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Chronic kidney disease Last updated: February 21, 2023

Summary

Epidemiology

Etiology

Pathophysiology

Clinical features

Diagnostic criteria and classification

Diagnostics

Management

Monitoring and management of ASCVD risk factors

Specific recommendations for ASCVD risk management in patients with CKD are reviewed below; see
also “Hypertension,” “Lipid disorders,” “Diabetes,” and “ASCVD.”
ASCVD risk assessment

Perform for all patients (CKD is an ASCVD risk-enhancing factor).

Includes:

Diabetes mellitus screening

Blood pressure monitoring

Screening for lipid disorders

ASCVD risk estimation (e.g., using the 2013 ACC/AHA pooled cohort equation)

Management of ASCVD risk not only reduces cardiovascular morbidity and mortality, but
also helps prevent CKD progression.

Cardiovascular disease (e.g., coronary artery disease, stroke) is the leading cause of death
in patients with CKD. The risk of cardiovascular events is higher in patients with more
advanced stages of CKD. [5]

[17]
Blood pressure control

Systolic blood pressure (SBP) target

[17]
SBP < 120 mm Hg is recommended (if tolerated).

Consider higher targets (e.g., < 130–140 mm Hg) for selected patients.

Pharmacological therapy

Consider for patients with SBP above target, particularly if they are in albuminuria categories A2–
A3.

First-line therapy: RAAS inhibitors (i.e., ACEI or ARB)

Benefits: nephroprotection and reduced proteinuria

Risks: may cause hyperkalemia and/or an initial decline in GFR

Consider combination therapy (e.g., RAAS inhibitor PLUS a calcium channel blocker and/or a
thiazide diuretic) :

For patients with an initial SBP ≥ 20 mm Hg above target

For patients who do not reach the target while on monotherapy at the optimal dose

Second-line agents include:

Loop diuretics or thiazide diuretics

Calcium channel blockers (CCBs)

Beta-blockers: usually reserved for patients with cardiovascular comorbidities

Aldosterone receptor antagonists: usually reserved for treatment resistant hypertension

See “Antihypertensive therapy” for information on medication dosages and contraindications.

Nonpharmacological management: Recommend for all patients; see “Lifestyle changes for managing
hypertension.”

Avoid any combination of an ACEI, ARB, and/or direct renin inhibitor because of the
increased risk of hyperkalemia and AKI.

Good blood pressure control is essential to prevent ASCVD complications, reduce

mortality, and help delay disease progression in patients with CKD.

[18][19]
Lipid management

Goal: reduction of ASCVD risk

Fasting lipid panel

Order at diagnosis and repeat only if the results may alter management.

May show dyslipidemia (↑ triglycerides are common)

Statin therapy; indications include:

Primary prevention of ASCVD

Start for all patients ≥ 50 years of age.

Consider for patients 18–49 years of age with concomitant diabetes mellitus and/or 10-year
ASCVD risk > 10%.

Secondary prevention of ASCVD

Dyslipidemia: See “Treatment of hypercholesterolemia in adults.”

Nonpharmacological management: Recommend as adjunctive therapy for all patients with

hypercholesterolemia.

For patients with eGFR < 60 mL/min/1.73 m2 (eGFR category G3–G5), adjustments to the
recommended statin doses are required to reduce their potential for toxicity.

Statin therapy may be indicated regardless of serum lipid levels, as patients with CKD have
a higher ASCVD risk than the general population.

Individuals with CKD often have dyslipidemia (e.g., ↑ triglycerides, ↑ LDL, ↓ HDL) due to
alterations in lipoprotein metabolism.

[20]
Diabetes management

HbA1c may not accurately reflect glycemic control in patients with CKD and eGFR < 30 mL/min/1.73
m2; correlate with results from ambulatory glucose monitoring.

Medications may need to be reduced or stopped as eGFR declines.

See “Diabetic kidney disease” for further information on managing DM in patients with renal
impairment.

SGLT-2 inhibitors and GLP-1 receptor agonists have been shown to slow CKD progression
and reduce urinary albumin excretion and ASCVD events. [20][21]

In patients with CKD category G4–G5 who were previously on metformin and/or an
SGLT-2 inhibitor, metformin should be discontinued; the SGLT-2 inhibitor may be
continued if tolerated.

