Chronic Kidney Disease (CKD) Overview

📋 Key Information Summary

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Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for >3 months, with implications for health — staged by GFR (G1–G5) and albuminuria (A1–A3) using the KDIGO 2012 classification.
CKD prevalence in Australia is approximately 11% of the adult population; rates are significantly higher among Aboriginal and Torres Strait Islander peoples.
The leading causes of CKD in Australia are diabetic nephropathy, hypertensive nephrosclerosis, and glomerulonephritis — identification of the underlying aetiology is critical for targeted management.
Albuminuria (ACR ≥3 mg/mmol) is an independent risk factor for CKD progression, cardiovascular events, and all-cause mortality — it must be quantified at diagnosis and monitored regularly.
Key complications include renal anaemia (EPO deficiency), CKD-mineral and bone disorder (CKD-MBD), cardiovascular disease, metabolic acidosis, and hyperkalaemia.
ACE inhibitors or ARBs are first-line renoprotective agents in albuminuric CKD (A2–A3) regardless of diabetes status — monitor potassium and creatinine within 1–2 weeks of initiation.
SGLT2 inhibitors (dapagliflozin, empagliflozin) are now PBS-listed for CKD with eGFR ≥20 mL/min/1.73 m² and provide significant renoprotective and cardioprotective benefits independent of glycaemic control.
Finerenone (non-steroidal MRA) is PBS-listed for diabetic kidney disease and reduces CKD progression and cardiovascular risk on top of standard therapy.
Blood pressure target <130/80 mmHg is recommended for most CKD patients with albuminuria; treat with lifestyle modification and pharmacotherapy.
Renal anaemia management uses iron repletion (ferritin >100 µg/L, TSAT >20%) before considering erythropoiesis-stimulating agents (ESAs) — haemoglobin target 100–115 g/L.
CKD-MBD management centres on phosphate restriction, phosphate binders, vitamin D analogues, and cinacalcet for secondary hyperparathyroidism in dialysis patients.
Timely nephrology referral is indicated for eGFR <30 mL/min/1.73 m², rapid decline (>5 mL/min/year), persistent ACR ≥30 mg/mmol, or difficult-to-manage complications.
Progression to end-stage kidney disease (ESKD, G5D) requires renal replacement therapy — haemodialysis, peritoneal dialysis, or kidney transplantation — with advance care planning initiated well in advance.
Cardiovascular disease is the leading cause of death in CKD patients — manage lipids, encourage smoking cessation, optimise glycaemic control, and consider antiplatelet therapy where indicated.

Introduction & Australian Epidemiology

Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for >3 months, with implications for health. CKD encompasses a broad spectrum of conditions ranging from mild dysfunction detectable only by laboratory abnormalities to end-stage kidney disease (ESKD) requiring renal replacement therapy. The condition is classified using the Kidney Disease: Improving Global Outcomes (KDIGO) 2012 framework, which stratifies patients by estimated glomerular filtration rate (G1–G5) and albuminuria category (A1–A3).

In Australia, CKD represents a significant public health burden. According to the Australian Institute of Health and Welfare (AIHW), approximately 1.7 million Australians (11% of the adult population) have indicators of CKD, though many remain undiagnosed due to the asymptomatic nature of early disease. CKD was recorded as an associated cause of over 17,000 deaths in Australia in 2021, and it is a leading contributor to the burden of cardiovascular disease.

The prevalence of CKD rises sharply with age: approximately 30% of Australians aged ≥75 years have an eGFR <60 mL/min/1.73 m². Diabetic kidney disease is the single most common cause of CKD in Australia, followed by hypertensive nephrosclerosis and glomerulonephritis. Aboriginal and Torres Strait Islander peoples experience CKD at rates 2–4 times higher than non-Indigenous Australians, with earlier onset and faster progression to ESKD.

The economic burden of CKD in Australia is substantial, with direct healthcare costs exceeding billion annually when dialysis and transplantation are included. Early detection through targeted screening (urine albumin-to-creatinine ratio and serum creatinine with eGFR calculation) remains the cornerstone of CKD management, enabling timely intervention to slow progression and reduce complications.

