Home Family Medicine Chronic Kidney Disease

Chronic Kidney Disease

📋 Key Information Summary

📋
  • Chronic kidney disease (CKD) is defined as GFR <60 mL/min/1.73 m² and/or markers of kidney damage (albuminuria, haematuria, structural abnormality) persisting for ≥3 months.
  • CKD staging uses two axes: GFR category (G1–G5) and albuminuria category (A1–A3) — both independently predict cardiovascular and renal outcomes.
  • Diabetes mellitus and hypertension account for >70 % of CKD in Australia; Aboriginal and Torres Strait Islander peoples carry a disproportionate burden.
  • CKD is often asymptomatic until advanced stages; routine screening with eGFR and uACR is recommended for high-risk groups.
  • First-line renoprotective therapy comprises an SGLT2 inhibitor (dapagliflozin or empagliflozin) plus an ACE inhibitor or ARB, titrated to maximum tolerated dose.
  • Finerenone (non-steroidal MRA) reduces progression and cardiovascular events in CKD with type 2 diabetes; now PBS-listed.
  • Acute kidney injury (AKI) is diagnosed by KDIGO criteria (rise in creatinine ≥26.5 µmol/L within 48 h or ≥1.5 × baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 h).
  • AKI and CKD are bidirectional risk factors — AKI accelerates CKD progression and pre-existing CKD increases AKI susceptibility.
  • Referral to nephrology is indicated for GFR <30, rapid decline (>5 mL/min/year), persistent A3 albuminuria, difficult-to-control hypertension, or suspected glomerulonephritis.
  • Manage cardiovascular risk aggressively: BP target <130/80 mmHg, statin therapy (atorvastatin), smoking cessation, and lifestyle modification.
  • Monitor electrolytes (potassium, bicarbonate, calcium, phosphate) and haemoglobin as CKD progresses; initiate erythropoiesis-stimulating agents for symptomatic CKD-related anaemia.
  • Nephrotoxic medications (NSAIDs, aminoglycosides, iodinated contrast) must be used cautiously or avoided in CKD; review all medications against renal function regularly.

Introduction & Australian Epidemiology

Chronic kidney disease (CKD) is a progressive condition characterised by structural or functional abnormalities of the kidneys persisting for ≥3 months. It encompasses a spectrum from mild kidney damage with preserved filtration to end-stage kidney disease (ESKD) requiring renal replacement therapy. CKD is a major public health concern in Australia: approximately 1.7 million Australians have evidence of CKD (stages 1–5), yet fewer than 10 % are aware of their diagnosis. CKD is the 10th leading cause of death in Australia and a powerful independent risk factor for cardiovascular disease, hospitalisation, and all-cause mortality.

The Australian Institute of Health and Welfare (AIHW) estimates that CKD contributes to nearly 15,000 deaths annually. In 2022, over 14,000 Australians received kidney replacement therapy (dialysis or transplant), with the ANZDATA Registry reporting a transplant rate of approximately 35 per million population. Diabetes is the leading cause of ESKD, followed by glomerulonephritis and hypertension.

⚠️
Health inequity: Aboriginal and Torres Strait Islander peoples experience CKD at 2.2 times the rate of non-Indigenous Australians and progress to ESKD at younger ages. Rural and remote communities face additional barriers to screening, monitoring, and specialist access.

Early identification and management of CKD in primary care can slow progression, reduce cardiovascular events, and delay or prevent the need for dialysis. General practitioners are central to this effort, as most CKD is managed in the community rather than in nephrology clinics.

CKD Classification & Staging

CKD is classified using the KDIGO 2012 system, which employs a two-dimensional grid based on estimated glomerular filtration rate (eGFR) and albuminuria. The GFR category (G1–G5) reflects the level of kidney function, while the albuminuria category (A1–A3) reflects the degree of kidney damage. Both axes independently predict the risk of CKD progression, cardiovascular events, and mortality.