Antiplatelet therapy

Usually indicated for secondary prevention of ASCVD

May be considered for primary prevention of ASCVD in high-risk individuals (e.g., patients with CKD
[5][21]
and diabetes)

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Monitoring for complications

Screening tests for complications are indicated in all patients with CKD at diagnosis to establish a
baseline.

Patients with CKD categories G3–G5 require repeat testing at regular intervals.

In CKD, close surveillance of serum potassium, calcium, and phosphate levels is essential.

[5]
Overview of screening for CKD complications

Screening test Screening Potential findings Management

frequency
(CKD category
G3–G5)

CBC Every 6–12 Normochromic, See “

months normocytic anemia Anemia of chronic
kidney disease
.”

Repeat as Hyperkalemia: usually seen in See “Chronic

Potassium [14]
needed. advanced CKD hyperkalemia” in
“Therapeutic approach
to hyperkalemia.”

Mineral PTH Every 3–12 ↑ PTH See “Management” in “

months Suggests CKD-MBD.”
and
secondary
bone hyperparathyroidism
disorder
May be seen with any
panel stage of CKD and worsens
[22] as GFR declines

Phosphate Every 1–12 Hyperphosphatemia and

months hypocalcemia : typically
and
seen in patients with eGFR <
total
30 mL/min/1.73 m2 [22]
calcium

Vitamin D Calcidiol: ↓ Calcidiol

Repeat as [22]
↓ Calcitriol
needed.

Calcitriol: No
specific
indication or
monitoring
frequency
exists.

Coagulation screen Measure in Normal PT, PTT, and See “

case of platelet count Hemostasis and
bleeding or if bleeding disorders
↑ Bleeding time due to
symptoms of .”
uremic platelet dysfunction
uremia
are present.

Blood gases Repeat as May show metabolic acidosis Consider oral

needed. [23] bicarbonate
supplementation for
patients with serum
bicarbonate < 22 mEq/L.

Screening and periodic monitoring for complications are indicated in all patients with CKD
and eGFR < 60 mL/min/1.73 m2.

Complications

For recommendations on screening tests and frequencies, see “Monitoring for complications.” Specialist
consultation (e.g., with a nephrologist) is advised for the management of complications.
Common acute complications [24]

Pulmonary edema

Hyperkalemia
[25]
Infection

Bacteremia secondary to UTI or pneumonia

IV catheter-related infection

Hemodialysis catheter-related infection

Peritoneal dialysis-associated peritonitis

[26]
Drug toxicity

See also “Complications of hemodialysis” and “Complications of peritoneal dialysis.”

Maintain a low threshold for suspecting infections and initiating empiric antibiotics, as
signs of sepsis may be vague or absent in patients with CKD. [24][27]

[5][28][29]
Anemia of chronic kidney disease

Pathophysiology: : ↓ synthesis of erythropoietin → ↓ stimulation of RBC production → normocytic,

normochromic anemia

Laboratory findings

↓ Hemoglobin (Hb)

MCV is usually normal.

Management

Manage correctable causes of anemia.

Obtain diagnostic studies for iron deficiency.

Consider evaluation for underlying causes of iron deficiency (e.g., GI bleeding).

Consider iron therapy for iron deficiency anemia in patients with TSAT < 30% and ferritin < 500
ng/mL.

Check for and potentially treat vitamin B12 deficiency and folate deficiency.
[29]
Consider erythropoietin-stimulating agents (ESAs): for patients with Hb < 10.0 g/dL ;

Treatment target: usually Hb concentration between 11 and 12 g/dL (without intentionally

exceeding 13 g/dL)

Measure TSAT and ferritin at least every 3 months to determine if adjunctive iron replacement
therapy is needed.

Adverse effects include increased risk of thrombosis, an increase in blood pressure, and headache.

Avoid blood transfusions: particularly in patients eligible for renal transplantation (risk of
alloimmunization)

Treatment with ESAs is not recommended for patients with Hb levels ≥ 10 g/dL because
their use has been associated with increased mortality, stroke, and
venous thromboembolism.

