Chronic kidney disease is a high-yield exam topic because it tests a two-axis classification, a clear set of protective treatments, and specific referral thresholds — and because SGLT2 inhibitors have changed its management. This guide covers CKD as examiners frame them, to the current NICE standard (NG203). Follow current guidance and local protocols in practice; this reflects guidance as of mid-2026.
What CKD is
Chronic kidney disease is a sustained reduction in kidney function or evidence of kidney damage persisting for at least three months. It is usually progressive and often silent, and it matters because it markedly increases cardiovascular risk — most people with CKD are far more likely to die of cardiovascular disease than to reach dialysis. The commonest causes in the UK are diabetes and hypertension. Other causes include glomerulonephritis, polycystic kidney disease, recurrent obstruction or infection, and long-term nephrotoxic drugs. CKD is usually detected on blood and urine testing rather than symptoms, which appear only at an advanced stage and include fatigue, oedema, breathlessness, pruritus and nausea.
Diagnosis and classification
CKD is defined by an eGFR below 60 mL/min/1.73m², or markers of kidney damage such as albuminuria, persisting for three months or more. Classification uses two axes, which examiners expect you to combine:
- GFR category, from G1 (90 or above) through G3a and G3b to G5 (below 15), which represents kidney failure.
- ACR category, based on the urine albumin-to-creatinine ratio: A1 (below 3), A2 (3 to 30) and A3 (above 30).
The combination of a lower GFR and a higher ACR predicts worse outcomes. Because CKD is silent, active testing is recommended in higher-risk groups: those with diabetes, hypertension, cardiovascular disease, a history of acute kidney injury, or who take nephrotoxic drugs. A single abnormal eGFR should be confirmed by repeating it, since transient falls — for example during acute illness — do not constitute CKD; the diagnosis requires the abnormality to persist beyond three months.
Management: protecting the kidney and heart
There is no cure; treatment slows progression and reduces cardiovascular risk.
- Blood pressure: control to below 140/90, or below 130/80 where the ACR is 70 mg/mmol or higher (or in diabetes with significant albuminuria).
- ACE inhibitor or ARB: offer to those with diabetes and an ACR of 3 or above, hypertension with an ACR above 30, or an ACR of 70 or above regardless of cause. Titrate to the maximum tolerated dose, and check eGFR and potassium one to two weeks after starting — a fall in eGFR of under 25%, or a creatinine rise of under 30%, is acceptable. Do not combine renin-angiotensin drugs, as this increases the risk of hyperkalaemia, hypotension and worsening renal function.
- SGLT2 inhibitor: dapagliflozin (and empagliflozin) is added to optimised ACE inhibitor or ARB therapy for eligible patients — both diabetic and non-diabetic CKD with albuminuria — because it slows progression and reduces cardiovascular death. Expect a small initial dip in eGFR that then stabilises.
- Statin: offer atorvastatin for cardiovascular risk reduction, since CKD is itself a major risk factor.
- Complications: treat anaemia (iron, then an erythropoiesis-stimulating agent) and renal bone disease (managing phosphate and vitamin D).
Lifestyle and risk-factor measures — smoking cessation, blood-pressure and glucose control, and an annual review of kidney function — run alongside, and nephrotoxic drugs are avoided or used with care.
When to refer to nephrology
Examiners reward knowing the referral thresholds: an eGFR below 30 (G4 or G5); an ACR of 70 mg/mmol or more (unless due to treated diabetes); an ACR of 30 or more with persistent haematuria; a sustained, rapid decline in eGFR; poorly controlled blood pressure despite four agents; a suspected genetic or rare cause; and a 5-year risk of needing renal replacement therapy above 5%. Earlier discussion with a nephrologist is always reasonable whenever the cause is uncertain or progression is faster than expected, even below these thresholds.
High-yield exam points and traps
- Classify with both axes — the GFR category and the ACR category — not GFR alone.
- A fall in eGFR of under 25% (or creatinine rise under 30%) after starting an ACE inhibitor or ARB is expected and acceptable, not a reason to stop.
- SGLT2 inhibitors now slow progression in both diabetic and non-diabetic CKD with albuminuria.
- Most patients with CKD die of cardiovascular disease rather than reaching dialysis — hence statins and risk-factor control.
- Refer when the eGFR falls below 30, or the ACR reaches 70, among the other thresholds.
- Hold ACE inhibitors, ARBs and SGLT2 inhibitors during acute illness with poor oral intake (sick-day rules).
- Confirm CKD on repeat testing after three months, since a single low eGFR may be transient rather than true CKD.
A few common questions
How is CKD classified? By two axes combined: the GFR category (G1 to G5) and the albuminuria (ACR) category (A1 to A3); a lower GFR and a higher ACR mean worse outcomes.
When is an ACE inhibitor or ARB indicated in CKD? For diabetes with an ACR of 3 or above, hypertension with an ACR above 30, or an ACR of 70 or above regardless of cause — titrated to the maximum tolerated dose.
Why are SGLT2 inhibitors used in CKD? SGLT2 inhibitors are used in CKD because dapagliflozin and empagliflozin slow progression and reduce cardiovascular death in eligible patients, including those without diabetes who have albuminuria.
What eGFR change is acceptable after starting an ACE inhibitor? A fall in eGFR of under 25%, or a rise in creatinine of under 30% — beyond that, recheck, consider other causes, and seek advice.
When should CKD be referred to a nephrologist? CKD should be referred to a nephrologist when the eGFR is below 30, the ACR is 70 or more, there is rapid decline or resistant hypertension, a rare cause is suspected, or the 5-year dialysis risk exceeds 5%.
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