CKD Classification (KDIGO G & A Staging)

The KDIGO 2012 classification system uses two orthogonal axes — glomerular filtration rate (G-stage) and albuminuria (A-stage) — to define CKD severity and prognostic risk. Both axes are independently associated with adverse outcomes including progression to ESKD, cardiovascular events, and all-cause mortality.

GFR Categories (G-Stage)

G-Stage	eGFR (mL/min/1.73 m²)	Description
G1	≥90	Normal or high — with evidence of kidney damage (albuminuria, haematuria, structural abnormality)
G2	60–89	Mildly decreased — with evidence of kidney damage
G3a	45–59	Mildly to moderately decreased
G3b	30–44	Moderately to severely decreased
G4	15–29	Severely decreased
G5	<15	Kidney failure (ESKD if on dialysis = G5D)

Albuminuria Categories (A-Stage)

A-Stage	ACR (mg/mmol)	Approximate Equivalent	Description
A1	<3	<30 mg/g	Normal to mildly increased
A2	3–30	30–300 mg/g	Moderately increased (formerly "microalbuminuria")
A3	>30	>300 mg/g	Severely increased (formerly "macroalbuminuria")

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CKD diagnosis requires duration >3 months: A single abnormal eGFR or ACR does not confirm CKD. Abnormalities must be present on at least two occasions separated by ≥3 months, unless structural or histological evidence of kidney damage is present (e.g., polycystic kidney disease on imaging, biopsy-proven glomerulonephritis).

Combined Risk Stratification (G × A Grid)

The KDIGO heat-map combines G-stage and A-stage to assign overall risk:

Risk Category	Typical G/A Combinations	Monitoring Frequency
Low risk	G1A1, G2A1	Annually
Moderate risk	G1A2, G2A2, G3aA1	Every 6 months
High risk	G3aA2, G3bA1, G3bA2, G4A1	Every 3–4 months
Very high risk	G3aA3, G3bA3, G4A2–A3, G5A1–A3	Every 1–3 months

Pathophysiology & Causes

CKD arises from a wide range of acute and chronic insults to the kidney. Regardless of the initial aetiology, common pathophysiological pathways converge on nephron loss, interstitial fibrosis, and tubular atrophy — a process often termed the "final common pathway" of CKD progression.

Mechanisms of Progressive Nephron Loss

Glomerular hyperfiltration: Loss of functioning nephrons causes compensatory hyperfiltration in remaining glomeruli, leading to increased intraglomerular pressure, podocyte injury, and progressive glomerulosclerosis.
Tubulointerstitial fibrosis: Chronic hypoxia, inflammation, and activation of fibroblasts drive collagen deposition in the renal interstitium, correlating more closely with declining function than glomerular changes.
Renin-angiotensin-aldosterone system (RAAS) activation: Sustained RAAS activation promotes vasoconstriction, sodium retention, fibrosis, and inflammation — central to both hypertensive nephrosclerosis and diabetic nephropathy.
Chronic inflammation and oxidative stress: Uraemic toxins, advanced glycation end-products, and immune dysregulation perpetuate a pro-inflammatory milieu accelerating nephron loss.

Major Causes of CKD in Australia

Aetiology	Proportion (approx.)	Key Features
Diabetic nephropathy	~35%	Type 2 DM > Type 1; progressive albuminuria, nodular glomerulosclerosis (Kimmelstiel-Wilson)
Hypertensive nephrosclerosis	~25%	Arterionephrosclerosis; risk ↑ with age, ATSI ethnicity; ACR usually A1–A2
Glomerulonephritis	~15%	IgA nephropathy most common primary GN in Australia; lupus nephritis, ANCA vasculitis
Polycystic kidney disease	~5%	ADPKD — bilateral renal cysts, positive family history; ADPLD less common
Reflux nephropathy / chronic pyelonephritis	~5%	Paediatric reflux leading to scarring; more common in females
Other / unknown	~15%	Obstructive uropathy, NSAID nephropathy, ischaemic nephropathy, myeloma cast nephropathy

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Renal biopsy: When the underlying aetiology is unclear — particularly with active urine sediment, rapid decline in GFR, or nephrotic-range proteinuria — referral for renal biopsy provides definitive histological diagnosis and guides immunosuppressive therapy.

