Summary

Chronic kidney disease (CKD) is defined as abnormal kidney structure or function present for more than 3 months, with implications for health. It is classified by cause, GFR category (G1-G5), and albuminuria category (A1-A3). CKD is common (affecting ~10% of the adult population), often asymptomatic in early stages, and is strongly associated with cardiovascular disease and mortality. The leading causes are diabetes (diabetic kidney disease) and hypertension. Management focuses on slowing progression (BP control, ACE inhibitors/ARBs, SGLT2 inhibitors), managing complications (anaemia, bone disease, acidosis, hyperkalaemia), reducing cardiovascular risk, and preparing for renal replacement therapy (dialysis or transplant) if progression to end-stage kidney disease (ESKD) occurs.

Key Facts

• Definition: Kidney damage (albuminuria, structural abnormality) OR GFR <60 mL/min for ≥3 months
• Prevalence: ~10% of adults; increases with age
• Main causes: Diabetes (40%), Hypertension (25%), Glomerulonephritis (10%)
• Staging: GFR categories (G1-G5) and albuminuria categories (A1-A3)
• Key threshold: eGFR <60 mL/min = Stage 3+ (clinically significant)
• Cardiovascular risk: CKD is major CV risk factor; patients more likely to die from CVD than reach dialysis
• ACE inhibitor: First-line for BP and renoprotection (especially with proteinuria)
• SGLT2 inhibitors: Now standard of care for CKD progression (dapagliflozin — DAPA-CKD trial)
• Complications: Anaemia, renal bone disease, acidosis, hyperkalaemia, CVD
• ESKD management: Dialysis (HD or PD) or kidney transplant

Clinical Pearls

"CKD Is a CV Risk Equivalent": Patients with CKD have CV risk equivalent to those with established coronary disease. Aggressive CV risk reduction is essential.

"Accept the ACEi Dip": An eGFR drop of up to 25% after starting ACE inhibitor is acceptable and expected. Don't stop unless >25% decline or hyperkalaemia. The long-term benefit is renoprotection.

"SGLT2 Inhibitors for All": DAPA-CKD and CREDENCE trials showed SGLT2 inhibitors (dapagliflozin, empagliflozin) slow CKD progression even in non-diabetics. Now standard of care for CKD.

"Refer Early to Nephrology": Patients with eGFR <30, rapid decline (>5/year), heavy proteinuria (ACR >70), or suspected glomerulonephritis need nephrology input for planning.

"Anaemia in CKD = EPO Deficiency": Kidneys produce erythropoietin. CKD causes EPO deficiency → normocytic anaemia. Treat with erythropoietin-stimulating agents (ESAs) once iron replete.

Why This Matters Clinically

CKD is common, often silent, and strongly associated with poor outcomes. Early detection (eGFR, ACR), BP control, use of cardio-renal protective drugs (ACEi, SGLT2i), and CV risk management can significantly slow progression and reduce mortality. Every clinician should be able to stage CKD, initiate first-line management, and know when to refer.[1,2]

Examination Findings

General:

• Pallor (anaemia)
• Excoriations (pruritus)
• Sallow complexion (uraemia)
• Fluid status (oedema, JVP, lung crackles)

Cardiovascular:

• Hypertension
• Pericardial rub (uraemic pericarditis — late)
• Cardiomegaly

Abdominal:

• Palpable kidneys (ADPKD)
• Transplant kidney (RIF/LIF)
• Dialysis catheter (tunnelled line, peritoneal)
• Fistula or graft (for haemodialysis)

Neurological:

• Peripheral neuropathy
• Asterixis (uraemic encephalopathy)

AV Fistula Assessment (Viva Favourite)

Progression

Survival

Key Guidelines

Landmark Trials

DAPA-CKD (2020)

• Dapagliflozin (SGLT2i) in CKD (with or without diabetes)
• 39% reduction in composite of eGFR decline, ESKD, or death
• Benefit in non-diabetic CKD confirmed
• PMID: 32970396

CREDENCE (2019)

• Canagliflozin in diabetic kidney disease
• 30% reduction in renal composite endpoint
• Established SGLT2i as renoprotective in DKD
• PMID: 30990260

RALES, RENAAL, IDNT

• Established benefit of RAAS blockade in CKD/DKD
• ACEi/ARB slow progression and reduce proteinuria

What is Chronic Kidney Disease?

