Management of the patient with CKD in palliative care

Three simultaneous jobs

Three simultaneous jobs, and they are separate:
- 1. Slow progression (BP, RAS blockade, SGLT2i, ns-MRA, acidosis)
- 2. Reduce cardiovascular risk - most CKD patients die of cardiovascular disease before reaching dialysis
- 3. Treat the complications of uraemia (anaemia, CKD-MBD, acidosis, K+, malnutrition)
Plus prescribing safely and planning for RRT before it is needed
Cardiovascular risk rises from CKD G3a and is driven by albuminuria as much as eGFR

~1 in 10 Australian adults have CKD; most are undiagnosed
Aboriginal and Torres Strait Islander peoples: ESKD rates up to 4x the non-Indigenous rate, and far higher in remote communities

Complication	%
Hypertension	82
Secondary hyperparathyroidism	72
Anaemia	51
Metabolic acidosis	31
25-OH vitamin D deficiency	27
Hyperphosphataemia	23
Hypoalbuminaemia	7.5

Nephron loss -> single-nephron hyperfiltration in survivors
- -> glomerular hypertension, podocyte stress, proteinuria
- -> tubulointerstitial inflammation and fibrosis
- -> further nephron loss (self-perpetuating, aetiology-independent)
Proteinuria is not just a marker - filtered protein is directly tubulotoxic. That is why every renoprotective drug lowers albuminuria
How each drug class interrupts the loop
- ACEi/ARB - efferent arteriolar dilatation -> dec intraglomerular pressure
- SGLT2i - restores tubuloglomerular feedback (inc distal Na delivery -> afferent constriction) -> dec hyperfiltration; also metabolic and cardiac benefit
- Non-steroidal MRA (finerenone) - blocks mineralocorticoid receptor-driven inflammation and fibrosis
- GLP-1 RA - weight, glycaemia, and direct anti-inflammatory renal effect (FLOW)

Staging - always eGFR and albuminuria (KDIGO heat map)

G stage	eGFR	A stage	UACR (mg/g)
G1	>=90	A1	<30
G2	60-89	A2	30-300
G3a	45-59	A3	>300
G3b	30-44
G4	15-29
G5	<15

CKD = eGFR <60 OR markers of damage, for >=3 months
*Albuminuria carries as much prognostic weight as eGFR* - G3a/A3 is higher risk than G4/A1
KFRE (Kidney Failure Risk Equation): age, sex, eGFR, UACR -> 2- and 5-year risk of kidney failure. Drives referral and RRT planning

Urinalysis + microscopy, UACR (first-void), renal ultrasound
FBE, UEC, Ca/PO4/PTH/ALP, 25-OH vitamin D, HCO3-, iron studies, lipids, HbA1c
Immunological screen and myeloma screen where the cause is unclear

eGFR <30, KFRE 5-yr risk >5%, UACR >300 mg/g, rapid decline (>5 mL/min/yr), unexplained cause, refractory HTN or K+, inherited disease

A. Slow progression

BP target <120 mmHg systolic (standardised office measurement)
- ACEi or ARB, maximally tolerated dose, for CKD with albuminuria (with or without diabetes) - not both together
- Tolerate a creatinine rise up to 30% and a modest K+ rise; do not stop reflexively
SGLT2i in essentially every proteinuric CKD patient (DAPA-CKD, EMPA-KIDNEY)
- Initiate down to eGFR 20; continue until dialysis or transplant
- Glycaemic effect wanes below eGFR 45 - the cardiorenal benefit does not
- Australian PBS access for dapagliflozin in CKD was widened in 2025 to include eGFR 20-<25 regardless of UACR, and higher eGFR with significant albuminuria
Non-steroidal MRA (finerenone) - add to RASi + SGLT2i in T2DM with albuminuria (FIDELIO/FIGARO); simultaneous initiation with an SGLT2i is now supported (~52% albuminuria reduction)
GLP-1 RA (semaglutide) - kidney and cardiovascular benefit in T2DM + CKD (FLOW); benefit preserved alongside an SGLT2i
Metabolic acidosis: oral NaHCO3 to keep HCO3- >=22 mmol/L - untreated acidosis accelerates decline
Avoid nephrotoxins; minimise IV contrast but do not withhold a needed scan; treat obstruction; stop smoking

