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Health condition · Clinically reviewed

Chronic kidney disease, two numbers, a clear plan, and modern medicines that change trajectory.

CKD is common, often silent and now genuinely treatable. Blood pressure control, SGLT2 inhibitors and finerenone have reshaped care.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE NG203, KDIGO and peer-reviewed nephrology sources you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice including SGLT2 inhibitors, finerenone and updated referral thresholds.

Key facts

CKD at a glance.

The essentials, in plain English - what CKD is, how it is staged and what changes outcomes in 2026.

  • What it is

    Abnormalities of kidney structure or function that have been present for more than three months and matter for health.

  • How common

    Around 10 to 13 per cent of UK adults have CKD - a large share are undiagnosed, picked up only on routine bloods.

  • How it is staged

    KDIGO stages by eGFR (G1 to G5) and albuminuria (A1 to A3) - the two together predict risk better than either alone.

  • Main causes

    Diabetes and hypertension drive most cases, followed by glomerulonephritis, polycystic disease and obstructive causes.

  • Biggest risk

    Cardiovascular disease is the leading cause of death in CKD - long before dialysis is on the table.

  • What changed care

    SGLT2 inhibitors and finerenone now slow progression and cut cardiovascular events across a wide slice of CKD.

Why this guide matters

A treatable disease, not a slow inevitability.

CKD is quietly common - and the last few years have handed clinicians the biggest set of new options in a generation.

  • Two numbers set the plan

    eGFR and urine ACR together (the KDIGO heat map) drive follow-up, referral and treatment decisions.

  • Cardiovascular risk leads

    CVD, not dialysis, is the leading cause of death in CKD - blood pressure, statins and SGLT2 inhibitors matter early.

  • Modern medicines change it

    SGLT2 inhibitors (dapagliflozin, empagliflozin) and finerenone have transformed slow-decline management in the last few years.

How the diagnosis is made

From a routine blood test to a clear kidney plan.

The steps a UK GP or nephrologist will normally follow per NICE NG203, in order - so you know what to expect and why.

  1. 01

    Assessing

    eGFR and urine ACR

    A blood eGFR (CKD-EPI) alongside an early-morning urine albumin to creatinine ratio - the two numbers that anchor every CKD plan.

  2. 02

    Assessing

    Confirm and repeat

    CKD is only diagnosed if abnormalities persist for more than three months - repeat testing avoids labelling a single dip.

  3. 03

    Assessing

    Stage by KDIGO

    Combine eGFR (G1 to G5) with albuminuria (A1 to A3) to place risk on the KDIGO heat map and steer follow-up.

  4. 04

    Confirming

    Cause-finding bloods

    FBC, U&Es, bone profile, PTH, vitamin D, HbA1c, lipids, urate, bicarbonate - plus selective immunology, serology and paraprotein screen.

  5. 05

    Confirming

    Renal ultrasound

    Kidney size, symmetry, cysts, stones and hydronephrosis - and a first look at whether obstruction is driving the picture.

  6. 06

    Confirming

    Kidney biopsy (selected)

    For suspected glomerulonephritis, rapidly progressive disease or unexplained CKD - a specialist decision with clear indications.

  7. 07

    Referral

    Nephrology referral

    NICE prompts referral for eGFR under 30, ACR over 70, rapid decline, uncontrolled hypertension or suspected hereditary or systemic cause.

Typical timeline: a first abnormal result to a settled plan in weeks, with lifelong monitoring after.

Symptoms

What CKD actually feels like.

Early CKD is usually silent. As things advance, a familiar mix of fatigue, fluid, itch and appetite change starts to appear - and there are red-flag features that mean urgent review.

  • Often silent

    Most people feel well - CKD is usually picked up on routine bloods or a urine dipstick, not from symptoms.

  • Fatigue and poor sleep

    A slow, grinding tiredness with reduced concentration and disturbed sleep is one of the earliest lived symptoms.

