Chronic kidney disease: diagnosis and staging

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

CKD is a time-based diagnosis. It includes sustained eGFR below 60 mL/min/1.73 m² and kidney damage shown by albuminuria, urine-sediment abnormality, histology, imaging or a transplanted kidney. A person with preserved filtration but persistent albuminuria can therefore have important CKD, while an older adult with a single eGFR of 58 during gastroenteritis has not yet been shown to have chronic disease.

The G and A grid is both description and prognosis. Lower filtration and higher albuminuria independently increase kidney-failure, acute kidney injury and cardiovascular risk. Serial values reveal trajectory, but biological and laboratory variation must be distinguished from sustained progression. Risk calculators such as the four-variable Kidney Failure Risk Equation can support referral and planning when used in their validated population.

Staging is incomplete without cause and complications. History, examination, urinalysis, ACR, blood tests and selective ultrasound commonly identify diabetes, vascular disease, obstruction or a glomerular signal. Nephrotic-range proteinuria, active urine findings, multisystem disease, family history, abrupt decline or discordance between mild CKD and marked anaemia should trigger a broader diagnostic frame.

Key points

CKD requires a kidney structural or functional abnormality present for more than 3 months; one low eGFR during acute illness is acute kidney injury until chronicity is demonstrated.
Classify eGFR as G1 at least 90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29 and G5 below 15 mL/min/1.73 m², but G1 or G2 alone is not CKD without another marker of damage.
Pair the G category with urine albumin:creatinine ratio: A1 below 3, A2 3–30 and A3 above 30 mg/mmol; the combination predicts renal and cardiovascular risk better than either value alone.
Repeat a newly reduced eGFR promptly to exclude acute deterioration, then use results separated by at least 90 days to establish stable CKD; inspect prior blood tests and clinical context.
Measure urine ACR rather than total protein for initial proteinuria detection, preferably on an early-morning specimen when confirmation is required, and interpret infection, menstruation, exercise and diabetes context.
Do not apply creatinine-based eGFR uncritically at extremes of muscle mass, amputation, malnutrition, oedema or rapidly changing renal function; discuss measured GFR when accuracy would change a major decision.
Aetiology matters: diabetes, hypertension, glomerular disease, obstruction, medicines, inherited disease and systemic inflammation need different investigations and disease-specific treatment.
Refer an adult for specialist CKD assessment, considering wishes and comorbidity, if 5-year KFRE risk is above 5%; ACR is at least 70 mg/mmol unless diabetes is the known cause and is already appropriately treated; ACR is above 30 mg/mmol with haematuria; eGFR falls by at least 25% with a category change within 12 months or by at least 15 mL/min/1.73 m² per year; blood pressure remains above the individual target despite at least 4 antihypertensives at therapeutic doses; or rare/genetic CKD or renal-artery stenosis is known or suspected.
Hyperkalaemia, pulmonary oedema, severe acidosis, uraemic complications or a rapidly rising creatinine are emergencies and should not wait for routine CKD staging.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Diabetic and metabolic injury

Diabetes is a major cause through glomerular hyperfiltration, metabolic and endothelial injury and progressive albuminuria, although non-albuminuric diabetic CKD and unrelated renal disease both occur.

Vascular and haemodynamic disease

Longstanding hypertension, atherosclerosis, renovascular disease, heart failure and repeated haemodynamic insults can cause nephron loss, ischaemic scarring and progressive filtration decline.

Glomerular and systemic disease

Primary glomerulopathies, lupus, vasculitis, infection and monoclonal immunoglobulin disorders damage the filtration barrier and may present with albuminuria, haematuria or systemic inflammation.

