Chronic kidney disease
Exam Tips
- In OSCE/viva, define CKD using the 3-month chronicity rule plus either reduced eGFR (<60) or marker of kidney damage (for example ACR >=3 mg/mmol).
- State CKD classification as Cause + GFR category + Albuminuria category (CGA), then estimate renal and cardiovascular risk from both G and A.
- A common exam trap is treating a single abnormal creatinine as CKD; confirm persistence over >=90 days and exclude AKI/UTI/obstruction first.
- For prescribing stations, mention renal dose adjustment, avoidance of NSAIDs, and post-initiation U&Es monitoring after ACEi/ARB/SGLT2 inhibitors.
- Link CKD to cardiovascular medicine: patients are more likely to die from CVD than to reach dialysis, so statin/BP/proteinuria control are high-yield management priorities.
- Use a structured complication screen: K+ and bicarbonate, fluid status, Hb/iron, bone-mineral profile, and uraemic symptoms.
Definition
Chronic kidney disease (CKD) is a sustained abnormality of kidney structure or function lasting at least 3 months, with clinical consequences such as reduced filtration, albuminuria, electrolyte disturbance, or structural renal disease. In practice, diagnosis is made by persistent eGFR <60 mL/min/1.73 m2 on at least two tests 90 days apart, and/or markers of kidney damage (for example ACR >=3 mg/mmol, persistent haematuria, abnormal imaging, or previous kidney transplant).
Pathophysiology
CKD reflects progressive nephron loss from causes such as diabetic kidney disease, hypertensive nephrosclerosis, glomerular inflammation, and tubulointerstitial damage. Surviving nephrons hyperfilter to maintain total GFR, but this adaptive response increases intraglomerular pressure, promotes proteinuria, and accelerates sclerosis and fibrosis. Ongoing RAAS activation, endothelial dysfunction, inflammation, and oxidative stress drive further decline in renal function. Falling GFR impairs potassium, phosphate, acid, water, and toxin excretion, causing hyperkalaemia, CKD-mineral bone disorder, metabolic acidosis, fluid overload, and uraemic symptoms. Cardiovascular risk rises markedly via shared risk factors plus CKD-specific mechanisms (arterial stiffness, vascular calcification, anaemia, chronic inflammation). See Figure: KDIGO CGA heat map (GFR category x albuminuria category) to visualize risk stratification and progression risk.
Risk Factors
- Diabetes mellitus (most common adult cause)
- Hypertension
- Previous acute kidney injury
- Established cardiovascular disease (IHD, heart failure, stroke, PAD)
- Family history of CKD stage 5 or inherited renal disease (for example ADPKD, Alport syndrome)
- Glomerular disease (including post-infectious and immune-mediated causes)
- Obstructive uropathy (BPH, neurogenic bladder, recurrent calculi, structural tract disease)
- Multisystem disease with renal involvement (SLE, vasculitis, myeloma, HIV)
- Nephrotoxin exposure (NSAIDs, lithium, calcineurin inhibitors, aminoglycosides, some chemotherapy/radiotherapy)
- Incidental proteinuria or persistent non-visible haematuria
Clinical Features
Symptoms
- Often asymptomatic in early CKD
- Fatigue, reduced exercise tolerance
- Nocturia/polyuria early, then oliguria in advanced disease
- Ankle swelling, breathlessness (fluid overload/pulmonary oedema)
- Anorexia, nausea, pruritus, metallic taste in uraemia
- Muscle cramps, restless legs, paraesthesia
- Bone pain or fragility symptoms in CKD-mineral bone disorder
Signs
- Hypertension
- Peripheral oedema, raised JVP, bibasal crackles if fluid overloaded
- Pallor (anaemia of CKD)
- Uraemic features in advanced disease (scratch marks, fetor, encephalopathy late)
- Evidence of systemic disease (rash/arthritis in lupus or vasculitis, enlarged kidneys in ADPKD)
- Signs of cardiovascular disease (carotid bruits, heart failure signs, peripheral vascular disease)
Investigations
Management
Lifestyle Modifications
- Smoking cessation and regular exercise to reduce cardiovascular and renal risk
- Salt restriction (typically <2 g sodium/day, about <5 g salt/day) and weight optimization
- Sick-day advice for dehydration/intercurrent illness (temporarily hold nephrotoxic or volume-depleting medicines when appropriate)
- Avoid non-prescribed NSAIDs and over-the-counter nephrotoxins
- Vaccination review (influenza, pneumococcal, hepatitis B in advanced CKD/dialysis planning)
- Dietetic input for potassium, phosphate, and protein balance in advanced disease
Pharmacological Treatment
RAAS blockade (renoprotection, proteinuria reduction, BP control)
- Ramipril 1.25-2.5 mg once daily initially, titrate to maximum tolerated dose
- Lisinopril 2.5-10 mg once daily initially, titrate as tolerated
- Losartan 50 mg once daily initially (up to 100 mg once daily)
Use ACE inhibitor or ARB (not both together routinely). Check creatinine/eGFR and potassium before and 1-2 weeks after initiation or dose increase. Acceptable creatinine rise is usually limited; stop/seek specialist advice if marked rise or significant hyperkalaemia. Contraindicated in pregnancy; caution in bilateral renal artery stenosis.
