TREATMENT FOR CKD
GENERAL APPROACH
• Goal of Treatment: The goal is to delay the progression of CKD, minimizing the
development or severity of complications.
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. 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. 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,
GENERAL APPROACH
• Goal of Treatment: The goal is to delay the progression of CKD, minimizing the
development or severity of complications.
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. 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. 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,
