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
| category | eGFR (mL/min/1.73 m²) | description |
|---|---|---|
| G1 | ≥90 | normal or high (CKD only if damage markers present) |
| G2 | 60–89 | mildly decreased (CKD only if damage markers present) |
| G3a | 45–59 | mild–moderate decrease |
| G3b | 30–44 | moderate–severe decrease |
| G4 | 15–29 | severe decrease |
| G5 | <15 | kidney failure |
albuminuria categories
| category | ACR (mg/mmol) | ACR (mg/g) | description |
|---|---|---|---|
| A1 | <3 | <30 | normal–mild |
| A2 | 3–30 | 30–300 | moderate |
| A3 | >30 | >300 | severe |
KDIGO risk heat map
| A1 | A2 | A3 | |
|---|---|---|---|
| G1 | low | moderate | high |
| G2 | low | moderate | high |
| G3a | moderate | high | very high |
| G3b | high | very high | very high |
| G4 | very high | very high | very high |
| G5 | very high | very high | very high |
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. Note: trial entry criterion was K⁺ ≤4.8 mmol/L.
- FIDELIO-DKD (2020) — 18% reduction in kidney composite endpoint
- Monitor K⁺ at 1 month and regularly; hold if K⁺ >5.5 mmol/L; restart at 10 mg once K⁺ ≤5.0
BP targets
<120 mmHg systolic (KDIGO 2024, standardised office measurement). CSN recommends a less aggressive target of <140/90 mmHg — reasonable in older or frail patients. Tolerate higher targets if symptomatic hypotension or eGFR declining with lower BP.
The Canadian Society of Nephrology commentary diverges on several points: BP target 140/90 (vs KDIGO <120 systolic), less restrictive sodium (individualised vs <2 g/d), against routine protein restriction, and anaemia screening only when eGFR <30 (vs G3a). CSN referral threshold of ACR >60 mg/mmol aligns with this note.
other measures
- Statin (or statin/ezetimibe) if age ≥50 with eGFR <60 (KDIGO). Age <50 with CKD: statin if other CV risk factors. Not initiated in dialysis-dependent patients (SHARP, AURORA, 4D)
- 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 rises as renal insulin clearance 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; PPI use (AIN risk)
- Lower urinary tract symptoms, UTI history
- Vasculitic screen: joint pain, rashes, oral ulcers, haematuria
- Volume status: dyspnoea, orthopnoea, PND, peripheral oedema
- Previous AKI episodes and circumstances
examination
- BP both arms (sitting) + standing — retake elevated readings after settling
- Volume status: JVP, lung crackles, peripheral oedema; weight trend
investigations
- Trend creatinine and ACR; urinalysis (blood, protein); HbA1c in diabetes
- Renal US if not done — size, echogenicity, obstruction
- Consider: calcium, phosphate, PTH, vitamin D (G3b+); haemoglobin and iron studies (G3a+)
nephrology referral indications
- eGFR <30 (G4–G5) or declining rapidly (>5 mL/min/yr sustained, or ≥25% decline from baseline)
- Kidney Failure Risk Equation (KFRE) 5-year risk ≥3–5% (KDIGO 2024) — developed in Canada (Tangri et al.); uses age, sex, eGFR, and ACR. Available at kidneyfailurerisk.com
- 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
- AKI-on-CKD or unexplained anaemia requiring ESA consideration
- Suspected systemic disease affecting kidneys (vasculitis, myeloma, amyloid)
CKD complications
anaemia
Screen haemoglobin from G3a onward. Target Hb 100–115 g/L — do not exceed 115 (↑ stroke and thromboembolism risk).
- Iron first: trial of IV or oral iron when TSAT ≤20% and ferritin ≤500 µg/L (KDIGO). Do not routinely give iron if ferritin >500. IV iron preferred in haemodialysis; oral or IV in non-dialysis CKD. Non-dialysis CKD thresholds for deficiency: ferritin <100 µg/L or TSAT <20%
- ESA (epoetin, darbepoetin): consider if Hb 90–100 g/L and iron replete. Titrate to avoid Hb >115
- ESA hyporesponsiveness → reassess iron stores, occult blood loss, infection, hyperparathyroidism, malignancy
CKD–mineral bone disease
Check calcium, phosphate, PTH, 25-OH vitamin D from G3b onward. Replete 25-OH vitamin D if deficient. Key principles:
- Hyperphosphataemia — dietary restriction first (processed foods, dairy, cola); phosphate binders with meals if persistent (calcium carbonate first-line; sevelamer/lanthanum if vascular calcification or hypercalcaemia)
- Secondary hyperparathyroidism — calcitriol/alfacalcidol only once phosphate controlled (risk of metastatic calcification); cinacalcet if refractory; parathyroidectomy rarely needed
- PTH target in dialysis: 2–9× upper limit of normal (KDIGO) — most titration is nephrologist-managed
metabolic acidosis
Oral NaHCO₃ (sodium bicarbonate) 500–1000 mg TDS once serum HCO₃⁻ <22 mmol/L (KDIGO 2024 target: maintain ≥22). Slows CKD progression and mitigates muscle wasting. Monitor volume and sodium load.
sick-day rules — SADMANS
Hold during acute dehydrating illness (vomiting, diarrhoea, febrile illness):
- Sulfonylureas
- ACEi
- Diuretics
- Metformin (some versions add MRAs — non-standard but clinically reasonable)
- ARBs
- NSAIDs
- SGLT2 inhibitors
KDIGO 2024 notes that evidence for sick-day rules preventing AKI is weak, and harm can occur from failure to restart medications. Patients on multi-drug renoprotective regimens (ACEi/ARB + SGLT2i + diuretic ± MRA) need a written plan with clear instructions for both holding and restarting.
urgent dialysis indications
AEIOU: refractory Acidosis, Electrolytes (hyperkalaemia), Ingestions (toxic alcohols, lithium, salicylates), fluid Overload, Uraemia (pericarditis, encephalopathy, bleeding) — see dialysis overview.
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.
related: acute kidney injury · nephrotic syndrome · hyponatraemia · hyperkalaemia · acid-base disorders · dialysis overview