Disclaimer
We’re actively expanding Guideline Genius to cover the full UKMLA content map. You may notice some conditions not uploaded yet, or articles that only include diagnosis and management for now. For updates, follow us on Instagram @guidelinegenius.
We openly welcome any feedback or suggestions through the anonymous feedback box at the bottom of every article and we’ll do our best to respond promptly.
Thank you for your support.
The Guideline Genius Team
Total Live Articles: 312
NICE guideline [NG203] Chronic kidney disease: assessment and management. Last updated: Nov 2021.
NICE CKS Chronic kidney disease. Last revised: May 2025.
Background information added accordingly, optimisations and improvements were made to the diagnosis and management sections.
Date: 21/12/25
CKD is defined as abnormalities in kidney function and/or structure, that present for at least 3 months
Top 4 causes of CKD: [Ref]
Diabetes, hypertension, and glomerular diseases all cause intrinsic kidney damage
Other causes of CKD (non-exhaustive list):
| Current or previous AKI | |
| Causes of obstructive uropathy |
|
| Multisystem disease with renal involvement |
|
| Hereditary kidney causes |
|
| Cardiovascular disease |
|
| Drugs | See section on nephrotoxic drugs below |
“Nephrotoxic drug” is a broad and often misused term. In practice, such drugs can be classified into two main groups: those associated with CKD, and those associated with AKI.
1) CKD-associated drugs are those that can cause intrinsic renal damage with prolonged use / repeated exposure:
Note that although ACE inhibitors / ARBs need to be temporarily stopped in AKI, they are renoprotective in the context of CKD (in fact, used as 1st line management for proteinuria in CKD).
2) AKI-associated drugs. This is often a source of confusion. In practice, AKI-associated drugs can be grouped into 3 distinct categories based on their mechanism.
| Drugs that cause pre-renal AKI |
|
| Drugs that cause intrinsic AKI | Drugs that cause acute tubular necrosis (direct tubular toxicity):
Drugs that cause acute interstitial nephritis:
|
| Drugs that should be withheld in AKI due to accumulation or toxicity risk, rather than direct nephrotoxicity |
|
The most exam-relevant “nephrotoxic drugs” to temporarily withhold in the acute setting of AKI:
Drugs associated with acute tubular necrosis can directly cause intrinsic AKI.
In contrast, drugs that cause pre-renal AKI typically impair renal haemodynamics and precipitate AKI in the presence of an additional insult, such as dehydration, sepsis, or hypotension.
CKD is often asymptomatic in early stages.
The clinical features of CKD itself, independent of the underlying cause, are often non-specific: [Ref]
Key complications include: [Ref]
| Impaired kidney excretory function | Impaired fluid excretion → fluid overload
|
Electrolyte and metabolic disturbances due to impaired excretion:
|
|
| In advanced CKD, impaired urea excretion → uraemia
Clinical syndrome of uraemia (non-exhaustive):
|
|
| Impaired kidney synthetic function | Impaired EPO production → anaemia of CKD
|
CKD-MBD:
Clinically manifest as renal osteodystrophy:
|
|
| Systemic consequences |
|
CKD testing is recommended in adults with any of the following:
If CKD testing is indicated (see above) or suspected, perform ALL the following investigations
| Test | Purpose |
|---|---|
| Serum creatinine and eGFR | eGFR reflects glomerular filtration (i.e. kidney function, indicating how effectively the kidneys filter creatinine) |
| Urine ACR | ACR quantifies proteinuria (which serves as a marker of structural kidney damage) |
| Urine dipstick | To check for haematuria
*Do NOT use a urine dipstick to test for proteinuria |
Be aware that testing with eGFR and ACR only provides information about whether a patient has CKD or not, without giving information about the underlying cause.
eGFR provides an estimate of the true GFR. NICE recommends using the CKD-EPI equation to calculate eGFR in adults, which incorporates the following variables:
The older MDRD equation, which also included a race adjustment, is no longer used. As race is a social construct, not a biological variable, it often overestimates kidney function in black patients. It also introduces health inequity.
Factors affecting eGFR interpretation:
| Factors that ↑ creatinine → falsely low eGFR (underestimated) | Factors that ↓ creatinine → falsely high eGFR (overestimated) |
|---|---|
|
|
1st line test: urine ACR
Note that transient elevations of albuminuria can occur with:
Therefore, it is important to repeat the urine ACR, if results are <70 mg/mmol to confirm if the albuminuria is transient (likely the listed causes here) or persistent (likely due to CKD).
Do NOT rely on urine reagent strips (dipsticks) to diagnose proteinuria, as they are insensitive and unreliable, particularly for low-level proteinuria. If urinalysis is +ve for protein (often an incidental finding), confirm with a urine ACR test.