Structural inherited and tubular disease

Polycystic and other genetic disorders, reflux, chronic obstruction, congenital anomalies, tubulointerstitial inflammation and nephrotoxic exposure can produce CKD with distinctive family, imaging or urine clues.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Nephron loss and hyperfiltration
Remaining nephrons increase single-nephron filtration after irreversible nephron loss; this initially preserves whole-kidney GFR but raises intraglomerular stress and promotes further damage.
2
Filtration barrier injury
Glomerular endothelial, basement-membrane or podocyte injury permits albumin leakage; filtered protein also activates tubular inflammatory pathways and predicts renal and cardiovascular risk.
3
Fibrosis and maladaptive repair
Persistent immune, metabolic, ischaemic or obstructive injury drives tubular atrophy, interstitial fibrosis and capillary loss, making function progressively less reversible.
4
Excretory and endocrine failure
As nephron reserve falls, salt, water, potassium, acid and uraemic solutes accumulate while erythropoietin production and vitamin-D activation decline, causing multisystem complications.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Often asymptomatic

Early and moderate CKD is commonly detected through eGFR or albuminuria surveillance rather than pain, urine-volume change or uraemic symptoms.

Albuminuric phenotype

Persistent raised ACR can precede falling filtration in diabetes or glomerular disease and materially changes cardiovascular risk and renoprotective eligibility.

Progressive phenotype

A reproducible downward eGFR trajectory, increasing albuminuria or new complications is more concerning than a stable category label over many years.

Glomerular signal

Albuminuria with haematuria, oedema, hypertension or systemic inflammatory features raises concern for glomerulonephritis and may warrant urgent nephrology input.

Obstructive signal

Lower urinary-tract symptoms, palpable bladder, hydronephrosis, pelvic malignancy or recurrent retention suggests post-renal disease requiring prompt imaging and decompression planning.

Advanced complications

Pruritus, anorexia, nausea, cognitive change, restless legs, fluid overload, anaemia, acidosis and CKD-mineral bone disorder become more likely as filtration declines.

Red flags requiring action

Pulmonary oedema, dangerous hyperkalaemia, severe metabolic acidosis, uraemic encephalopathy or pericarditis requires immediate hospital and renal assessment, not outpatient confirmation of chronicity.
A rapid creatinine rise or oliguria indicates possible acute kidney injury superimposed on CKD and needs same-day evaluation of volume, obstruction, sepsis and nephrotoxins.
Visible haematuria, persistent non-visible haematuria with substantial albuminuria, or rapidly progressive renal impairment may signal glomerulonephritis or urological malignancy and requires the appropriate urgent pathway.
New bilateral hydronephrosis, an obstructed solitary kidney or infected obstruction is a time-critical urological problem; seek drainage advice while treating sepsis and electrolyte disturbance.
Severe hypertension with retinal, neurological, cardiac or renal target-organ injury is a hypertensive emergency and should not be managed as routine CKD blood-pressure review.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Serial creatinine and eGFRFirst step
Why
Confirm chronicity, establish the G category and detect acute or sustained progression.
Interpretation and limitations
Repeat an unexpected new reduction rapidly to exclude acute decline, then demonstrate persistence beyond 3 months; eGFR is unreliable during changing creatinine and at unusual muscle mass.
02
Urine albumin:creatinine ratio
Why
Detect and quantify albuminuria for A staging, prognosis and treatment selection.
Interpretation and limitations
Use A1, A2 and A3 categories; confirm a moderately raised result on an early-morning sample while very high ACR, compatible symptoms or urgent glomerular features need not await serial delay.
03
Urine reagent strip and microscopy when indicated
Why
Identify haematuria, infection and an active sediment suggesting glomerular inflammation.
Interpretation and limitations
Persistent blood alongside albuminuria changes referral urgency; casts and dysmorphic cells support renal inflammation, whereas infection or menstruation can confound sampling.
04
Renal tract ultrasound
Why
Assess kidney size, structure, asymmetry, cysts and urinary obstruction when clinical criteria are met.
Interpretation and limitations
Small echogenic kidneys support chronic parenchymal disease; hydronephrosis requires correlation with bladder and ureteric obstruction, while a normal scan does not exclude glomerular CKD.
05
Cause-directed blood profile
Why
Look for diabetes, systemic inflammation, paraprotein or immunological disease when history and urine findings suggest them.
Interpretation and limitations
HbA1c, blood count, calcium and targeted immunology or electrophoresis should answer a specific diagnostic question; indiscriminate panels generate misleading incidental results.
06
Four-variable Kidney Failure Risk Equation
Why
Estimate two- and five-year treated kidney-failure risk from age, sex, eGFR and ACR in an appropriate CKD population.
Interpretation and limitations
Use the UK-validated four-variable equation only with stable CKD inputs. A 5-year kidney-failure risk above 5% is a NICE criterion for specialist assessment; do not calculate or act on a precise-looking score during AKI or from a transient or contaminated ACR.
07
CKD complication screen
Why
Detect anaemia, potassium disturbance, acidosis and mineral-bone abnormalities as disease advances.
Interpretation and limitations
Interpret haemoglobin, bicarbonate, potassium, calcium, phosphate and PTH against stage and trend; a discordant abnormality needs its own differential rather than automatic attribution to CKD.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute kidney injury

