Decision support only — not a substitute for KDIGO 2024, the Kidney Health Australia primary-care handbook, eTG, or your renal team. CKD = abnormal kidney structure/function ≥3 months, classified by cause, GFR (G1–5) and albuminuria (A1–3). Two jobs: slow progression and reduce cardiovascular risk — most people with CKD die of cardiovascular disease, not dialysis. Verify all doses.
1 Kidney-protection pillars — slow progression & protect the heart
RAAS inhibitionACEi / ARB
Albuminuria and/or hypertension.
Titrate to max tolerated. Accept ≤30% creatinine rise; continue even when eGFR <30.
SGLT2idapagliflozin / empagliflozin
CKD with proteinuria — with or without diabetes.
Foundational DAPA-CKD · EMPA-KIDNEY. Start eGFR ≥20, continue below once on it. Sick-day hold.
Finerenonenonsteroidal MRA
T2D + albuminuria + eGFR >25 + normal K⁺, despite max RAASi.
Add for residual albuminuria FIDELIO-DKD · FIGARO-DKD. Monitor potassium.
GLP-1 RAdiabetic CKD
T2D + CKD not at glycaemic target on metformin + SGLT2i.
Semaglutide is renoprotective FLOW — weight, glucose, kidney and CV benefit.
Under every pillar: BP control, glycaemic control, a statin, lifestyle, and nephrotoxin stewardship. The non-diabetic evidence for SGLT2i is established; the non-diabetic role of finerenone/GLP-1 is still being defined (KDIGO focused update underway). Albuminuria itself is a treatment target — falling uACR tracks slower progression.
2 Classify & risk-stratify
The CGA heat map (GFR × albuminuria)
eGFR ↓ / uACR →
A1 <3
A2 3–30
A3 >30
G1–2 ≥60
low
mod
high
G3a 45–59
mod
high
v high
G3b 30–44
high
v high
v high
G4–5 <30
v high
v high
v high
uACR in mg/mmol. Risk rises with both axes — albuminuria matters as much as eGFR.
How to test & predict
- uACRQuantitative uACR, not a dipstick — albuminuria is an independent risk marker and a treatment target.
- eGFRCreatinine-based; add cystatin C when accuracy matters (drug dosing, borderline decisions).
- KFREKidney Failure Risk Equation for 2- & 5-yr risk — guides referral and planning better than eGFR alone.
- CauseIdentify it (diabetes, vascular, GN, PKD, obstructive) — changes specific management.
3 Investigate the aetiology
Everyone — the core workup
- UrineuACR + dipstick (blood/protein) + microscopy — dysmorphic RBCs / red-cell casts point to glomerular disease. The cheapest, highest-yield step.
- eGFRTrend it; add cystatin C if borderline. A single value can't separate acute from chronic.
- UltrasoundSize & symmetry, obstruction, cysts, scarring. Small kidneys = chronicity; asymmetry → renovascular/reflux.
- Bloods + drugsFBC, electrolytes, Ca/PO₄/PTH, HbA1c, lipids; review the full drug history (NSAIDs, lithium, PPIs, calcineurin inhibitors, analgesics).
Look harder when it doesn't fit
- Not DN?Don't assume diabetic nephropathy if there's no retinopathy, rapid decline, active sediment, nephrotic-range proteinuria, or short diabetes duration → seek a non-diabetic cause.
- GlomerularProteinuria + haematuria / active sediment → ANCA, anti-GBM, complement (C3/C4), ANA/dsDNA, hepatitis B/C, HIV ± biopsy.
- MyelomaOlder + anaemia + unexplained CKD/AKI ± hypercalcaemia → SPEP/UPEP + serum free light chains.
- RenovascularAsymmetry, bruit, flash pulmonary oedema, or a sharp Cr rise on ACEi → Doppler / CTA / MRA.
Large or normal-sized kidneys with CKD point toward diabetes (early), polycystic disease, amyloid, myeloma, or HIV-associated disease. Biopsy when the cause is unclear and would change management — particularly glomerular disease, rapid decline, or systemic features that might warrant immunosuppression.
4 Slow progression & cut cardiovascular risk
Blood pressure
- TargetKDIGO: SBP <120 by standardised measurement SPRINT.
- CaveatTechnique-dependent — individualise for frailty, orthostasis, falls. KHA pragmatically uses <130/80.
- AgentACEi/ARB first if albuminuria.
Lipids & lifestyle
- StatinFor most with CKD (CV risk) SHARP. Don't start de novo on dialysis — no benefit 4D · AURORA.
- SaltSodium restriction; weight; smoking cessation; activity.
- AvoidNSAIDs; nephrotoxin stewardship; sick-day rules.
Glycaemia & urate
- GlucoseIndividualised HbA1c; SGLT2i + GLP-1 RA do double duty (pillars above).
- UrateLower only if symptomatic — don't treat asymptomatic hyperuricaemia to protect kidneys.
5 Manage the complications
Anaemia — don't over-correct
- Iron firstReplace iron before reaching for an ESA.
- TargetHb ~100–115 g/L — not normal. Targeting normal Hb with ESAs causes harm TREAT · CHOIR · CREATE.
- HIF-PHIOral HIF stabilisers (roxadustat) an emerging option.
Bone, acid & potassium
- CKD-MBDManage phosphate (diet ± binders), PTH, vitamin D; avoid hypercalcaemia.
- AcidosisSodium bicarbonate if HCO₃ <22 — may slow progression.
- K⁺Don't reflexively stop RAASi for mild hyperkalaemia — use diet/binders (patiromer, SZC) to keep the renoprotective drug on board.
6 Prepare, refer & traps
Referral & planning
- RefereGFR <30, uACR ≥30 (A3) or rapid decline, high KFRE 5-yr risk, suspected GN/hereditary, refractory complications.
- PlanModality choice (HD/PD/transplant/conservative); timely AV fistula; pre-emptive transplant work-up.
- ProtectVaccinate; avoid unnecessary contrast; advance care planning for the conservative pathway.
Traps
- SGLT2iDon't withhold for "low eGFR" or absence of diabetes — start ≥20, continue below, benefit is independent of diabetes.
- RAASiA ≤30% creatinine rise on starting is expected and acceptable — don't stop reflexively.
- DrugsDose-adjust (metformin, DOACs, antibiotics); avoid morphine; caution with gadolinium at low eGFR (NSF).
Sources.
KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of CKD (CGA staging, SGLT2i eGFR ≥20 ± diabetes, finerenone, GLP-1 RA, statins, cystatin C, nephrotoxin stewardship; focused update on non-diabetic CKD underway 2026). KDIGO 2021 BP guideline (SBP <120). Kidney Health Australia "CKD Management in Primary Care"; CARI. eTG; PBS for subsidised agents.
Key trials: DAPA-CKD, EMPA-KIDNEY (SGLT2i); FIDELIO-DKD, FIGARO-DKD (finerenone); FLOW (semaglutide); CREDENCE (canagliflozin, diabetic CKD); SHARP (statin in CKD) & 4D/AURORA (no benefit starting on dialysis); SPRINT (intensive BP); TREAT/CHOIR/CREATE (ESA — harm targeting normal Hb).
Caveats: the SBP <120 target depends on standardised/automated measurement and must be individualised. PBS authority criteria govern SGLT2i/finerenone/GLP-1 access — confirm before prescribing. Drug dosing in CKD is dynamic; verify against eTG/product information. Companion to the AKI sheet — the same patient on a continuum.