  • Fluid overload

    Ankle and leg swelling, puffy eyes and breathlessness on exertion as sodium and water retention build.

  • Reduced appetite and nausea

    Metallic taste, early fullness, nausea and unintended weight loss as uraemia progresses.

  • Itch and restless legs

    Uraemic pruritus, dry skin, restless legs and cramps - classic markers of advanced kidney disease.

  • Foamy or bloody urine

    Frothy urine can signal heavy proteinuria; visible blood needs urgent assessment for a renal or urological cause.

  • Rising blood pressure

    New or worsening hypertension often runs alongside CKD and drives further kidney injury if untreated.

  • Red flag - rapid decline

    A fast fall in eGFR, new heavy proteinuria or systemic features (rash, joints, lungs) needs same-week nephrology input.

Treatment

How CKD is treated in the UK.

Blood pressure, albuminuria and cardiovascular risk sit at the centre. SGLT2 inhibitors and finerenone are the biggest recent additions - kidney replacement therapy is reserved for kidney failure.

  • Treat the underlying cause

    Optimise diabetes and blood pressure, relieve obstruction, and address glomerular or systemic disease early - it changes trajectory.

  • ACE inhibitor or ARB

    First-line for albuminuria and blood pressure - target under 130/80 (under 125/75 if albuminuric). Monitor potassium and creatinine. Avoid during AKI.

  • SGLT2 inhibitor

    Dapagliflozin or empagliflozin per DAPA-CKD and EMPA-KIDNEY - now used in diabetic and non-diabetic CKD to slow decline and cut cardiovascular events.

  • Finerenone

    Non-steroidal MRA (Kerendia) for diabetic CKD with albuminuria - FIDELIO-DKD and FIGARO-DKD showed reduced progression and heart failure.

  • Statin therapy

    Atorvastatin 20 mg for most adults with CKD 3 to 5 to lower the very high cardiovascular risk that comes with kidney disease.

  • Anaemia and bone care

    Iron (oral or IV), erythropoiesis-stimulating agents or oral HIF-PHI - plus phosphate binders, vitamin D analogues and cinacalcet for CKD-MBD.

  • Potassium and acidosis

    Patiromer or sodium zirconium (Lokelma) for stubborn hyperkalaemia and oral sodium bicarbonate for metabolic acidosis.

  • Kidney replacement or CKM

    Transplant (best long-term outcomes, ideally pre-emptive), haemodialysis or peritoneal dialysis - or conservative kidney management where appropriate.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and international specialty standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or nephrologist knows your kidneys, medicines and history and can tell you which parts apply to you. If in doubt, get seen.

  • NICE. Chronic kidney disease: assessment and management (NG203).

  • KDIGO 2024. Clinical Practice Guideline for the Evaluation and Management of CKD.

  • NICE. SGLT2 inhibitors (dapagliflozin, empagliflozin) for CKD - technology appraisals.

  • MHRA and NICE. Finerenone (Kerendia) for chronic kidney disease with type 2 diabetes.

  • The Renal Association / UK Kidney Association. Clinical practice guidelines.

Red flags

When CKD needs urgent attention.

Most CKD is managed steadily in primary care with nephrology support. These are the situations where waiting is the wrong call.

  • Rapidly progressive kidney injury

    A sudden fall in eGFR, new heavy proteinuria or haematuria with systemic features needs same-week nephrology input for possible glomerulonephritis.

  • Severe hyperkalaemia

    Potassium above 6.0 mmol/L, especially with ECG changes, is a medical emergency - stop offending drugs and treat urgently.

  • Fluid overload and breathlessness

    New orthopnoea, leg oedema and reduced urine output can signal decompensated CKD or heart failure and needs urgent review.

  • Uraemic symptoms

    Persistent nausea, vomiting, confusion, pericarditis or intractable itch in advanced CKD prompt urgent nephrology assessment for KRT.

  • Obstructive uropathy

    Loin pain with reduced urine output or new hydronephrosis on imaging is urological - it needs relief of obstruction before nephron loss.

