What is Chronic Kidney Disease?
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for >3 months, with implications for health. Classified by GFR category (G1–G5) using CKD-EPI 2021 equation and albuminuria category (A1–A3). CKD encompasses a spectrum from mildly reduced eGFR to kidney failure requiring renal replacement therapy.
Pathophysiology
Progressive nephron loss triggers adaptive hyperfiltration in remaining nephrons, generating glomerular hypertension and proteinuria that accelerate further injury. RAAS activation, TGF-β-driven fibrosis, and chronic inflammation drive tubulointerstitial scarring. Cardiovascular risk is disproportionately elevated: patients with CKD G3b–G4 are more likely to die from cardiovascular events than to reach end-stage renal disease.
Clinical Features & Symptoms
- Often asymptomatic in early stages (G1–G3)
- Fatigue, reduced exercise tolerance
- Oedema (hypoalbuminaemia, fluid retention)
- Anaemia symptoms (pallor, breathlessness)
- Pruritus (late CKD)
- Nausea, anorexia, vomiting (uraemia — late)
- Hypertension (very common — cause and consequence)
- Nocturia and changes in urine output
Diagnosis
CKD requires ≥2 measurements of: eGFR <60 mL/min/1.73m² (CKD-EPI 2021) or uACR ≥3 mg/mmol (30 mg/g) — persisting >3 months apart. Classify by KDIGO heat map: G1–G5 (eGFR) × A1–A3 (uACR). Screen annually in diabetes and hypertension. Investigate for underlying cause: renal ultrasound, urine microscopy, immunological screen if indicated.
Current Treatment Guidelines
SGLT2 inhibitor
Class I, Level ADapagliflozin 10 mg or empagliflozin 10 mg. Reduces CKD progression and cardiovascular events in CKD G2–G4 with uACR ≥22 mg/mmol regardless of diabetes status (DAPA-CKD, EMPA-KIDNEY). First Class I recommendation in non-diabetic CKD (KDIGO 2024).
RAAS blockade
Class I, Level AACE inhibitor or ARB for all CKD patients with uACR ≥30 mg/g (>3 mg/mmol). Reduces proteinuria and slows GFR decline. Maximum tolerated dose. Monitor eGFR and potassium at 1–4 weeks after initiation/dose change.
Finerenone
Class IIa, Level A (diabetic CKD)Non-steroidal MRA. Reduces CKD progression and cardiovascular events in diabetic CKD on RAAS blockade (FIDELIO-DKD, FIGARO-DKD). KDIGO 2024: add to SGLT2-i + RAAS blockade in diabetic CKD with eGFR ≥25 and potassium <5.0 mmol/L.
Blood pressure control
Class I, Level ATarget <130/80 mmHg in most CKD patients. More intensive targets (120/80) if proteinuric CKD and well tolerated. ACE-I/ARB preferred as first-line antihypertensive in CKD with proteinuria.
Protein intake
Class IIa, Level BModerate protein restriction 0.8 g/kg/day in non-dialysis CKD (avoid high protein >1.3 g/kg/day). Ensure adequate caloric intake to avoid malnutrition. Plant-based protein sources reduce acid load and may slow CKD progression.
Nephrology referral
Class I, Level CRefer if: eGFR <30 (G4–G5), rapidly declining eGFR (>5 ml/min/1.73m²/year), uACR >70 mg/mmol, suspected underlying glomerulopathy, or refractory hypertension. Timely referral for transplant/dialysis planning.
Monitoring & Treatment Targets
eGFR and uACR every 3–12 months depending on CKD stage and rate of progression. BP at every visit. HbA1c in diabetic CKD. Potassium and haemoglobin regularly. Annual: lipid profile, calcium/phosphate, 25-OH vitamin D, PTH in advanced CKD.
Key Clinical Trials
Clinical Guidelines
External Resources
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Frequently Asked Questions
What eGFR defines chronic kidney disease?
CKD requires eGFR <60 mL/min/1.73m² (GFR category G3a or below) OR evidence of kidney damage (uACR ≥3 mg/mmol, haematuria of renal origin, pathological abnormality) persisting for >3 months on ≥2 separate measurements. A single low eGFR may reflect acute kidney injury rather than CKD.
When should SGLT2 inhibitors be used in CKD?
KDIGO 2024 recommends SGLT2 inhibitors in all CKD patients with eGFR ≥20 and uACR ≥22 mg/mmol, regardless of diabetes status. Dapagliflozin and empagliflozin both have Class I evidence. They can be continued until dialysis initiation. The renoprotective effect is independent of their glucose-lowering action.
Medical disclaimer: This content is intended for qualified healthcare professionals and does not constitute medical advice. Always apply clinical judgment and refer to current local guidelines and institutional protocols.