A new low eGFR during illness, obstruction or medicine change may be AKI; prior results and prompt repeat testing are essential before assigning chronicity.

Acute kidney disease

Kidney dysfunction present for 7 to 90 days has not yet met the greater-than-3-month CKD definition and requires continued cause assessment and follow-up.

Creatinine-estimate mismatch

Low or high muscle mass, amputation, oedema, diet, creatine and tubular-secretion inhibitors can make creatinine-based eGFR diverge from true filtration and the clinical phenotype.

Transient albuminuria

Urinary infection, fever, exercise, menstruation, marked hyperglycaemia and decompensated heart failure can temporarily raise ACR; confirmation in a stable, uncontaminated sample prevents misclassification.

Non-albumin protein or bleeding

Paraprotein or tubular protein may produce proteinuria with little albumin, while urological bleeding can cause haematuria without glomerular disease; ACR, PCR, microscopy and context distinguish them.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01CONFIRMNew low eGFRFirst stepAn adult has a first creatinine-based eGFR below 60 mL/min/1.73 m².

1Check prior results, current illness, hydration, urine output, medicines and obstruction symptoms, and assess immediately for AKI or a renal emergency.
2Repeat renal function within the NICE-recommended acute exclusion interval when deterioration is new, adjusting urgency to the clinical picture.
3If stable, document at least two results separated by 90 days or another unequivocal chronic marker before labelling CKD.
4Stage with both eGFR and ACR, determine likely cause, review cardiovascular risk and agree a stage- and trajectory-based monitoring plan.

02ALBUMINRaised urine ACRAlbuminuria is detected with any eGFR, including preserved filtration.

1Exclude transient contamination or illness, quantify ACR and repeat an intermediate result on an early-morning specimen where guidance advises confirmation.
2Measure blood pressure, eGFR, urinalysis and diabetes status and ask about oedema, systemic disease, family history and nephrotoxic medicines.
3Combine A category, haematuria and trajectory to decide renoprotective therapy, monitoring frequency and renal referral.
4EscalationEscalate rapidly for nephrotic syndrome, inflammatory sediment, rapid loss of function or severe systemic features.

03REFERNephrology discussion or referralRisk, progression, albuminuria, haematuria, hypertension or suspected cause exceeds routine primary-care management.

1Calculate kidney-failure risk where valid and document the sustained eGFR and ACR trajectory rather than sending one isolated result.
2Apply NICE NG203 exactly: 5-year KFRE risk above 5%; ACR at least 70 mg/mmol unless due to diabetes and already appropriately treated; ACR above 30 mg/mmol with haematuria; sustained eGFR fall at least 25% with category change within 12 months or at least 15 mL/min/1.73 m² per year; hypertension above target despite at least 4 therapeutic-dose agents; known or suspected rare or genetic CKD; or suspected renal-artery stenosis.
3Provide medicine list, urine findings, imaging, complication bloods, comorbidity and the person's goals so triage can identify urgency.
4Continue safe blood-pressure, cardiovascular and nephrotoxin management while awaiting review; referral does not transfer all care automatically.

04LIMITSCreatinine estimate may misleadBody composition, diet, amputation, oedema or a high-stakes decision makes eGFRcreatinine potentially inaccurate.

