Chronic kidney disease

Last updated: September 11, 2023

Summarytoggle arrow icon

Chronic kidney disease (CKD) is defined as an abnormality of kidney structure or function that persists for > 3 months. The most common causes of CKD in the United States are diabetes mellitus, hypertension, and glomerulonephritis. The kidney's efficient compensatory mechanisms and significant renal reserve mean that most patients remain asymptomatic until their kidney function is severely impaired. While patients are most commonly initially identified because of gradual asymptomatic elevation in serum creatinine, at advanced disease stages, patients may present with symptoms of fluid overload (e.g., peripheral edema) and/or uremia (e.g., fatigue, pruritus). Patients with CKD also have a significantly increased risk of developing atherosclerotic cardiovascular disease (ASCVD). Laboratory studies may show metabolic complications, such as hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis. The goal of management is to slow CKD progression and prevent and manage complications. This includes treatment of the underlying disease, avoiding nephrotoxic substances, maintaining adequate hydration and nutrition, management of ASCVD (e.g., using statin therapy and adequate treatment of diabetes mellitus), and addressing complications such as anemia of chronic kidney disease and CKD-mineral and bone disorder. Renal replacement therapy (i.e., dialysis or kidney transplantation) is required if CKD progresses to end-stage renal disease (ESRD).

See also “Acute kidney injury” (AKI) and “Diabetic kidney disease.”

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Pathophysiologytoggle arrow icon

Pathophysiology depends on the underlying condition, any of which will eventually lead to progressive nephron loss, structural damage, and impaired kidney function.

Underlying conditions

Diabetic nephropathy [6]

Hypertensive nephropathy

Glomerulonephritis (GN)


Reduced GFR

Reduced endocrine activity

Reduced gluconeogenesis

Clinical featurestoggle arrow icon

Patients are often asymptomatic until later stages due to the exceptional compensatory mechanisms of the kidneys.

Manifestations of Na+/H2O retention

Manifestations of uremia

Kidney OUTAGES: hyperKalemia, renal Osteodystrophy, Uremia, Triglyceridemia, Acidosis (metabolic), Growth delay, Erythropoietin deficiency (anemia), Sodium/water retention (consequences of chronic kidney disease)

Diagnostic criteria and classificationtoggle arrow icon

Diagnostic criteria [5]

CGA classification of chronic kidney disease [4][5]

CKD is classified according to the cause, eGFR category, and albuminuria category; this is referred to as the CGA classification.

Cause [5]

  1. Systemic vs. primary cause: Determine if kidney disease is associated with a systemic disease (e.g., diabetes) or if it is primary kidney disease (e.g., polycystic kidney disease).
  2. Location: Determine the location (presumed or confirmed) of the damage within the kidney.
    • Glomerular
    • Tubulointerstitial
    • Vascular
    • Cystic and congenital

eGFR and albuminuria [5]

Risk of progression and complications of CKD based on eGFR and albuminuria category [5]
eGFR category (mL/min/1.73 m2) Albuminuria category (UACR)

A1: < 30 mg/g or < 3 mg/mmol

(normal to mildly increased)

A2: 30–300 mg/g or 3–30 mg/mmol


A3: > 300 mg/g or > 30 mg/mmol


Stage G1 CKD: ≥ 90 (normal or high) Low risk* Moderate risk High risk
Stage G2 CKD: 60–89 (mildly low)
Stage G3 CKD G3a: 45–59 (mildly to moderately low) Moderate risk High risk Very high risk
G3b: 30–44 (moderately to severely low) High risk Very high risk
Stage G4 CKD: 15–29 (severely low) Very high risk
Stage G5 CKD: < 15 (kidney failure)

*Stages G1A1 and G2A1 do not indicate CKD in the absence of other markers of kidney damage.

Diagnosticstoggle arrow icon

The goals of the diagnostic evaluation include confirming the chronicity of kidney dysfunction and identifying the cause of kidney disease.

Approach [5]

The diagnosis of CKD requires the persistence of eGFR < 60 mL/min/1.73 m2 and/or of a marker of kidney damage for more than 3 months.

A rapid rise in creatinine level (i.e., over days rather than weeks or months), recent onset of uremia, and/or oliguria or anuria suggest AKI (with or without underlying CKD).