Complications (Anaemia, Bone Disease, CVD)

CKD has systemic consequences far beyond the kidney. As GFR declines, a constellation of metabolic, haematological, cardiovascular, and musculoskeletal complications emerge, collectively driving morbidity and mortality. Identification and proactive management of these complications is central to CKD care.

Renal Anaemia

Anaemia is a common complication of CKD, affecting approximately 50% of patients with eGFR <30 mL/min/1.73 m². The primary mechanism is reduced erythropoietin (EPO) production by peritubular interstitial cells, compounded by iron deficiency (absolute or functional), uraemic inhibition of erythropoiesis, chronic inflammation (hepcidin-mediated iron sequestration), and shortened red cell survival.

Mild

Hb 100–115 g/L

Often asymptomatic; check iron studies first. Optimise iron stores before considering ESA therapy.

Setting: Primary care / nephrology outpatients

Moderate

Hb 80–99 g/L

Fatigue, exertional dyspnoea, reduced exercise tolerance. Iron repletion ± ESA initiation indicated.

Setting: Nephrology management

Severe

Hb <80 g/L

Symptomatic anaemia; may require transfusion if haemodynamically unstable. Urgent review for bleeding, haemolysis, or nutritional deficiency.

Setting: Hospital / specialist review

Iron targets before ESA initiation: Ferritin >100 µg/L (non-dialysis) or >200 µg/L (dialysis), and transferrin saturation (TSAT) >20%.

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Iron polymaltose (Ferrum H®)

IV iron · Oral iron alternative

IV dose (repletion) 500–1000 mg IV infusion over ≥15 min; dose by Ganzoni formula: Weight (kg) × (Target Hb − Actual Hb) (g/L) × 0.24 + 500

Oral dose Iron polymaltose 100–200 mg PO daily (less effective in CKD due to hepcidin-mediated malabsorption)

Renal adjustment No dose adjustment required

PBS status ✔ PBS General Benefit

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Erythropoietin alfa / Darbepoetin alfa

Eprex® / Aranesp® · ESA

Epoetin alfa (Eprex®) 50 IU/kg SC three times weekly; titrate to Hb 100–115 g/L

Darbepoetin (Aranesp®) 0.45 µg/kg SC every 2 weeks; titrate by response

Key monitoring Hb every 2–4 weeks during titration; do not exceed Hb 130 g/L — increased thrombotic risk

PBS status ⚠ PBS Authority Required

CKD-Mineral and Bone Disorder (CKD-MBD)

CKD-MBD encompasses a spectrum of abnormalities in calcium, phosphate, parathyroid hormone (PTH), and vitamin D metabolism that lead to renal osteodystrophy, vascular calcification, and increased fracture risk. It becomes clinically significant from G3a onwards.

Hyperphosphataemia: Reduced phosphate excretion leads to elevated serum phosphate, driving vascular calcification and secondary hyperparathyroidism. Target serum phosphate 0.9–1.5 mmol/L (G3–G4) and as close to normal as possible (G5/dialysis).
Hypocalcaemia & vitamin D deficiency: Reduced 1-alpha hydroxylase activity impairs calcitriol synthesis, contributing to hypocalcaemia, secondary hyperparathyroidism, and osteomalacia.
Secondary hyperparathyroidism: Sustained hyperphosphataemia, hypocalcaemia, and calcitriol deficiency drive parathyroid gland hyperplasia. Target intact PTH: 2–9 × upper limit of normal for dialysis patients.
Adynamic bone disease: Over-suppression of PTH (excessive cinacalcet or vitamin D) can cause low-turnover bone disease with increased fracture risk.