SGLT2 inhibitors (reno- and cardioprotection where indicated)
- Dapagliflozin 10 mg once daily
- Empagliflozin 10 mg once daily
Consider in CKD with albuminuria/diabetes according to current NICE criteria and eGFR thresholds. Warn about genital mycotic infection risk, volume depletion, and rare euglycaemic DKA; pause during acute illness/fasting/surgery.
Antihypertensives for BP targets
- Amlodipine 5 mg once daily (increase to 10 mg once daily if needed)
- Indapamide 2.5 mg once daily (or SR 1.5 mg once daily)
- Furosemide 40 mg once daily, titrate for oedema/fluid overload
Choice depends on albuminuria, ethnicity, comorbidity, and volume status. Monitor for postural hypotension, electrolyte disturbance, and AKI risk during intercurrent illness.
Lipid lowering for cardiovascular risk reduction
- Atorvastatin 20 mg once daily
Recommended for many adults with CKD not on dialysis for primary/secondary CV prevention. Check interactions and liver adverse effects; do not initiate statin solely for dialysis-dependent patients without another indication.
CKD complications: acidosis, hyperkalaemia, anaemia, CKD-MBD
- Sodium bicarbonate 500 mg to 1 g three times daily (titrate to bicarbonate target)
- Patiromer 8.4 g once daily (titrate as needed) or sodium zirconium cyclosilicate 10 g three times daily for up to 48 h then maintenance
- Ferrous sulfate 200 mg two to three times daily (if iron deficiency), then consider IV iron
- Epoetin alfa (specialist initiation; for example 50 IU/kg 3 times weekly, adjusted to Hb response)
- Phosphate binders such as calcium acetate 667 mg three times daily with meals or sevelamer 800 mg three times daily with meals
Usually specialist-led in advanced CKD. Sodium bicarbonate may worsen fluid overload/hypertension; potassium binders require monitoring and interaction timing; ESA therapy carries hypertension/thrombotic risk; avoid overcorrection of Hb; calcium-based binders risk hypercalcaemia/vascular calcification.
Surgical / Interventional
- Renal replacement therapy planning in advanced CKD: haemodialysis access formation (arteriovenous fistula), peritoneal dialysis catheter insertion
- Kidney transplantation assessment and listing where appropriate
- Relief of obstruction (for example stenting/nephrostomy/prostate surgery) when obstructive uropathy contributes
Complications
- Accelerated CKD progression and end-stage kidney disease
- Acute kidney injury episodes superimposed on CKD
- Hypertension and treatment-resistant hypertension
- Major cardiovascular events (myocardial infarction, stroke, heart failure, PAD)
- Hyperkalaemia and life-threatening arrhythmia risk
- Metabolic acidosis
- Fluid overload and pulmonary oedema
- Anaemia of CKD
- CKD-mineral and bone disorder (fracture and vascular calcification risk)
- Peripheral neuropathy/myopathy and restless legs symptoms
- Malnutrition and uraemic symptom burden
- Increased all-cause mortality
Prognosis
Course is heterogeneous and depends on cause, baseline eGFR, and albuminuria; many patients remain stable for years, while a smaller subgroup shows accelerated decline. Risk of death (mainly cardiovascular) generally exceeds risk of progression to end-stage kidney disease, and both risks rise as eGFR falls and albuminuria increases. Good BP control, reduction of albuminuria, and aggressive cardiovascular risk management slow progression and improve outcomes.
Sources & References
🏥BMJ Best Practice(5)
💊BNF Drug References(4)
- Difelikefalin[management.pharmacological]
- Etelcalcetide[management.pharmacological]
- Orlistat[cautions]
- Paricalcitol[management.pharmacological]
✅NICE Guidelines(1)
- Chronic kidney disease[overview]
📖Textbook References(20)
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1748)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 992)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1236)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 830)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 833)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 992, 993)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1663)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1169)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 923)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1040)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 794, 795)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1175)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 258, 259)[context]
- David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 881)[context]
- Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 439)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 677, 678)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 678)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 318, 319)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 75, 76)[context]
- [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 703, 704)[context]