Initial laboratory studies

Parameters of renal function

Urine studies

If the UPCR is significantly higher than the UACR, plasma cell dyscrasia should be suspected. Send a urine sample for protein electrophoresis to identify urine proteins other than albumin (e.g., Bence Jones protein).


Ultrasound of the kidneys and urinary tract

Consider obtaining an ultrasound of the kidneys and urinary tract as part of the routine evaluation of all patients with CKD.

Additional investigations to identify underlying causes

Additional investigations should be considered based on clinical suspicion or if an underlying cause of CKD is not apparent following an initial assessment.

Integration of information from the patient's clinical presentation, laboratory tests, imaging, and in some cases, pathology, is needed to determine the underlying cause.

Noninvasive testing

Investigations for specific underlying causes of CKD
Examples Suggestive features Common additional studies
Multiple myeloma
Renal artery stenosis

Renal biopsy [5][14]

  • Not routinely indicated
  • Consider in either of the following situations:
    • Rapid and unexplained decline in eGFR
    • Need for diagnostic confirmation of the underlying etiology (e.g., glomerulonephritis) prior to initiating disease-specific therapy

Renal biopsy is only indicated in patients in whom the underlying cause of CKD is still unclear after noninvasive testing, the results are likely to influence management, and the potential benefits are thought to outweigh the risks.

Managementtoggle arrow icon

The following guidance applies to patients with CKD category G1–G5 who are not on dialysis and have not had a kidney transplant.


The goals of treatment are to delay the progression of CKD and prevent and manage complications.

  • Treat the underlying causes of CKD (if identified).
  • Start comprehensive management.
    • Provide recommendations regarding nutrition and vaccinations, and adjust current medications as required.
    • Primary prevention of ASCVD.
    • Assess for evidence of metabolic complications and start management under specialist guidance.
  • Monitor for CKD progression and continuously evaluate the need for advanced care.

If CKD progression or complications are detected during follow-up, review the current management and assess for reversible causes of progression (e.g., nephrotoxin exposure, medications affecting glomerular perfusion, urinary tract obstruction).

Pay attention to the prevention of AKI, as this may further compromise kidney function.

If there are indications for acute dialysis, urgently initiate renal replacement therapy.

Nephrology consultation [5]

Nutritional management [15]

Dietary protein restriction must ONLY be prescribed under close clinical supervision and in consultation with a nutritionist.

Obtain a nutritionist consult for all patients with CKD.


Patients with CKD are at an increased risk of vaccine-preventable infections.

Patients with CKD may be immunocompromised. Decisions regarding the use of live vaccines should therefore take into account the patient's current immune status and be made in consultation with a specialist. [5]

Medication management [5][14]

Weigh the risks and benefits of potentially nephrotoxic substances on a case-by-case basis.

Given the increased risk of AKI in acutely ill patients with CKD, consider temporarily holding renally cleared medications and medications that can detrimentally affect glomerular perfusion (e.g., NSAIDs, ACEIs, ARBs).

Renal replacement therapy [5]

Monitoring and management of ASCVD risk factorstoggle arrow icon

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

ASCVD risk assessment

Management of ASCVD 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]

Blood pressure control [17]

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.

Lipid management [18][19]

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.

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

Diabetes management [22]

  • 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. [22][23]

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

Monitoring for complicationstoggle arrow icon

  • 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.

Overview of screening for CKD complications [5]
Screening test

Screening frequency

(CKD category G3–G5)

Potential findings Management
  • Every 6–12 months
Potassium [14]
  • Repeat as needed.
Mineral and bone disorder panel [24] PTH
  • Every 3–12 months
  • See “Management” in “CKD-MBD.”
Phosphate and total calcium
  • Every 1–12 months
Vitamin D
  • Calcidiol: Repeat as needed.
  • Calcitriol: No specific indication or monitoring frequency exists.
Coagulation screen
Blood gases
  • Repeat as needed.

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

Complicationstoggle arrow icon

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 [26]

Maintain a low threshold for suspecting infections and initiating empiric antibiotics, as signs of sepsis may be vague or absent in patients with CKD. [26][29]

Calciphylaxis [30][31]

Anemia of chronic kidney disease [5][32][33]


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) [34][35]

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

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

Special patient groupstoggle arrow icon

Chronic kidney disease in pregnancy [36]

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Referencestoggle arrow icon

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