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Sevelamer carbonate

Renvela® · Non-calcium phosphate binder

Dose 800–1600 mg PO TDS with meals; titrate to phosphate <1.5 mmol/L

Advantage Does not cause hypercalcaemia; may reduce LDL cholesterol and vascular calcification

PBS status ⚠ PBS Authority Required (G4–G5)

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Cinacalcet

Mimpara® · Calcimimetic

Dose 30 mg PO daily; titrate every 2–4 weeks to max 180 mg/day

Indication Secondary hyperparathyroidism in dialysis patients (PTH >2 × ULN despite vitamin D and phosphate management)

Monitoring Corrected calcium at 1 week and monthly; risk of symptomatic hypocalcaemia

PBS status ⚠ PBS Authority Required

Cardiovascular Disease in CKD

Cardiovascular disease (CVD) is the leading cause of death in CKD patients, accounting for approximately 40–50% of all deaths in this population. CKD is now recognised as an independent cardiovascular risk equivalent. The relationship between CKD and CVD is bidirectional — CVD accelerates kidney decline through renal hypoperfusion and atheroembolic disease.

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CVD risk in CKD: Patients with eGFR <60 mL/min/1.73 m² have a 2–3-fold increased risk of cardiovascular death compared to the general population. Standard risk calculators (e.g., Framingham) underestimate risk in CKD — consider CKD as a high-risk state warranting aggressive primary and secondary prevention.

Left ventricular hypertrophy (LVH): Present in >70% of patients starting dialysis; driven by volume overload, hypertension, and anaemia.
Heart failure: Both heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF) are common; cardiorenal syndrome complicates management.
Atherosclerotic CVD: Accelerated atherosclerosis due to dyslipidaemia, chronic inflammation, oxidative stress, and vascular calcification.
Arrhythmias: Hyperkalaemia and uraemia predispose to atrial fibrillation; sudden cardiac death is a major cause of mortality in dialysis patients.
Vascular calcification: Medial arterial calcification (Mönckeberg type) is particularly prevalent in CKD-MBD, contributing to arterial stiffness and systolic hypertension.

Lipid management: Atorvastatin 10–80 mg daily or rosuvastatin 10–40 mg daily is recommended for CKD patients aged 50–75 years with eGFR <60 mL/min/1.73 m² (regardless of baseline LDL). No dose adjustment is required for statins in CKD, but combination with fibrates should be avoided. The SHARP trial demonstrated a 17% reduction in major atherosclerotic events with simvastatin/ezetimibe in CKD patients not on dialysis.

Management & Slowing Progression

The primary goals of CKD management are to slow the rate of GFR decline, prevent or manage complications, reduce cardiovascular risk, and prepare for renal replacement therapy if needed. Management is tailored to the underlying aetiology, CKD stage, and individual patient factors.

Blood Pressure Control

Hypertension accelerates CKD progression and is a modifiable cardiovascular risk factor. Target blood pressure is <130/80 mmHg for most CKD patients, particularly those with albuminuria (A2–A3), and <140/90 mmHg for those without albuminuria. Lifestyle modifications (sodium restriction <6 g NaCl/day, weight loss, regular exercise, limited alcohol) are first-line adjuncts to pharmacotherapy.

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Perindopril

Coversyl® · ACE inhibitor

Adult dose 5–10 mg PO daily; start 2.5 mg if eGFR <30 or elderly

Renal adjustment Start low; titrate cautiously in eGFR <30. Monitor K⁺ and creatinine at 1–2 weeks.

Key indication First-line renoprotection in albuminuric CKD (A2–A3); reduces intraglomerular pressure and proteinuria

PBS status ✔ PBS General Benefit

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Irbesartan

Karvea® · ARB

Adult dose 150–300 mg PO daily

Renal adjustment No specific dose reduction; monitor K⁺ and creatinine

Key indication Alternative to ACEi if ACEi-intolerant (e.g., cough). Do NOT combine ACEi + ARB — increased hyperkalaemia and AKI risk with no additional benefit.

PBS status ✔ PBS General Benefit

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ACEi/ARB initiation and monitoring: Expect an initial rise in creatinine of up to 30% — this is acceptable and indicates haemodynamic GFR reduction (not structural damage). Discontinue if creatinine rises >30% or if hyperkalaemia (K⁺ >5.5 mmol/L) persists. Hold during intercurrent illness, peri-operatively, or in the context of dehydration (sick-day rules).