GFR Categories

Stage eGFR (mL/min/1.73 m²) Description
G1 ≥90 Normal or high (kidney damage markers present)
G2 60–89 Mildly decreased
G3a 45–59 Mildly to moderately decreased
G3b 30–44 Moderately to severely decreased
G4 15–29 Severely decreased
G5 <15 Kidney failure

Albuminuria Categories

Category uACR (mg/mmol) AER (mg/24 h) Description
A1 <3.0 <30 Normal to mildly increased
A2 3.0–30.0 30–300 Moderately increased (previously "microalbuminuria")
A3 >30.0 >300 Severely increased (previously "macroalbuminuria")

KDIGO Risk Stratification Grid

The intersection of GFR and albuminuria categories determines overall risk and guides monitoring frequency and referral urgency:

A1 (<3 mg/mmol) A2 (3–30 mg/mmol) A3 (>30 mg/mmol)
G1 (≥90) Low risk Moderate risk High risk
G2 (60–89) Low risk Moderate risk High risk
G3a (45–59) Moderate risk High risk Very high risk
G3b (30–44) High risk Very high risk Very high risk
G4 (15–29) Very high risk Very high risk Very high risk
G5 (<15) Very high risk Very high risk Very high risk
ℹ️
Coding note: Use the SNOMED CT concept for CKD staging and MBS item 69971 (eGFR) and 69981 (uACR) for Medicare-billed pathology monitoring in Australian general practice.

Causes & Risk Factors

Major Causes of CKD in Australia

Cause Proportion (%) Notes
Diabetic kidney disease ~36 % Leading cause; both type 1 and type 2 diabetes
Glomerulonephritis ~18 % IgA nephropathy most common primary GN in Australia
Hypertension / vascular ~15 % Often co-exists with diabetes
Polycystic kidney disease ~5 % ADPKD is most common inherited cause
Reflux nephropathy ~4 % Often diagnosed in childhood
Obstructive uropathy ~4 % BPH, urolithiasis, malignancy
Other / unknown ~18 % Analgesic nephropathy, amyloidosis, myeloma, etc.

Risk Factors for Developing CKD

  • Modifiable: Hypertension, diabetes mellitus, obesity, smoking, dyslipidaemia, recurrent UTI, nephrotoxic medication use (NSAIDs, lithium, aminoglycosides)
  • Non-modifiable: Age >60 years, family history of CKD or ESKD, Aboriginal or Torres Strait Islander heritage, prior AKI, low birth weight, cardiovascular disease history
  • Structural: Solitary kidney, renal tract malformations, previous nephrectomy, prostatic hypertrophy
🚨
Nephrotoxin alert: Long-term NSAID use (including OTC ibuprofen and naproxen) is a preventable cause of CKD progression and AKI. In patients with eGFR <60, avoid regular NSAID use. Where unavoidable, use the lowest dose for the shortest duration and monitor renal function within 1–2 weeks.

Clinical Approach & Investigations

When to Screen for CKD

Screen with eGFR and urine albumin-to-creatinine ratio (uACR) in all patients with:

  • Diabetes mellitus (type 1 from 5 years after diagnosis; type 2 at diagnosis) — annually
  • Hypertension — at diagnosis and periodically
  • Cardiovascular disease (coronary artery disease, heart failure, peripheral vascular disease, cerebrovascular disease)
  • Family history of CKD or ESKD
  • Obesity (BMI ≥30 kg/m²)
  • Smokers (current or ex)
  • Aboriginal and Torres Strait Islander adults aged ≥18 years — at annual health check (MBS 715)
  • History of recurrent nephrolithiasis
  • Incidental findings: haematuria, proteinuria, structural abnormality on imaging

Initial Investigations

Essential
Serum creatinine with eGFR (CKD-EPI equation)
MBS 66511. Use CKD-EPI 2021 creatinine equation (race-free). Confirm abnormal result at 3 months before diagnosing CKD.
Essential
Urine albumin-to-creatinine ratio (uACR)
MBS 69981. First-void morning specimen preferred. Abnormal if ≥3.0 mg/mmol. Confirm with repeat sample.
Essential
Urinalysis with microscopy
Assess for haematuria, casts (RBC casts suggest glomerulonephritis), leucocytes, crystals.
Available
Full blood count
Assess for anaemia (normocytic normochromic in CKD-related erythropoietin deficiency).
Available
Electrolytes, bicarbonate, calcium, phosphate, PTH
CKD-mineral bone disease (CKD-MBD) monitoring. Abnormalities typically emerge at G3b–G4.
Available
Lipid studies
Cardiovascular risk assessment — CKD is a coronary risk equivalent.
Available
HbA1c (if diabetic)
Glycaemic control monitoring. Note: may be unreliable in advanced CKD (G4–G5).
Specialist
Renal ultrasound
Indicated if: suspected obstruction, polycystic kidney disease, unexplained CKD, prior to nephrology referral. Assess kidney size, cortical thickness, hydronephrosis, and echogenicity.
Specialist
Autoimmune serology (ANA, ANCA, anti-GBM, complement, immunoglobulins)
If glomerulonephritis suspected: haematuria + proteinuria, rapid decline in eGFR, systemic features.

