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chronic kidney disease

in review 5 min read Updated 2026-08-24
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chronic kidney disease

Sustained eGFR <60 mL/min/1.73 m² or markers of kidney damage (albuminuria, sediment abnormalities, structural abnormalities) for ≥3 months. Staging combines GFR category (G1–G5) and albuminuria category (A1–A3) — the combination drives prognosis and management intensity. Renoprotective pillars: RAS blockade, SGLT2 inhibitors, BP control, and finerenone in diabetic CKD.


staging

GFR categories

categoryeGFR (mL/min/1.73 m²)description
G1≥90normal or high (CKD only if damage markers present)
G260–89mildly decreased (CKD only if damage markers present)
G3a45–59mild–moderate decrease
G3b30–44moderate–severe decrease
G415–29severe decrease
G5<15kidney failure

albuminuria categories

categoryACR (mg/mmol)ACR (mg/g)description
A1<3<30normal–mild
A23–3030–300moderate
A3>30>300severe

KDIGO risk heat map

A1A2A3
G1lowmoderatehigh
G2lowmoderatehigh
G3amoderatehighvery high
G3bhighvery highvery high
G4very highvery highvery high
G5very highvery highvery high
confirm chronicity before labelling CKD

A single eGFR <60 may be acute kidney injury. Trend creatinine as far back as possible (provincial lab systems — OLIS, ClinicalConnect). Small, echogenic kidneys on US suggest chronicity. Prior abnormal urinalysis or ACR supports the diagnosis.


renoprotective strategies

RAS blockade

ACEi or ARB — first-line for CKD with albuminuria (A2–A3). Titrate to maximum tolerated dose. Accept up to 30% rise in creatinine after initiation; beyond that, investigate renal artery stenosis.

  • Hold in AKI, volume depletion, hyperkalaemia >5.5 mmol/L
  • Do not combine ACEi + ARB (ONTARGET — no benefit, more hyperkalaemia and AKI)

SGLT2 inhibitors

Add regardless of diabetes status if eGFR ≥20 mL/min/1.73 m² and ACR ≥20 mg/mmol (or eGFR 20–45 even without significant albuminuria per EMPA-KIDNEY).

  • DAPA-CKD (2020) — dapagliflozin reduced sustained ≥50% eGFR decline, ESKD, or renal/CV death by 39% vs placebo; benefit in diabetic and non-diabetic CKD
  • EMPA-KIDNEY (2023) — empagliflozin reduced progression or CV death by 28%; included patients with eGFR 20–45 without significant albuminuria
  • CREDENCE (2019) — canagliflozin in diabetic nephropathy; 30% reduction in primary renal composite

Expect an initial eGFR dip of 3–5 mL/min (haemodynamic, not injury) — do not stop for this. Withhold perioperatively and in acute illness (sick-day rules).

finerenone (non-steroidal MRA)

Add in type 2 diabetes with CKD (eGFR ≥25, K⁺ <5.0 mmol/L, ACR ≥3 mg/mmol) already on maximised RAS blockade.

  • FIDELIO-DKD (2020) — 18% reduction in kidney composite endpoint
  • Monitor K⁺ at 1 month and regularly; hold if K⁺ >5.5 mmol/L

BP targets

<120/80 mmHg (KDIGO 2024, standardised office measurement). Tolerate higher targets if symptomatic hypotension, advanced age/frailty, or eGFR declining with lower BP.

other measures

  • Statin or statin/ezetimibe for all CKD G3–G5 not on dialysis (SHARP trial)
  • Sodium restriction <2 g/d (≈5 g NaCl) — potentiates RAS blockade
  • Protein: avoid high-protein diets; 0.8 g/kg/d in G4–G5 (controversial, modest benefit)
  • Glycaemic control in diabetes — HbA1c ≤53 mmol/mol (≤7%); individualise in advanced CKD (hypoglycaemia risk increases as renal clearance of insulin falls)
  • Avoid nephrotoxins: NSAIDs, aminoglycosides, iodinated contrast without hydration

outpatient assessment framework

history — nephrology-specific

  • Creatinine and ACR trend — start with a one-line trajectory summary
  • Duration and control of diabetes (HbA1c, microvascular complications) and hypertension (home readings)
  • NSAID use — ask by brand name (patients often don’t recognise “NSAID”)
  • PPI use — common cause of AIN; question ongoing need
  • Lower urinary tract symptoms, UTI history
  • Vasculitic screen: joint pain, rashes, oral ulcers, haematuria
  • Volume status symptoms: dyspnoea, orthopnoea, PND, peripheral oedema
  • Previous AKI episodes and circumstances

examination

  • BP both arms (sitting) + standing (one arm) — retake elevated readings after settling
  • Volume status: JVP, lung crackles, peripheral oedema
  • Weight trend for diuresis assessment

investigations

  • Trend creatinine and ACR over time
  • Urinalysis — blood (glomerular source?), protein
  • HbA1c trend in diabetes
  • Renal US if not done — size, echogenicity, obstruction
  • Consider: calcium, phosphate, PTH, vitamin D (G3b+); haemoglobin (G3+); iron studies

nephrology referral indications

  • eGFR <30 (G4–G5) or declining rapidly (>5 mL/min/yr sustained)
  • ACR >60 mg/mmol (A3) or nephrotic-range proteinuria
  • Persistent haematuria with proteinuria (glomerular disease likely)
  • Refractory hypertension despite ≥3 agents
  • Refractory hyperkalaemia or metabolic acidosis
  • Suspected systemic disease affecting kidneys (vasculitis, myeloma, amyloid)

traps

  • Stopping ACEi/ARB for a modest creatinine rise — up to 30% increase is expected and acceptable. Stopping prematurely removes long-term renoprotection.
  • Ignoring albuminuria when eGFR is normal — A3 albuminuria with G1 eGFR is still high-risk CKD. ACR drives prognosis independently of GFR.
  • Attributing all CKD to diabetes/hypertension without confirmation — atypical features (active sediment, rapid decline, no retinopathy in a diabetic with advanced nephropathy) warrant biopsy consideration.
  • NSAIDs in CKD — patients self-medicate without mentioning it. Ask by brand name every visit.
  • Forgetting sick-day rules — patients on ACEi/ARB + SGLT2i + diuretics need a clear plan to hold these during acute illness (vomiting, diarrhoea, febrile illness).

key trials

trialyearpopulationresult
CREDENCE2019T2DM + CKD, ACR >33 mg/mmolcanagliflozin ↓ renal composite 30%
DAPA-CKD2020CKD ± diabetes, eGFR 25–75dapagliflozin ↓ renal composite 39%
FIDELIO-DKD2020T2DM + CKD on max RASfinerenone ↓ kidney composite 18%
EMPA-KIDNEY2023CKD broad (eGFR 20–45 or 45–90 + ACR ≥20)empagliflozin ↓ progression/CV death 28%

related: acute kidney injury · nephrotic syndrome · hyponatraemia · hyperkalaemia · dialysis overview

Key references