SGLT2 Inhibitors — A Paradigm Shift in CKD Management

SGLT2 inhibitors have emerged as a cornerstone of CKD management, offering renoprotective and cardioprotective benefits independent of glycaemic control. Landmark trials (DAPA-CKD, EMPA-KIDNEY, CREDENCE) demonstrated significant reductions in CKD progression, heart failure hospitalisation, and cardiovascular mortality.

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Dapagliflozin

Forxiga® · SGLT2 inhibitor

Dose 10 mg PO once daily

Indication CKD with eGFR ≥20 mL/min/1.73 m² (with or without diabetes); reduces risk of eGFR decline ≥50%, ESKD, CV death, and HF hospitalisation

Initiation Can initiate down to eGFR 20; may continue below 20 until dialysis. Expect initial eGFR dip (reversible haemodynamic effect).

PBS status ⚠ PBS Authority Required (CKD indication)

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Empagliflozin

Jardiance® · SGLT2 inhibitor

Dose 10 mg PO once daily

Indication CKD with eGFR ≥20 mL/min/1.73 m² (PBS-listed for CKD and heart failure)

PBS status ⚠ PBS Authority Required (CKD/HF indication)

Non-Steroidal MRA — Finerenone

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Finerenone

Kerendia® · Non-steroidal MRA

Dose 10 mg PO daily if eGFR 25–59; 20 mg daily if eGFR ≥60. Reduce to 10 mg if eGFR drops <25.

Indication Diabetic kidney disease (type 2 DM with albuminuria A2–A3) — reduces CKD progression and CV events on top of ACEi/ARB

Monitoring Serum potassium at 4 weeks and every 4 months thereafter; hold if K⁺ >5.5 mmol/L

PBS status ⚠ PBS Authority Required

Glycaemic Control in Diabetic CKD

For patients with diabetic kidney disease, individualised HbA1c targets apply. A target of ≤53 mmol/mol (7.0%) is appropriate for most patients, while less stringent targets (≤64 mmol/mol / 8.0%) may be appropriate for elderly patients or those with limited life expectancy, recurrent hypoglycaemia, or advanced CKD.

Metformin: Safe to continue down to eGFR 30 mL/min/1.73 m²; reduce dose to 500 mg BD at eGFR 30–45. Cease at eGFR <30 due to lactic acidosis risk.
SGLT2 inhibitors: First-line add-on therapy (see above) — glycaemic efficacy reduced in advanced CKD but renoprotective benefit persists.
GLP-1 receptor agonists: Liraglutide (Victoza®) and semaglutide (Ozempic®) have demonstrated cardiovascular and renal benefits. Dose adjustment not required in CKD, but GI side effects may limit use.
Insulin: Requirements may decrease in advanced CKD due to reduced renal insulin clearance — risk of hypoglycaemia increases. Monitor closely and reduce doses as GFR declines.

Metabolic Acidosis

Metabolic acidosis (serum bicarbonate <22 mmol/L) is common in CKD G4–G5 and accelerates muscle wasting, bone disease, and CKD progression. Treatment with oral sodium bicarbonate (600–1200 mg PO TDS) to maintain serum bicarbonate ≥22 mmol/L is recommended. Monitor for sodium/fluid overload and hypokalaemia during therapy.

Hyperkalaemia Management

Hyperkalaemia (K⁺ >5.5 mmol/L) is a common and potentially life-threatening complication, particularly in patients taking ACEi/ARBs, spironolactone, or finerenone. Management strategies include:

Dietary potassium restriction (<2 g/day if recurrent hyperkalaemia)
Sodium zirconium cyclosilicate (Lokelma®) or patiromer (Veltassa®) — novel potassium binders enabling continuation of renoprotective RAAS inhibitor therapy
Loop diuretics (furosemide) to enhance renal potassium excretion
Review medications — cease or reduce K⁺-sparing agents, NSAIDs, trimethoprim