Confirming the Diagnosis

CKD requires either a GFR <60 mL/min/1.73 m² or markers of kidney damage (albuminuria, haematuria, electrolyte abnormalities, structural abnormality) present on at least two occasions separated by ≥3 months. This distinguishes CKD from acute kidney injury.

Monitoring Frequency

Risk Category eGFR Monitoring uACR Monitoring
Low (G1–G2, A1) Every 12 months Every 12 months
Moderate (G1–G2 A2, G3a A1) Every 6–12 months Every 6–12 months
High (G3a A2–A3, G3b) Every 3–6 months Every 3–6 months
Very high (G4–G5) Every 1–3 months Every 3 months

Management of CKD

Renoprotective Pharmacotherapy

The cornerstone of CKD management is dual blockade of the renin-angiotensin system and the sodium-glucose cotransporter 2 pathway. The CREDENCE, DAPA-CKD, and EMPA-KIDNEY trials demonstrated significant renoprotective and cardioprotective benefits of SGLT2 inhibitors across a broad CKD population, regardless of diabetes status.

💊
Perindopril
Coversyl® · ACE inhibitor
Adult dose 5 mg PO once daily; titrate to 10 mg daily
Renal adjustment Initiate at 2.5 mg daily if eGFR <30; monitor K⁺ and creatinine within 1–2 weeks
PBS status ✔ PBS General Benefit
💊
Irbesartan
Avapro® · ARB
Adult dose 150 mg PO once daily; titrate to 300 mg daily
Renal adjustment Start 75 mg if eGFR <30; monitor K⁺ and creatinine
PBS status ✔ PBS General Benefit
💊
Dapagliflozin
Forxiga® · SGLT2 inhibitor
Adult dose 10 mg PO once daily
Renal adjustment Initiate if eGFR ≥20 mL/min/1.73 m² (KDIGO 2024); may continue below this if already tolerated
PBS status ✔ PBS General Benefit (with authority for CKD indication)
💊
Empagliflozin
Jardiance® · SGLT2 inhibitor
Adult dose 10 mg PO once daily
Renal adjustment Initiate if eGFR ≥20 mL/min/1.73 m²
PBS status ✔ PBS General Benefit (with authority for CKD indication)
💊
Finerenone
Kerendia® · Non-steroidal MRA
Adult dose 10 mg PO once daily (20 mg if K⁺ ≤4.8 mmol/L after 4 weeks)
Indication CKD (G2–G4 with A2–A3) with type 2 diabetes, on maximum tolerated ACEi/ARB
Renal adjustment Not recommended if eGFR <25; monitor K⁺ at 4 weeks, then every 4 months
PBS status Authority Required
Triple therapy: KDIGO 2024 recommends an ACEi/ARB + SGLT2 inhibitor as first-line for all patients with CKD at risk of progression. Add finerenone in those with type 2 diabetes and persistent albuminuria despite dual therapy. This combination addresses complementary pathophysiological pathways and maximises renoprotection.

Blood Pressure Management

  • Target: Systolic <120 mmHg (office) for most CKD patients per SPRINT-trial evidence; at minimum <130/80 mmHg.
  • ACEi or ARB is first-line (do not combine ACEi + ARB — increased hyperkalaemia and AKI risk without benefit).
  • Second-line agents: dihydropyridine CCB (amlodipine), thiazide-like diuretic (indapamide), or mineralocorticoid receptor antagonist.
  • Monitor serum potassium and creatinine 1–2 weeks after initiating or uptitrating RAAS blockade.

Cardiovascular Risk Reduction

  • Statin therapy: Atorvastatin 20–80 mg daily for all CKD patients ≥50 years or with additional CV risk factors. CKD is a coronary risk equivalent. ✔ PBS General Benefit
  • Antiplatelet: Low-dose aspirin (100 mg daily) for secondary prevention; primary prevention benefit less certain in CKD.
  • Smoking cessation: Counselling + pharmacotherapy (varenicline or NRT) — strongest modifiable CV risk factor.
  • Weight management: Target BMI 18.5–25 kg/m²; consider GLP-1 receptor agonists (semaglutide) for dual CV and potential renal benefit.

Management of CKD Complications

CKD-Related Anaemia

Monitor haemoglobin from G3a onwards. Initiate investigation when Hb <110 g/L. Iron deficiency is the most common correctable cause — aim ferritin >100 µg/L (or >200 µg/L if on ESA) and transferrin saturation >20 %. Use IV iron (ferric carboxymaltose) if oral iron intolerant or insufficient. Erythropoiesis-stimulating agents (ESAs) such as darbepoetin alfa (Aranesp®) are indicated once iron stores are replete and Hb remains <100 g/L — target Hb 100–115 g/L.

CKD-Mineral Bone Disease (CKD-MBD)

  • Monitor calcium, phosphate, and PTH from G3b onwards.
  • Phosphate binders (calcium carbonate or sevelamer) if phosphate >1.5 mmol/L despite dietary restriction.
  • Vitamin D: Cholecalciferol 1000–2000 IU daily for 25-OH vitamin D <50 nmol/L. Calcitriol reserved for G4–G5 with elevated PTH under specialist guidance.

Metabolic Acidosis

Target serum bicarbonate ≥22 mmol/L. Oral sodium bicarbonate 500 mg–1 g TDS (or sodium bicarbonate tablets 840 mg) may slow CKD progression. Monitor for sodium and fluid overload.

Hyperkalaemia

Common barrier to optimal RAAS blockade. Dietary potassium counselling, ensure adequate diuresis, correct acidosis. Patiromer (Veltassa®) or sodium zirconium cyclosilicate (Lokelma®) are potassium binders that allow continuation of ACEi/ARB/finerenone — available via authority PBS for recurrent hyperkalaemia.

Nephrology Referral Criteria

⚠️
Refer to nephrology if:
  • eGFR <30 mL/min/1.73 m² (G4–G5)
  • Rapid decline in eGFR: >5 mL/min/year or >25 % drop from baseline
  • Persistent A3 albuminuria (uACR >30 mg/mmol) despite 3 months of RAAS blockade
  • Suspected glomerulonephritis (haematuria + proteinuria, RBC casts)
  • Difficult-to-control hypertension (≥4 agents)
  • Refractory hyperkalaemia or metabolic acidosis
  • Hereditary kidney disease (e.g., ADPKD, Alport syndrome)
  • Recurrent nephrolithiasis with CKD

Acute Kidney Injury (AKI)

Acute kidney injury (AKI) is a clinical syndrome characterised by a rapid decline in renal function occurring over hours to days. AKI and CKD are closely linked: AKI is both a consequence of and a risk factor for CKD, and recurrent AKI episodes accelerate progression to end-stage kidney disease.

KDIGO AKI Diagnostic Criteria

Criterion Definition
Creatinine rise ≥26.5 µmol/L increase within 48 hours, or ≥1.5 × baseline within 7 days
Urine output <0.5 mL/kg/h for ≥6 hours

AKI Staging (KDIGO)

Stage 1
Mild AKI
Creatinine rise ≥26.5 µmol/L or 1.5–1.9 × baseline; UO <0.5 mL/kg/h for 6–12 h
Setting: Close monitoring, remove offending agents, optimise volume
Stage 2
Moderate AKI
Creatinine 2.0–2.9 × baseline; UO <0.5 mL/kg/h for ≥12 h
Setting: Hospital admission, nephrology consultation, consider ICU
Stage 3
Severe AKI
Creatinine ≥3.0 × baseline or ≥353.6 µmol/L or initiation of RRT; UO <0.3 mL/kg/h for ≥24 h or anuria ≥12 h
Setting: ICU admission, urgent nephrology, likely dialysis

Aetiology — Prerenal, Intrinsic, Postrenal

Category Causes Key Features
Prerenal (~60 %) Dehydration, haemorrhage, sepsis, heart failure, hepatorenal syndrome, ACEi/ARB + diuretic FENa <1 %; bland urine sediment; responds to fluid resuscitation
Intrinsic renal (~30 %) Acute tubular necrosis (ATN — most common), acute interstitial nephritis (AIN), glomerulonephritis, vasculitis, thrombotic microangiopathy Muddy brown casts (ATN); WBC casts (AIN); RBC casts (GN)
Postrenal (~10 %) BPH, calculi, malignancy, retroperitoneal fibrosis, blocked catheter Hydronephrosis on USS; bilateral obstruction or solitary kidney obstruction

AKI Management in Primary Care

1
Stop nephrotoxins
Immediately cease or withhold NSAIDs, aminoglycosides, ACEi/ARBs (temporarily), metformin (if eGFR <30), gadolinium contrast, and high-dose diuretics.
2
Optimise volume status
Oral rehydration if mild; IV 0.9 % sodium chloride 250–500 mL bolus if dehydrated. Avoid fluid overload in heart failure — reassess fluid balance frequently.
3
Exclude obstruction
Renal tract ultrasound if postrenal cause suspected. Ensure urinary catheter is patent if in situ.
4
Urgent referral
Refer to emergency department or nephrology for: Stage 2–3 AKI, hyperkalaemia (K⁺ >6.0 mmol/L), pulmonary oedema, metabolic acidosis (pH <7.2), suspected GN/vasculitis, or need for dialysis.
5
Follow up
Recheck creatinine within 48–72 h. If AKI resolves, recheck at 3 months to assess for residual CKD. If CKD persists, classify and manage per CKD staging.
🚨
Emergency indications for dialysis (AEIOU): Acidosis (pH <7.1 refractory to bicarbonate), Electrolytes (refractory hyperkalaemia), Intoxication (lithium, methanol, ethylene glycol), Overload (pulmonary oedema unresponsive to diuretics), Uraemia (encephalopathy, pericarditis, bleeding).

Contrast-Associated AKI Prevention

For patients with eGFR <45 receiving iodinated contrast: pre-procedure IV 0.9 % NaCl 1 mL/kg/h for 6–12 h (or oral hydration if outpatient); use low-osmolar or iso-osmolar contrast at minimum volume; avoid nephrotoxic co-medications for 48 h; recheck creatinine 48–72 h post-procedure. Gadolinium-based MRI contrast is relatively contraindicated in eGFR <30 (risk of nephrogenic systemic fibrosis).

Special Populations

🤰

Pregnancy

  • ACEi and ARBs are teratogenic — contraindicated in pregnancy (FDA category D). Discontinue at least 3 months pre-conception or immediately if unplanned pregnancy.
  • Safe antihypertensives in pregnancy: labetalol, nifedipine SR, methyldopa.
  • SGLT2 inhibitors are not recommended in pregnancy — discontinue when planning conception.
  • CKD increases risk of pre-eclampsia, fetal growth restriction, preterm delivery, and AKI. Nephrology and obstetric co-management recommended for CKD G3–5.
  • eGFR equations are unreliable in pregnancy; use 24-hour creatinine clearance for monitoring.
👶

Paediatrics

  • Use the bedside CKiD or updated CKiD-U25 eGFR equation for children (not CKD-EPI).
  • Common causes: congenital anomalies of kidney and urinary tract (CAKUT), reflux nephropathy, glomerulonephritis.
  • CKD in children impairs growth — monitor height velocity, refer to paediatric endocrinology if growth faltering.
  • Phosphate binders and ESAs require weight-based dosing. Refer all paediatric CKD to a paediatric nephrologist.
👴

Elderly (≥65 years)

  • Age-related decline in eGFR (~1 mL/min/year after age 40) must be distinguished from pathological CKD. An eGFR of 45–59 in an older adult without albuminuria or other markers may not represent CKD.
  • Frailty and sarcopenia may lead to overestimation of eGFR (creatinine production is reduced). Consider cystatin C-based equations if suspicion.
  • Medication review is critical — polypharmacy is common; renally dose all medications.
  • Shared decision-making for dialysis initiation in the very elderly; conservative kidney care may be appropriate.
🫘

Renal Impairment

  • In patients already on renal replacement therapy, primary care management shifts to cardiovascular risk management, infection prevention, and transplant follow-up.
  • Post-transplant: monitor tacrolimus/ciclosporin levels, renal function, HbA1c, lipids, and skin cancer surveillance.
  • Dialysis access: avoid venepuncture and IV cannulation in the ipsilateral arm of AV fistulae.
🫁

Hepatic Impairment

  • Hepatorenal syndrome (HRS) is a diagnosis of exclusion in cirrhotic patients with rapidly progressive AKI. Requires specialist management (terlipressin + albumin).
  • eGFR equations may overestimate renal function in cirrhosis due to reduced creatinine production. Use cystatin C or measured creatinine clearance.
  • Dose-adjust medications hepatically metabolised that are renally excreted; avoid NSAIDs completely in cirrhosis.
🛡️

Immunocompromised

  • HIV-associated nephropathy (HIVAN): collapsing FSGS, presents with nephrotic-range proteinuria. Antiretroviral therapy is renoprotective.
  • Post-transplant CKD: calcineurin inhibitor nephrotoxicity (tacrolimus, ciclosporin) is common; monitor drug levels and adjust.
  • Immunosuppressed patients with AKI should be assessed for opportunistic infections (CMV, BK virus in transplant) and drug toxicity.

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander peoples experience a disproportionate burden of CKD, with rates 2.2 times higher than the non-Indigenous population. The rate of treated ESKD in remote Indigenous communities is up to 20 times the national average. Culturally safe, community-centred approaches are essential.

Screening
CKD screening is recommended for all Aboriginal and Torres Strait Islander adults aged ≥18 years at every Annual Health Check (MBS item 715). Include eGFR, uACR, HbA1c, BP, and urinalysis. Point-of-care testing (POCT) for eGFR and uACR is available in many Aboriginal Community Controlled Health Organisations (ACCHOs) through the Quality Assurance for Aboriginal and Torres Strait Islander Medical Practices (QAAMS) programme.
Epidemiology
Diabetic kidney disease is the leading cause of ESKD in Indigenous Australians, accounting for >50 % of cases. CKD onset occurs at younger ages, with faster progression to ESKD. Cardiovascular mortality is markedly elevated in Indigenous Australians with CKD.
Remote and rural access
Specialist nephrology services are concentrated in major cities. Telehealth nephrology consultations (MBS items 99200–99215) are funded by Medicare and enable remote specialist review. Patient-assisted travel schemes (PATS) assist with transport to dialysis centres. Satellite dialysis units in regional centres reduce relocation burden.
Cultural safety
Use the AIDA (Australian Indigenous Doctors' Association) cultural safety framework. Engage Aboriginal Health Workers and Aboriginal Health Practitioners in CKD education and management. Acknowledge the social and emotional determinants of health: housing, food security, education, racism, and intergenerational trauma — all of which influence CKD outcomes.
Transplant access
Indigenous Australians are significantly under-represented on kidney transplant waitlists. Barriers include late referral, geographic isolation, cultural concerns about organ donation, and health literacy. Initiatives to improve transplant access include dedicated transplant coordinators and community-based education programmes.
Rheumatic fever and CKD
Endocarditis from rheumatic heart disease can cause immune-complex glomerulonephritis. Acute post-streptococcal glomerulonephritis remains more common in remote Indigenous communities. Consider this aetiology in Indigenous children and young adults presenting with haematuria and oedema following skin or throat infections.
📋
Key resources: Kidney Health Australia's Chronic Kidney Disease Management in Primary Care (4th edition) includes dedicated Indigenous health sections. The RHDAustralia guidelines provide renal dosing for antimicrobials commonly used in remote communities. AIHW reports on Indigenous kidney disease are available at aihw.gov.au.

📚 References

  1. 1. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117–S314.
  2. 2. Kidney Disease: Improving Global Outcomes (KDIGO) AKI Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1–138.
  3. 3. Australian Institute of Health and Welfare. Chronic kidney disease: Australian facts. AIHW Cat. no. PHE 229. Canberra: AIHW; 2023.
  4. 4. ANZDATA Registry. 46th Annual Report 2023. Adelaide: Australia and New Zealand Dialysis and Transplant Registry; 2023.
  5. 5. Kidney Health Australia. Chronic Kidney Disease (CKD) Management in Primary Care. 4th ed. Melbourne: Kidney Health Australia; 2020.
  6. 6. Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and renal outcomes in type 2 diabetes and nephropathy (CREDENCE). N Engl J Med. 2019;380(24):2295–2306.
  7. 7. Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in patients with chronic kidney disease (DAPA-CKD). N Engl J Med. 2020;383(15):1436–1446.
  8. 8. The EMPA-KIDNEY Collaborative Group. Empagliflozin in patients with chronic kidney disease (EMPA-KIDNEY). N Engl J Med. 2023;388(2):117–127.
  9. 9. Bakris GL, Agarwal R, Anker SD, et al. Effect of finerenone on chronic kidney disease outcomes in type 2 diabetes (FIDELIO-DKD). N Engl J Med. 2020;383(23):2219–2229.
  10. 10. SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control (SPRINT). N Engl J Med. 2015;373(22):2103–2116.
  11. 11. Royal Australian College of General Practitioners. Management of type 2 diabetes: A handbook for general practice. Melbourne: RACGP; 2020.
  12. 12. Australian Bureau of Statistics. National Aboriginal and Torres Strait Islander Health Survey 2018–19. ABS Cat. no. 4715.0. Canberra: ABS; 2019.
  13. 13. Hoy WE, Mathews JD, McCredie DA, et al. The multidimensional nature of renal disease: rates and associations of albuminuria in an Australian Aboriginal community. Kidney Int. 1998;54(4):1296–1304.
  14. 14. Caring for Australasians with Renal Impairment (CARI). CARI Guidelines: Early chronic kidney disease. Sydney: CARI; 2022.
  15. 15. National Health and Medical Research Council. NHMRC additional levels of evidence and grades for recommendations for developers of guidelines. Canberra: NHMRC; 2009.
for PBS scripts. Utilise ACCHS pharmacies and Remote Area Aboriginal Health Worker programs for medication supply in remote areas. Avoid initiating benzodiazepines; support holistic pain management including community-based exercise programs.
Preventive health
Promote bone health: encourage vitamin D supplementation (1000 IU daily in deficient individuals), smoking cessation support, reduction of alcohol intake, and weight-bearing exercise. MBS Item 715 health checks provide a structured opportunity to assess bone health, screen for osteoporosis risk factors, and discuss musculoskeletal health in a culturally safe context.

Quick Reference: Differential Diagnosis at a Glance

Costovertebral dysfunction
Paracetamol ± NSAID; manual therapy
2–6 weeks
Provocable on palpation; no red flags
Thoracic compression fracture
Paracetamol; ± calcitonin; DXA + osteoporosis Rx
6–12 weeks healing
Elderly; osteoporosis; acute onset
ACS (posterior MI)
Aspirin 300 mg, GTN, heparin; urgent PCI
Time-critical
ECG, troponin; CV risk factors
Aortic dissection
IV labetalol; urgent CT aortogram; surgery (Type A)
Time-critical
Tearing pain; BP differential >20 mmHg
Vertebral osteomyelitis
IV antibiotics (vancomycin + ceftriaxone initially); ID consult
6 weeks IV antibiotics
Fever, elevated CRP, IV drug use
Biliary colic / cholecystitis
Paracetamol ± morphine; lap cholecystectomy
Surgical within 72 h (cholecystitis)
RUQ/infrascapular; post-prandial; RUQ US