B. Cardiovascular risk

Statin in everyone >=50 with CKD not on dialysis (do not initiate de novo on dialysis)
Weight, smoking, glycaemia, aspirin only for secondary prevention

C. Anaemia of CKD

Correct iron first: target ferritin >100 microgram/L and TSAT >20% before starting an ESA
- On ESA therapy: ferritin 200-500 microgram/L, TSAT 20-30%
ESA target Hb 100-115 g/L - do not normalise; higher targets increase stroke, VTE and mortality
Exclude B12/folate deficiency, blood loss, haemolysis, myeloma before attributing to CKD
HIF prolyl-hydroxylase inhibitors (daprodustat, roxadustat) - oral alternative, limited Australian availability

D. Prescribing in CKD

Diabetes agents
- Metformin down to eGFR 30; dose-reduce below 45; withhold when sick (lactic acidosis)
- DPP-4 inhibitors - usable at eGFR <30 with dose adjustment (linagliptin needs none)
- Sulfonylureas - accumulate, hypoglycaemia; avoid glibenclamide
- Insulin requirements fall as eGFR falls (reduced renal insulin clearance)
Avoid NSAIDs, aminoglycosides, high-dose ciprofloxacin, lithium without monitoring
Tenofovir disoproxil (TDF) - avoid at CKD G3-5; causes proximal tubulopathy with hypophosphataemia, hypomagnesaemia, glycosuria. *Tenofovir alafenamide (TAF) has substantially lower nephrotoxicity and is now the usual choice*
Dose by absolute CrCl (Cockcroft-Gault), not body-surface-normalised eGFR, for narrow-therapeutic-index drugs (DOACs, digoxin, vancomycin)

E. Sick day rules - give in writing

Withhold during acute illness with volume depletion: ACEi/ARB, ARNI, diuretics, metformin, SGLT2i, NSAIDs, MRA
SGLT2i also: euglycaemic DKA risk - withhold 3 days pre-operatively and during acute illness or fasting

F. Preparing for kidney failure

Education and modality choice at eGFR ~20 or KFRE 2-yr risk >10%
Vein preservation (no cannulation or PICC in the non-dominant forearm); AV fistula ~6 months before anticipated need
Pre-emptive transplant workup at eGFR ~15-20; live donor is the best outcome
Hepatitis B vaccination (double dose, 4 doses), influenza, COVID, pneumococcal
Advance care planning and conservative kidney management as a legitimate pathway in the frail elderly

Cardiovascular disease - LVH, heart failure, AF, accelerated atherosclerosis, sudden cardiac death
Anaemia, CKD-MBD, hyperkalaemia, metabolic acidosis, hyperuricaemia
Protein-energy wasting - inflammation + acidosis + anorexia; predicts mortality better than any biochemical marker
Uraemic pruritus, restless legs, sleep disturbance, sexual dysfunction
Depression - very common, under-treated
Increased infection risk (uraemic immune dysfunction) and increased malignancy risk
Cognitive impairment, gout, secondary and tertiary hyperparathyroidism

Decline is usually linear for a given patient - plot 1/creatinine or eGFR over time and extrapolate
- An abrupt deviation means a superimposed insult, not natural progression
Most CKD patients die - of cardiovascular disease - before reaching ESKD
AKI on CKD is the commonest accelerant; each episode leaves a lower baseline

inc muscle protein degradation -> muscle wasting
Bone dissolution -> renal bone disease, hypercalciuria, stones
dec albumin synthesis -> hypoalbuminaemia
Accelerated CKD progression, inflammation, impaired insulin secretion and sensitivity, beta-2 microglobulin amyloid, increased mortality

Rapid progression = eGFR decline >5 mL/min/1.73m2/yr - triggers reassessment of cause and adherence

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