Chronic kidney disease-mineral and bone disorder (CKD-MBD) [30][31]

Definition: abnormalities in mineral and/or bone metabolism in CKD

Pathophysiology

CKD results in hypocalcemia via different mechanisms.

↓ Renal excretion of phosphate → hyperphosphatemia → calcium phosphate precipitation in

tissues → ↓ Ca2+

↓ Renal hydroxylation of vitamin D → ↓ 1,25-dihydroxyvitamin D → ↓ intestinal Ca2+

absorption → ↓ Ca2+

Chronically decreased calcium levels can cause secondary hyperparathyroidism, which can progress
to tertiary hyperparathyroidism.

Histological classification

Secondary hyperparathyroidism: high turnover bone disease or osteitis fibrosa cystica; (metabolic
bone disease)

Osteomalacia: defective bone mineralization

Mixed uremic bone disease: secondary hyperparathyroidism with osteomalacia

Adynamic bone disease: decreased bone formation without osteomalacia

Clinical features (may be asymptomatic initially)

Musculoskeletal

Fractures

Bone and periarticular pain

Muscular weakness and pain

Extraskeletal

Focal vascular calcification (atherosclerotic plaques)

Diffuse vascular calcification (medial calcific sclerosis and calcific uremic arteriolopathy)

Diagnostics [31]

Laboratory studies: frequent monitoring with a mineral and bone disorder panel

Imaging (not routinely indicated)

X-ray may show sclerotic changes (rugger jersey spine), brown tumors, and/or subperiosteal bone
thinning.

Consider bone mineral density testing for patients with CKD category G3–G5.

Treatment (under specialist guidance): The goal is to normalize phosphate, calcium, and PTH levels. [30]
[31]

Treatment of hyperphosphatemia, e.g.:

Dietary phosphate restriction

Phosphate binders (e.g., sevelamer)

Treatment of hyperparathyroidism, e.g.:

Cholecalciferol or ergocalciferol supplementation for vitamin D deficiency or insufficiency

Calcitriol (not routinely recommended)

Calcimimetics (e.g., cinacalcet)

Parathyroidectomy (last-line therapy)

Hyperphosphatemia, hypocalcemia, and insufficient production of vitamin D in patients

with CKD may lead to secondary hyperparathyroidism and consequent
renal osteodystrophy.

Growth delay and developmental delay in children

Contributing factors include:

Malnutrition (protein and calorie deficit)

Metabolic acidosis

Growth hormone resistance

Anemia

Renal osteodystrophy

We list the most important complications. The selection is not exhaustive.

Special patient groups

Chronic kidney disease in pregnancy [32]

Overview

Prevalence of CKD in women of childbearing age is estimated to be 0.1–4%.

Research suggests that pregnancy negatively affects kidney function in women with CKD (as
evidenced by, e.g., doubling of creatinine, progression to next stage).

CKD negatively influences pregnancy outcomes by increasing the risk of maternal and fetal
complications (see below).

Physiological anatomic (e.g., dilation of the renal collecting system, changes in kidney length and
volume) and hemodynamic changes (e.g., decreased mean arterial pressure) can pose a challenge to
monitoring kidney function and diagnosing complications.

Maternal complications

Preeclampsia

Concomitant hypertension and proteinuria

Preterm delivery

Cesarean delivery

Fetal complications

Intrauterine growth restriction

Low birth weight

Fetal/neonatal death

Management

Patients should be cared for by a multidisciplinary team, including nephrologists, neonatologists, and
health care personnel specialized in high-risk obstetrics.

Optimization of blood pressure (i.e., < 140/90 mm Hg) to reduce the risk of preeclampsia and other
complications (see “Overview of antihypertensives to avoid during pregnancy” for details)

Minimization of proteinuria: Treatment depends on the underlying etiology (e.g., pregnancy-safe

immunosuppression with prednisone or calcineurin inhibitors in lupus nephritis).

Consideration of anticoagulation in individuals with severe proteinuria

Prevention of preeclampsia with aspirin before 16 weeks of gestation and calcium and vitamin D
supplementation throughout the pregnancy

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References

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