Lifestyle and Dietary Measures

Sodium restriction: <6 g NaCl/day (approximately 2.3 g sodium) — reduces blood pressure, proteinuria, and oedema.
Protein intake: 0.75–1.0 g/kg/day for CKD G3–G4 (not on dialysis); avoid high-protein diets (>1.3 g/kg/day) which accelerate GFR decline. Increase to 1.0–1.2 g/kg/day on dialysis to prevent malnutrition.
Phosphate restriction: 800–1000 mg/day for CKD G4–G5; avoid phosphate additives in processed foods.
Exercise: ≥150 min/week moderate-intensity activity; improves cardiovascular fitness, blood pressure, insulin sensitivity, and quality of life.
Smoking cessation: Essential — smoking accelerates CKD progression and doubles cardiovascular risk.
Weight management: Target BMI 20–25 kg/m²; obesity contributes to glomerular hyperfiltration and nephropathy progression.

Nephrology Referral Criteria

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Refer to nephrology when any of the following are present:

eGFR <30 mL/min/1.73 m² (G4–G5)
Rapid decline in eGFR: >5 mL/min/1.73 m² per year, or >25% decline within 12 months
Persistent albuminuria ACR ≥30 mg/mmol (A3), or rapidly rising albuminuria
Uncertain aetiology — need for renal biopsy
Resistant hypertension (≥4 agents at maximum tolerated doses)
Recurrent nephrolithiasis or structural kidney disease
Hereditary kidney disease (e.g., ADPKD, Alport syndrome)
Planning for renal replacement therapy (pre-emptive transplant workup, dialysis access creation)

Renal Replacement Therapy (RRT)

When CKD progresses to ESKD (G5D, eGFR <10–15 mL/min/1.73 m² with uraemic symptoms), renal replacement therapy becomes necessary. Modality selection depends on patient preference, comorbidities, social circumstances, and geographic accessibility.

Modality	Key Features	Access
Haemodialysis	Centre-based (3×/week, 4–5 hours) or home haemodialysis. Most common modality in Australia.	AV fistula (preferred), AV graft, central venous catheter
Peritoneal dialysis	CAPD (4 exchanges/day) or APD (overnight cycler). Home-based; better preservation of residual renal function.	Tenckhoff catheter
Kidney transplantation	Best long-term survival and quality of life. Living donor preferred; deceased donor waitlist 3–7 years in Australia.	Pre-emptive transplant possible before dialysis initiation
Conservative / supportive care	Appropriate for patients who decline RRT, have limited life expectancy, or significant comorbidities. Focus on symptom management, advance care planning, and palliative care.	N/A

Investigations

A systematic approach to CKD investigation establishes diagnosis, identifies aetiology, stages disease severity, and assesses for complications. The following investigations should be performed at diagnosis and repeated at intervals determined by CKD stage and risk category.

Essential

Serum creatinine with eGFR (CKD-EPI equation)

MBS Item 66500 (renal function). Use CKD-EPI 2021 (race-free) equation. Repeat every 3–12 months depending on stage.

Essential

Urine albumin-to-creatinine ratio (ACR)

MBS Item 66910. First-morning void preferred. Confirm abnormal result (A2–A3) with repeat within 3 months. Repeat annually or per risk category.

Essential

Full blood examination (FBE)

MBS Item 65070. Assess for renal anaemia (normocytic, normochromic). Monitor Hb every 3–6 months in CKD G3–G5.

Essential

Serum electrolytes (Na⁺, K⁺, Cl⁻, HCO₃⁻, urea)

MBS Item 66500. Monitor for hyperkalaemia (especially on ACEi/ARB/finerenone), metabolic acidosis, and uraemia. Frequency: every 3–6 months for G3; monthly or more for G4–G5.

Available

Iron studies (ferritin, TSAT)

MBS Item 66815. Essential if Hb <120 g/L. Target: ferritin >100 µg/L (non-dialysis), >200 µg/L (dialysis); TSAT >20%.

Available

Calcium, phosphate, intact PTH, 25-OH vitamin D

MBS Item 66815 (Ca, PO₄), 66840 (PTH), 66836 (Vit D). Assess CKD-MBD. Check from G3a onwards. PTH frequency: every 6–12 months (G3); every 3–6 months (G4–G5).

Available

Lipid profile (total cholesterol, LDL, HDL, triglycerides)

MBS Item 66509. Assess cardiovascular risk. At diagnosis and annually.

Available

HbA1c (if diabetic)

MBS Item 66552. Target ≤53 mmol/mol (7.0%) for most patients. Every 3–6 months.

Available

Renal ultrasound

MBS Item 55021. At diagnosis in all CKD patients. Assess kidney size (small = chronic), echogenicity, hydronephrosis, cysts, stones, asymmetry. Repeat if clinical change.

Specialist

Renal biopsy

Indicated for unexplained CKD, active sediment, rapid GFR decline, nephrotic syndrome, or suspected GN. Performed by nephrologist under ultrasound guidance.

Specialist

Renal angiogram / CT angiogram

For suspected renovascular disease (renal artery stenosis). Avoid gadolinium contrast in eGFR <30 (nephrogenic systemic fibrosis risk).

Special Populations

🤰 Pregnancy

ACEi/ARBs are absolutely contraindicated in pregnancy — teratogenic (renal dysgenesis, oligohydramnios, pulmonary hypoplasia). Discontinue immediately when pregnancy is planned or confirmed. Switch to labetalol, methyldopa, or nifedipine.

SGLT2 inhibitors: Cease in pregnancy — insufficient safety data.

CKD G1–G2 with A1: Generally tolerates pregnancy well; monitor closely.

CKD G3–G5: High risk of pre-eclampsia, preterm delivery, and accelerated CKD progression. Joint obstetric-nephrology care essential. Consider pre-pregnancy counselling.

Statins: Contraindicated in pregnancy — cease when planning conception.

👶 Paediatrics

eGFR estimation: Use bedside Schwartz formula (eGFR = 0.413 × height [cm] / creatinine [µmol/L]) or CKiD equations in children.

Common causes: Congenital anomalies of the kidney and urinary tract (CAKUT), reflux nephropathy, nephrotic syndrome, and inherited disorders (ADPKD, Alport syndrome).

Growth and development: CKD impairs growth — monitor height velocity; recombinant growth hormone may be indicated in severe CKD with growth failure.

ACEi: Enalapril 0.08–0.6 mg/kg/day PO in divided doses; safe and renoprotective in paediatric CKD.

Specialist care: All paediatric CKD should be managed by a paediatric nephrologist.

👴 Elderly (≥75 years)

eGFR interpretation: Age-related GFR decline is physiological; isolated eGFR 45–59 without albuminuria may represent ageing rather than CKD. Confirm with repeat testing and ACR.

Frailty and polypharmacy: Review medications for renal dosing; cease nephrotoxic agents (NSAIDs, aminoglycosides, iodinated contrast without precautions).

RRT decisions: Dialysis may not extend survival in frail elderly with multiple comorbidities. Shared decision-making and advance care planning are essential. Conservative management is a valid option.

Blood pressure: Avoid excessive lowering — increased fall risk. Target <140/90 mmHg may be more appropriate in frail elderly.

🫘 Dose Adjustment in CKD

Key principle: Many drugs require dose reduction or extended dosing intervals when eGFR <30 mL/min/1.73 m². Use the AMH, eTG, or product information for specific adjustments.

High-risk drugs: Metformin (cease <30), digoxin (renally cleared — reduce dose), DOACs (apixaban preferred in CKD; rivaroxaban and dabigatran require dose reduction), lithium, vancomycin, gentamicin.

NSAIDs: Avoid in CKD — risk of AKI, hyperkalaemia, and accelerated CKD progression. Use paracetamol as first-line analgesic.

Contrast media: Use low-osmolar or iso-osmolar iodinated contrast with IV hydration (NaCl 0.9% 1 mL/kg/hr for 6–12 hours pre/post) if eGFR <45. Avoid gadolinium if eGFR <30.

🫁 Hepatic Impairment

Hepatorenal syndrome: Progressive AKI in advanced cirrhosis — type 1 (rapid) and type 2 (slow). Managed with terlipressin + albumin (if available) and liver transplantation.

Drug metabolism: Compounded impairment with dual hepatic and renal dysfunction. Avoid statins if Child-Pugh C; adjust paracetamol to ≤2 g/day.