Urine ACR is preferred over PCR to test for proteinuria, as it is more sensitive for low levels of proteinuria. PCR should only be used as an alternative to ACR if ACR is ≥70 mg/mmol (where it is able to provide adequate quantification).
If a urine dipstick shows 1+ or more blood on the dipstick:
CKD can only be diagnosed if ANY of the following (right column) are present for at least 3 months
| eGFR |
|
| Markers of kidney damage |
|
The selection of additional tests to investigate the underlying cause should be individualised based on the clinical context and working diagnosis.
A standard panel would include:
1st line: renal ultrasound (to evaluate for structural abnormalities / obstruction / polycystic kidney disease)
Indicated if any of the following are present:
Classic ultrasound findings in CKD:
However, some causes of CKD are associated with preserved or enlarged kidney size despite long-standing disease: [Ref1][Ref2]
However, note that advanced scarring from chronic injury can still cause kidney atrophy.
CKD staging based on eGFR:
| CKD stage | Criteria |
|---|---|
| 1 | eGFR >90 + marker of kidney damage |
| 2 | eGFR 60-89 + marker of kidney damage |
| 3a | eGFR 45-59 |
| 3b | eGFR 30-44 |
| 4 | eGFR 15-29 |
| 5 (end-stage renal disease) | eGFR <15 |
Although the reference range of CKD is often listed as >90, an eGFR of 60-89 alone does NOT constitute CKD
NICE recommends stratifying the risk of progression and complications of CKD based on BOTH eGFR and ACR
| A1 (ACR <3) | A2 (ACR 3-30) | A3 (ACR >30) | |
|---|---|---|---|
| G1 (eGFR ≥90) | Low risk
*There is no CKD if there are no other markers of kidney damage |
Moderate risk | High risk |
| G2 (eGFR 60-89) | |||
| G3a (eGFR 45-59) | Moderate risk | High risk | Very high risk |
| G3b (eGFR 30-44) | High risk | Very high risk | |
| G4 (eGFR 15-29) | Very high risk | ||
| G5 (eGFR <15) |
Modern CKD classification incorporates both eGFR and ACR because they provide complementary prognostic information. Albuminuria is independently associated with faster CKD progression and increased cardiovascular risk, even when eGFR is preserved.
Classifying CKD using both parameters, therefore provides superior prognostic accuracy than eGFR alone.
It is essential to identify and treat (or optimise the treatment of) the underlying cause of CKD. The management principles outlined below apply to the non-specific management of CKD, regardless of aetiology.
Assess 5-year risk of needing RRT with the 4-variable Kidney Failure Risk Equation
Refer adults with CKD for specialist assessment if any of the following:
Monitor CKD progression with eGFR and urine ACR
Tests to monitor potential CKD complications:
Lifestyle advice is very personalised in CKD, depending on various factors (e.g. polyuric or oligouric, electrolyte levels, fluid status).
Some key lifestyle advice:
There are 3 main aspects of CKD management (irrespective of underlying cause):
Manage hypertension as per those outlined in the Hypertension (Primary) article.
BP targets in CKD depend on ACR level:
1st line: ACE inhibitor / ARB
2nd line: SGLT-2 inhibitor (dapagliflozin / empagliflozin)
The exact indications outlined by NICE are often not strictly adhered to in practice. All patients with CKD are typically started on an ACE inhibitor / ARB (unless contraindicated). It is more important to be aware that both ACE inhibitors (or ARB) and SGLT-2 inhibitors are used to treat proteinuria in CKD, than learning the exact indications outlined by NICE.
CKD alone is an indication for statin therapy (primary prevention):
NICE recommends atorvastatin 20mg for both primary and secondary prevention in CKD.
The following outlines the key complications of CKD that are amenable to treatment or require specific management strategies.
Otherwise, the risk of other complications is best reduced by optimising the management of CKD itself and any underlying causes.
Test of choice: FBC to exclude iron deficiency
First, correct any iron deficiency (if present)
If there is persistent anaemia, despite correction of reversible causes / iron deficiency:
Hyperphosphataemia is often only seen in CKD stage 4 / 5.
Step 1: dietary management
Step 2: phosphate binders
Although inexpensive and effective, calcium-based phosphate binders (e.g. calcium acetate, calcium carbonate) carry a significant risk of hypercalcaemia and accelerated vascular calcification.
Non-calcium binders (e.g. sevelamer carbonate, sucroferric oxyhydroxide, lanthanum carbonate) are associated with a lower risk of these complications, therefore preferred in patients with hypercalcaemia, vascular calcification, or related comorbidities.
Vitamin D should only be measured if deficiency is suspected
1st line (any CKD stage): standard oral vitamin D supplementation (cholecaliferol or ergocalciferol)
Active vitamin D (alfacalcidol / calcitriol) should only be offered if:
