NephrologyTier 1Disease (DEADMAN)

Chronic kidney disease (CKD)

Description

Definition

eGFR <60 mL/min/1.73m2 for >3 months, OR
>3 months of any marker of kidney damage regardless of GFR:
- Albuminuria, glomerular (dysmorphic) haematuria, structural abnormality on imaging, pathological abnormality on biopsy, electrolyte abnormality from tubular disorder, history of transplantation
*The 3-month requirement is what separates CKD from AKI - a single low eGFR is not CKD*

Staging - eGFR AND albuminuria, always both

G stage	eGFR		A stage	ACR (mg/mmol)
G1	>=90	CKD only if a damage marker present	A1 normal	<2.5 (M) / <3.5 (F)
G2	60-89	same caveat	A2 micro	2.5-25 (M) / 3.5-35 (F)
G3a	45-59		A3 macro	>25 (M) / >35 (F)
G3b	30-44
G4	15-29
G5	<15 or on dialysis

Macroalbuminuria is a poor prognostic marker independent of eGFR - G3a/A3 carries higher risk than G4/A1
KHA colour-coded heat map (green/yellow/orange/red) sets monitoring frequency and referral

~1 in 10 Australian adults; most undiagnosed until stage 3
Leading causes of incident ESKD in Australia (ANZDATA):
- Diabetic nephropathy ~35-40%, glomerulonephritis ~15%, hypertension/renovascular ~13%, polycystic ~6%, reflux nephropathy ~3%
Aboriginal and Torres Strait Islander peoples: ESKD incidence up to 4x, and up to 20x in remote communities; younger onset
Prevalence rises steeply with age; >50% of over-75s have eGFR <60 (much of it not progressive)

Causes - classify by compartment

Glomerular - diabetes, GN (IgA, FSGS, membranous), lupus, amyloid, myeloma
Vascular - hypertensive nephrosclerosis, renovascular disease, vasculitis, TMA, atheroembolic
Tubulointerstitial - reflux nephropathy, chronic pyelonephritis, drugs (lithium, CNI, analgesics, aristolochic acid), sarcoid, myeloma cast nephropathy
Obstructive - prostate, stones, retroperitoneal fibrosis, malignancy
Cystic/inherited - ADPKD, Alport, Fabry, ADTKD, nephronophthisis

Final common pathway

Nephron loss -> hyperfiltration in surviving nephrons
- -> glomerular capillary hypertension, podocyte stress, proteinuria
- -> filtered protein is directly tubulotoxic -> interstitial inflammation and fibrosis
- -> further nephron loss
Self-perpetuating and aetiology-independent once established - which is why the same drugs slow progression whatever the cause
*Interstitial fibrosis and tubular atrophy, not the glomerular lesion, predicts renal survival on biopsy*

Measuring function

eGFR by CKD-EPI creatinine (Australian labs report automatically when creatinine is ordered)
- Reported as mL/min/1.73m2 - body surface normalised
- Not valid: acute changes in function, extremes of muscle mass (amputee, body-builder, cachexia, paraplegia), high-protein or creatine supplement intake, pregnancy, children, some ethnic groups
- 2021 CKD-EPI equation removed the Black race coefficient
Cystatin C-based eGFR where creatinine is unreliable, or to confirm a borderline eGFR before a consequential decision
Cockcroft-Gault CrCl (absolute, mL/min) for drug dosing of narrow-therapeutic-index agents
24h urine creatinine clearance - overestimates GFR (tubular secretion); rarely needed

Albuminuria

First-void spot urine ACR is the standard; confirm a positive on 2 of 3 samples over 3 months
False positives: UTI, exercise within 24h, menstruation, febrile illness, heart failure, hyperglycaemia

Determine the cause

Urinalysis + microscopy for dysmorphic RBCs and casts
Renal ultrasound - size (small = chronic; large = diabetes, amyloid, ADPKD, HIV, infiltration), asymmetry, obstruction, cysts
Immunology and myeloma screen where the cause is unclear: ANA, ANCA, anti-GBM, C3/C4, SPEP + serum free light chains, hepatitis B/C, HIV
Renal biopsy if the cause is unclear, proteinuria is significant, or there is unexplained rapid decline

When to refer

eGFR <30, or sustained decline >5 mL/min/yr
ACR >30 mg/mmol (or >3 mg/mmol with haematuria)
KFRE 5-yr kidney failure risk >5%
Glomerular haematuria, refractory HTN or hyperkalaemia, suspected genetic disease, CKD in the young

Three separate jobs: slow progression, cut cardiovascular risk, treat uraemic complications.

1. Slow progression

BP <120 mmHg systolic (standardised office measurement)
ACEi or ARB, maximally tolerated, for albuminuric CKD with or without diabetes
- Tolerate a creatinine rise up to 30%; do not use ACEi and ARB together
SGLT2i - dapagliflozin or empagliflozin for proteinuric CKD irrespective of diabetes
- Initiate down to eGFR 20; continue to dialysis
Finerenone (non-steroidal MRA) added to RASi + SGLT2i in T2DM with albuminuria
GLP-1 RA (semaglutide) in T2DM + CKD - kidney and cardiovascular benefit (FLOW)
NaHCO3 to keep HCO3- >=22 mmol/L
Glycaemic control (HbA1c ~53 mmol/mol / 7%, relaxed in the frail), weight, smoking cessation, avoid nephrotoxins

2. Cardiovascular risk

Statin for everyone >=50 with CKD not on dialysis (do not start de novo once on dialysis)
CKD is a cardiovascular risk equivalent - most patients die of cardiovascular disease before reaching ESKD

3. Complications

Anaemia - iron first (ferritin >100 microgram/L, TSAT >20%), then ESA to Hb 100-115 g/L
CKD-MBD - phosphate toward normal, restrict calcium-based binders, PTH 2-9x ULN on dialysis
Hyperkalaemia - dietary, loop diuretic, NaHCO3, K+ binders (sodium zirconium cyclosilicate, patiromer) to preserve RAS blockade rather than stop it
Volume - loop diuretic, Na restriction <2 g/day
Uraemic symptoms: pruritus, restless legs, nausea, sleep disturbance

4. Prescribing and sick-day rules

Withhold during acute illness: ACEi/ARB, diuretics, metformin, SGLT2i, NSAIDs, MRA
Dose-adjust to CrCl; avoid NSAIDs entirely

5. Prepare for kidney failure

Modality education at eGFR ~20 or KFRE 2-yr risk >10%
Vein preservation; fistula ~6 months ahead; pre-emptive transplant workup at eGFR 15-20
Vaccination (double-dose hepatitis B, influenza, pneumococcal, COVID)
Conservative kidney management is a valid pathway - discuss early in the frail elderly

Cardiovascular disease - LVH, heart failure, AF, accelerated atherosclerosis, sudden cardiac death
Diabetes, hypertension, obesity, metabolic syndrome
Anaemia, CKD-MBD, hyperkalaemia, metabolic acidosis, hyperuricaemia and gout
Protein-energy wasting, sarcopenia, frailty
Depression, cognitive impairment, sexual dysfunction, restless legs
Increased infection risk and increased malignancy risk (especially urothelial)
AKI - CKD is the strongest risk factor for AKI, and each AKI accelerates CKD

Progression is usually linear for a given patient - plot eGFR over time and extrapolate to RRT
- A sudden deviation means a superimposed insult (AKI, obstruction, drug, volume depletion), not natural history
Rapid progression = eGFR decline >5 mL/min/1.73m2 per year
Most people with CKD die - of cardiovascular disease - before reaching ESKD
KFRE (age, sex, eGFR, ACR) gives 2- and 5-yr kidney failure risk and drives referral and access planning

Predictors of progression

Albuminuria - the single strongest modifiable predictor
Lower baseline eGFR, hypertension, poor glycaemic control, male sex, smoking, obesity
Interstitial fibrosis and tubular atrophy on biopsy
Repeated AKI episodes, ongoing nephrotoxin exposure, Aboriginal and Torres Strait Islander identity

Monitoring intervals (eGFR + ACR)

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