia
and hyperkalemia.
VITAMIN D THERAPY
• Reasonable control of calcium and phosphorus must be achieved before initiation
and during continued vitamin D therapy.
• Calcitriol, 1,25-dihydroxyvitamin D3, directly suppresses PTH synthesis and secre-
tion and upregulates vitamin D receptors. The dose depends on the stage of CKD
(Table 74–4).
• The newer vitamin D analogues paricalcitol and doxercalciferol may be associated
with less hypercalcemia and, for paricalcitol, hyperphosphatemia. Vitamin D therapy,
regardless of agent, is associated with decreased mortality.

794
 TABLE 74–3 Phosphate-Binding Agents for Treatment of Hyperphosphatemia in CKD Patients
Drug Brand Name Compound Content Starting Doses Dose Titrationa Comments
Calcium Tums, Os-Cal, 40% elemental calcium 0.5–1 g (elemental Increase or decrease by 500 First-line agent; dissolution characteristics and phosphate
carbonateb Caltrate calcium) three times a mg per meal (200 mg binding may vary from product to product
day with meals elemental calcium)
Approximately 39 mg phosphorus bound per 1 g calcium
carbonate
Calcium PhosLo 25% elemental calcium 0.5–1 g (elemental Increase or decrease by 667 First-line agent; comparable efficacy to calcium carbonate
acetate (169 mg elemental calcium calcium) three times a mg per meal (169 mg with lower dose of elemental calcium
(25% per 667 mg capsule) day with meals elemental calcium) Approximately 45 mg phosphorus bound per 1 g
elemental calcium acetate
calcium)
Phoslyra 667 mg calcium acetate
per 5 mL
Sevelamer Renvela 800 mg tablet 800–1,600 mg three Increase or decrease by First-line agent; also lowers low-density lipoprotein

Chronic Kidney Disease   |   CHAPTER 74

carbonate 0.8 and 2.4 g powder for times a day with meals 800 mg per meal cholesterol
oral suspension (once-daily dosing also Consider in patients at risk for extraskeletal calcification
effective)
Associated with a lower risk of acidosis and GI adverse
events than Renagel (sevelamer hydrochloride) that is
no longer available
Lanthanum Fosrenol 500, 750, and 1,000 mg 1,500 mg daily in divided Increase or decrease by First-line agent; potential for accumulation of lanthanum
carbonate chewable tablets doses with meals 750 mg/day due to GI absorption (long-term consequences
unknown)
Aluminum AlternaGel Content varies (range 300–600 mg three times Not for long-term use Not a first-line agent; risk of aluminum toxicity; do not use
hydroxideb 100–600 mg/unit) a day with meals requiring titration concurrently with citrate-containing products
Reserve for short-term use (4 weeks) in patients with
hyperphosphatemia not responding to other binders
Based on phosphorus levels, titrate every 2–3 weeks until phosphorus goal reached.
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a
b
Multiple preparations available that are not listed.
796

SECTION 14   |   Renal Disorders

TABLE 74–4 Vitamin D Agents
Brand Form of Dosage
Generic Name Name Vitamin D Forms Initial Dose Dosage Range Frequency of Administration
Nutritional Vitamin D
Ergocalciferola Generic D2 po Varies based on 25OHD levels 400–50,000 Daily (doses of 400–2,000
international international units)
units
Cholecalciferola Generic D3 po Weekly or monthly for higher
doses (50,000 international
units)
Active Vitamin D
Calcitriol Calcijex D3 IV 1–2 mcg 0.5–5 mcg Three times per week
Rocaltrol po 0.25 mcg 0.25–5 mcg Daily or three times per week
Vitamin D Analogs
Paricalcitol Zemplar D2 po CKD nondialysis: 1 mcg daily or 2 mcg three times per 1–4 mcg Daily or three times per week
week if PTH ≤500 pg/mL (≤500 ng/L; ≤54 pmol/L);
2 mcg daily or 4 mcg three time per week if PTH
>500 pg/mL (>500 ng/L; >54 pmol/L)
Stage 5 CKD: mcg dose based on ratio of PTH/80 and
administered three times per week
IV Stage 5 CKD: 0.04–1 mcg three times per week 2.5–15 mcg Three times per week
Doxercalciferol Hectorol D2 po CKD nondialysis: 1 mcg daily 5–20 mcg Daily or three times per week
Stage 5 CKD: 10 mcg three times per week
IV Stage 5 CKD: 4 mcg three times per week 2–8 mcg Three times per week
a
Multiple preparations are available that are not listed.
 Chronic Kidney Disease   |   CHAPTER 74

CALCIMIMETICS
• Cinacalcet reduces PTH secretion by increasing the sensitivity of the calcium-
sensing receptor. The most common adverse events include nausea and vomiting.
• The most effective way to use cinacalcet with other therapies has not been decided.
The starting dose is 30 mg daily, which can be titrated to the desired PTH and cal-
cium concentrations every 2 to 4 weeks to a maximum of 180 mg daily.
Hyperlipidemia
• The prevalence of hyperlipidemia increases as renal function declines.
• National guidelines differ on how aggressively dyslipidemia should be managed in
patients with CKD. KDIGO guidelines recommend treatment with a statin (eg, ator-
vastatin 20 mg, fluvastatin 80 mg, rosuvastatin 10 mg, simvastatin 20 mg) in adults
aged 50 and older with stage 1 to 5 CKD not on dialysis.
• In patients with ESRD, lipid profile should be reassessed at least annually and 2 to 3
months after changing treatment.
• For more information on dyslipidemias, see Chap. 8.

See Chapter 29, Chronic Kidney Disease, authored by Joanna Q. Hudson and Lori D.
Wazny, for a more detailed discussion of this topic.

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