CKD means your kidneys don't work as well as they should, and this has been the case for at least 3 months. Your kidneys filter waste and excess fluid from your blood.

What causes it?

The most common causes are:

• Diabetes — high blood sugar damages kidney filters
• High blood pressure — damages blood vessels in the kidneys
• Other kidney diseases — inflammation, inherited conditions

How is it diagnosed?

CKD is diagnosed with:

• A blood test (eGFR) to see how well your kidneys filter
• A urine test (ACR) to check for protein in the urine

How is it treated?

There is no cure, but treatments can slow progression:

• Blood pressure medicines (ACE inhibitors like ramipril)
• SGLT2 inhibitors (like dapagliflozin) — newer medicines that protect kidneys
• Control blood sugar if diabetic
• Healthy lifestyle — low salt diet, stop smoking, exercise
• Avoid painkillers like ibuprofen which harm kidneys

What if kidneys fail completely?

If kidneys stop working (end-stage kidney disease), options include:

• Dialysis — a machine filters your blood (haemodialysis) or fluid exchanges in your tummy (peritoneal dialysis)
• Kidney transplant — receiving a healthy kidney from a donor

High-Yield Exam Topics

Sample Viva Questions

Q1: A 65-year-old with type 2 diabetes has eGFR 45 and ACR 50. How do you classify and manage?

Model Answer: This is CKD stage G3a (eGFR 45-59) with moderately increased albuminuria (A2: ACR 3-30 actually — 50 is A3). Classification: CKD G3a A3 (if ACR 50). Management: Optimise BP (<130/80 given A3); first-line ACE inhibitor (ramipril) for renoprotection; add SGLT2 inhibitor (dapagliflozin) — evidence from DAPA-CKD showing benefit even in established CKD; optimise glycaemic control; statin for CV risk; avoid NSAIDs; dietary advice (low salt); annual monitoring of eGFR, ACR, FBC, bone profile. Consider nephrology referral given significant proteinuria (A3).

Q2: What is the significance of SGLT2 inhibitors in CKD?

Model Answer: SGLT2 inhibitors (dapagliflozin, empagliflozin) represent a paradigm shift in CKD management. The DAPA-CKD trial (2020) showed 39% reduction in the composite outcome of sustained eGFR decline, ESKD, or death in patients with CKD — importantly, including those without diabetes. The mechanism is thought to involve reduced intraglomerular pressure (via afferent arteriole vasoconstriction), reduced hyperfiltration, and anti-inflammatory effects. SGLT2 inhibitors are now recommended for all patients with CKD with eGFR ≥25 and ACR ≥22.6 mg/mmol, regardless of diabetes status.

Q3: What complications occur in advanced CKD and how are they managed?

Model Answer:

• Anaemia: Due to reduced EPO production. Treat with ESAs once iron replete. Target Hb 100-120.
• Renal bone disease (CKD-MBD): High PTH, high PO4, low Ca. Phosphate binders (sevelamer), alfacalcidol for vitamin D, cinacalcet for resistant hyperparathyroidism.
• Metabolic acidosis: Reduced acid excretion. Oral sodium bicarbonate.
• Hyperkalaemia: Dietary restriction, avoid K-sparing drugs, potassium binders (sodium zirconium cyclosilicate).
• Cardiovascular disease: Major cause of death in CKD. Statins, BP control, lifestyle.
• Fluid overload: Loop diuretics, fluid restriction, dialysis if refractory.

Common Exam Errors

Last Reviewed: 2025-12-24 | MedVellum Editorial Team

Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.