Coagulopathy: INR may be elevated but does not necessarily reflect bleeding risk in liver disease — assess with viscoelastic testing (TEG/ROTEM) if available.

🛡️ Immunocompromised

HIV-associated nephropathy: Collapsing FSGS; early ART is renoprotective. Tenofovir alafenamide (TAF) preferred over tenofovir disoproxil fumarate (TDF) to reduce nephrotoxicity.

Transplant recipients: CNI toxicity (tacrolimus, cyclosporine) contributes to chronic allograft nephropathy. Monitor drug levels and eGFR closely.

Infection risk: CKD patients on immunosuppression are at increased risk of opportunistic infections — ensure Pneumocystis prophylaxis, avoid live vaccines.

Vaccination: CKD patients are immunocompromised due to uraemia — prioritise pneumococcal, influenza, hepatitis B, and COVID-19 vaccination. Higher-dose hepatitis B vaccine (H-B-Vax II Dialysis/Fortis) may be required.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health

Epidemiological burden

Aboriginal and Torres Strait Islander peoples experience CKD at 2–4 times the rate of non-Indigenous Australians. ESKD incidence is approximately 6–8 times higher. CKD onset is earlier, progression is faster, and outcomes are poorer across all stages. AIHW data indicate that CKD is the 7th leading contributor to the health gap for Indigenous Australians.

Key risk factors

Type 2 diabetes (prevalence ~3× higher), hypertension, obesity, recurrent childhood infections (post-streptococcal GN), low birth weight/nephron deficit, and socioeconomic disadvantage. Rheumatic heart disease and acute post-streptococcal glomerulonephritis remain significant in remote communities.

Remote and rural access

Many Indigenous Australians live in remote areas with limited access to nephrology services, dialysis units, and pathology. Patients requiring haemodialysis may need to relocate hundreds of kilometres from Country and community, contributing to psychological distress, treatment disengagement, and high rates of dialysis withdrawal. Remote dialysis units and community-based peritoneal dialysis programmes are expanding but remain insufficient.

Cultural safety

CKD care must be delivered in a culturally safe framework. Aboriginal Health Workers and Practitioners (AHW/AHPs) should be integral to the care team. Acknowledge connection to Country, community, and kinship systems. Engage family and community Elders in care planning. Support for Sorry Business, cultural obligations, and traditional healing practices should be incorporated into treatment plans.

Screening recommendations

RACGP and Kidney Health Australia recommend annual screening for CKD in all Aboriginal and Torres Strait Islander adults aged ≥18 years with diabetes or hypertension, and all adults aged ≥30 years in the context of periodic health assessments (MBS 715). Screen with urine ACR and serum creatinine (eGFR).

AMR considerations

Higher rates of antibiotic-resistant organisms in remote communities, including CA-MRSA and ESBL-producing Gram-negative bacteria, may complicate management of CKD-associated infections (e.g., urinary tract infections, dialysis access infections). Antibiotic selection should be guided by local antibiograms and AMR data. RHDAustralia guidelines apply for rheumatic heart disease management in the context of CKD.

Transplant access

Indigenous Australians are significantly underrepresented on kidney transplant waitlists. Barriers include geographical isolation, delayed referral, psychosocial factors, and comorbidity burden. Active efforts to improve transplant access include dedicated Indigenous transplant coordinators, pre-emptive transplant workup, and culturally appropriate education programmes.

Closing the Gap

Addressing CKD disparities requires a multi-pronged approach: early screening and detection, management of diabetes and hypertension in primary care, expanding dialysis services in remote areas, improving transplant access, investing in the Indigenous health workforce, and addressing the social determinants of health (housing, nutrition, education, employment). The National Agreement on Closing the Gap (2020) includes health outcome targets relevant to CKD.

📚 References

1. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International Supplements. 2013;3(1):1–150.
2. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney International. 2024;105(4S):S117–S314.
3. Australian Institute of Health and Welfare (AIHW). Chronic kidney disease: Australian facts. Cat. no. PHE 227. Canberra: AIHW; 2023.
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