  • Suspected renal artery disease

    A sharp rise in creatinine after starting an ACE inhibitor or ARB, or flash pulmonary oedema, suggests bilateral renal artery stenosis.

  • Systemic illness clues

    Rash, joint pain, haemoptysis, sinus disease or weight loss with CKD point to vasculitis, lupus or myeloma - do not delay work-up.

  • Pregnancy in CKD

    Pregnancy with reduced eGFR or proteinuria carries higher maternal and fetal risk - joint obstetric and nephrology care is essential.

  • Contrast and nephrotoxic drugs

    NSAIDs, aminoglycosides and IV contrast can accelerate decline - always review before scans, procedures and new prescriptions.

Living with it

A long-term condition, with a clear playbook.

Four things that make the biggest difference day to day - knowing your numbers, taming blood pressure, moving lifestyle levers and checking every new medicine.

A quiet reminder

Small, steady wins, kept up for years.

CKD rewards steady habits and consistent medication far more than short bursts of intensity.

  1. 01 Numbers

    Know your eGFR and ACR

    These two numbers set the plan. Ask what yours are, how often they will be repeated and what would trigger a referral.

  2. 02 Pressure

    Blood pressure is the lever

    Steady control - usually with an ACE inhibitor or ARB - slows CKD more than almost anything else you can change.

  3. 03 Lifestyle

    Weight, salt, smoking, movement

    Keeping salt under 6 g a day, staying active, not smoking and treating weight and cholesterol all add up over years.

  4. 04 Meds

    Check every new prescription

    Ask a pharmacist about kidney doses before starting anything new, and avoid regular NSAIDs where you can.

Frequently asked

Everything we get asked about CKD.

Quick answers on staging, causes, medicines and what happens if kidneys fail.

  • What is chronic kidney disease?

    Chronic kidney disease means abnormalities of kidney structure or function that have been present for more than three months and matter for health. It ranges from mild reductions in filtering (eGFR) or small amounts of protein in the urine (albuminuria) through to kidney failure needing dialysis or a transplant.

  • How is CKD staged?

    The KDIGO system stages CKD by eGFR (G1 above 90 with damage, G2 60 to 89, G3a 45 to 59, G3b 30 to 44, G4 15 to 29, G5 below 15) and by albuminuria (A1 under 3, A2 3 to 30, A3 over 30 mg/mmol). The two together predict risk of kidney failure and cardiovascular events far better than either on its own.

  • What causes CKD?

    The commonest causes in the UK are diabetes (around 30 per cent) and hypertension (around 25 per cent). Others include glomerulonephritis (IgA nephropathy, membranous, FSGS, lupus, ANCA vasculitis), polycystic kidney disease, chronic interstitial nephritis, obstruction (stones, BPH, tumours), vascular and systemic disease (SLE, amyloid, myeloma, sickle cell) and hereditary conditions such as Alport and Fabry.

  • Which medicines actually slow CKD?

    ACE inhibitors and ARBs remain first-line, especially with albuminuria. SGLT2 inhibitors (dapagliflozin, empagliflozin) are now used in both diabetic and non-diabetic CKD after DAPA-CKD and EMPA-KIDNEY. Finerenone is used in diabetic CKD with albuminuria. Statins reduce cardiovascular risk. All work best alongside blood pressure control and the treatment of the underlying cause.

  • When should I see a kidney specialist?

    NICE recommends nephrology referral for eGFR under 30, ACR over 70, a rapid decline in kidney function, uncontrolled hypertension despite four agents, suspected genetic or systemic cause, or an unexplained acute kidney injury that has not recovered.

  • What are the treatment options for kidney failure?

    Kidney replacement therapy includes haemodialysis (in-centre or home), peritoneal dialysis and kidney transplantation. Transplant, ideally pre-emptive and from a living donor, gives the best long-term outcomes. For older or frailer patients, conservative kidney management focuses on symptoms and quality of life without dialysis and is a valid choice.

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