1Identify why creatinine generation or distribution is atypical and avoid interpreting a small numerical change as biological certainty.
2Discuss cystatin C, measured clearance or reference-method GFR with renal or laboratory specialists when the result would change dosing, donation or another major decision.
3Use trends from a consistent method and incorporate albuminuria, imaging and the clinical phenotype.
4Dose medicines using the product-specific renal-function method and pharmacist advice rather than silently substituting a different estimate.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Kidney failure and acute injury

Progressive nephron loss can lead to kidney-replacement or conservative-care decisions, while reduced reserve greatly increases vulnerability to superimposed AKI.

Cardiovascular disease

Albuminuria and reduced GFR independently increase atherosclerotic events, heart failure, arrhythmia and cardiovascular death, often before kidney failure develops.

Fluid electrolyte and acid disturbance

Advanced CKD can cause hypertension, oedema, pulmonary congestion, hyperkalaemia and metabolic acidosis, with severity altered by diet, medicines and intercurrent illness.

Anaemia and mineral bone disorder

Reduced erythropoietin and disordered iron handling cause anaemia, while phosphate retention, altered vitamin-D metabolism and secondary hyperparathyroidism contribute to bone and vascular disease.

Uraemia and medicine toxicity

Accumulating uraemic solutes can cause pruritus, anorexia, cognitive change, neuropathy, platelet dysfunction and pericarditis; reduced clearance also increases toxicity from renally eliminated medicines.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Set eGFR monitoring frequency from G and A category, prior rate of decline, diabetes, heart failure, intercurrent illness and medicines that affect kidney haemodynamics.
Recheck ACR at a clinically useful interval to confirm persistence and assess disease-modifying response, avoiding samples during urinary infection or major transient stress where possible.
Record blood pressure with an appropriate standardised method and review home readings when white-coat effect, variability or treatment intensification matters.
Track potassium and creatinine after starting or increasing renin–angiotensin-system blockade, diuretics, mineralocorticoid antagonists or other haemodynamically active therapy.
Screen haemoglobin, bicarbonate, calcium, phosphate and PTH more closely as CKD advances, using local renal protocols rather than testing every marker at every visit.
Recalculate kidney-failure risk and revisit modality planning when eGFR or ACR changes materially; communicate risk in natural frequencies and alongside competing health risks.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

G1 is not normal by definition

A person can have G1 CKD through persistent A3 albuminuria, a structural abnormality or a kidney transplant despite apparently preserved filtration.

Creatinine follows muscle

Low muscle mass can conceal poor filtration, while high muscle mass or creatine intake can lower estimated GFR without equivalent parenchymal disease.

Albuminuria is vascular information

ACR predicts cardiovascular as well as renal events and may change blood-pressure targets and drug eligibility before symptoms appear.

Trajectory beats snapshot

A stable eGFR of 34 over years and a fall from 80 to 45 in months share no equivalent urgency despite category labels.

Risk equations need a stable input

Using KFRE during acute kidney injury or with a contaminated ACR gives a precise-looking answer built from invalid assumptions.

Cause survives the stage

Writing only ‘CKD 3b’ can hide treatable obstruction, inflammatory glomerular disease, paraprotein injury or an inherited condition with family implications.

11Common pitfallsFrequent interpretation and management errors.

01
Do not code CKD from a single low eGFR obtained during sepsis, dehydration or medication-associated acute kidney injury.
02
Do not call G1 or G2 CKD without albuminuria, structural disease, urine abnormality, histology or another accepted chronic marker.
03
Do not stage with eGFR alone; omit ACR and you lose important prognosis, referral and treatment information.
04
Do not treat eGFR as measured truth in amputation, cachexia, body-building, major oedema or changing creatinine.
05
Do not attribute new severe anaemia, haematuria or rapid decline to ‘known CKD’ without investigating a superimposed cause.
06
Do not let routine referral paperwork delay emergency treatment for hyperkalaemia, pulmonary oedema, obstruction or uraemic complications.