📚 References

  1. 1. Briggs AM, Smith AJ, Straker LM, Bragge P. Thoracic spine pain in the general population: prevalence, incidence and associated factors in children, adolescents and adults. A systematic review. BMC Musculoskelet Disord. 2009;10:77.
  2. 2. National Health and Medical Research Council (NHMRC). Evidence-based management of acute musculoskeletal pain. Canberra: NHMRC; 2003 (updated 2020).
  3. 3. Australian Institute of Health and Welfare (AIHW). Aboriginal and Torres Strait Islander Health Performance Framework: Summary report 2023. Canberra: AIHW; 2023.
  4. 4. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760–765.
  5. 5. Stochkendahl MJ, Kjaer P, Hartvigsen J, et al. National Clinical Guidelines for non-surgical treatment of patients with recent onset low back pain or lumbar radiculopathy. Europ Spine J. 2018;27(1):60–75.
  6. 6. Erwin WM, Jackson PC, Homonko DA. Innervation of the human costovertebral joint: implications for clinical back pain syndromes. J Manipulative Physiol Ther. 2000;23(6):395–403.
  7. 7. Royal Australian College of General Practitioners (RACGP). Guidelines for preventive activities in general practice. 9th edn. Melbourne: RACGP; 2018 (updated 2023).
  8. 8. Hirsch JA, Singh V, Falco FJE, et al. Thoracic facet joint interventions. Pain Physician. 2016;19(4):E581–E593.
  9. 9. Erwin WM, Jackson PC. The costovertebral joint: anatomy, biomechanics, and clinical significance in thoracic back pain syndromes. J Can Chiropr Assoc. 2003;47(2):112–120.
  10. 10. Strayer RJ, Gunnerson JM, Brown LH, et al. Aortic dissection: clinical features, diagnosis, and management. Aust Crit Care. 2019;32(2):144–153.
  11. 11. Ombregt L. A system of orthopaedic medicine. 3rd edn. Edinburgh: Churchill Livingstone Elsevier; 2013. Chapter 18: Thoracic spine.
  12. 12. Lin CC, Chen KH, Li DM, et al. Characteristics and outcomes of patients presenting with thoracic back pain to the emergency department. Emerg Med Australas. 2020;32(5):805–811.
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).
for PBS-listed medicines at participating pharmacies.
Cultural safety
Engagement with Aboriginal Community Controlled Health Organisations (ACCHOs) is essential. Cultural safety training for non-Indigenous clinicians, use of Aboriginal Health Workers and Liaison Officers, and incorporation of traditional healing practices alongside Western medicine improve treatment adherence and outcomes. Avoidance of eye contact, respect for gender-sensitive examination practices, and understanding of sorry business protocols are critical elements of culturally safe care.
Medication adherence
Complex DMARD regimens with frequent monitoring requirements present adherence challenges. Long-acting depot injections (e.g., methotrexate SC) may improve adherence compared to oral regimens. Community pharmacy partnerships through the Indigenous Pharmacy Programmes improve medication management.
Specific conditions
Rheumatic heart disease (RHD) requires secondary prophylaxis with benzathine penicillin G (BPG) 1.2 MU IM every 3–4 weeks for a minimum of 10 years or until age 21 (whichever is longer). RHD registers (e.g., NT RHD Register) facilitate recall and follow-up. The Australian RHD Endgame Strategy targets elimination by 2031.
Referral pathways
Referral through ACCHOs and Aboriginal Hospital Liaison Officers (AHLOs) improves engagement. The Specialist Outreach Assistance Programme provides funded specialist visits to remote communities. NT, WA, and QLD have specific rheumatology outreach programmes targeting Indigenous communities.

📚 References

  1. 1. Australian Institute of Health and Welfare (AIHW). Autoimmune disease in Australia. Cat. no. PHE 312. Canberra: AIHW; 2023.
  2. 2. Fraenkel L, Bathon JM, England BR, et al. 2021 American College of Rheumatology guideline for the treatment of rheumatoid arthritis. Arthritis Care Res. 2021;73(7):924–939.
  3. 3. Fanouriakis A, Kostopoulou M, Alber K, et al. 2019 update of the EULAR recommendations for the management of systemic lupus erythematosus. Ann Rheum Dis. 2019;78(6):736–745.
  4. 4. Chung SA, Langford CA, Maz M, et al. 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of antineutrophil cytoplasmic antibody-associated vasculitis. Arthritis Care Res. 2021;73(11):1583–1599.
  5. 5. Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis with synthetic and biological disease-modifying antirheumatic drugs: 2022 update. Ann Rheum Dis. 2023;82(1):3–18.
  6. 6. Australian Technical Advisory Group on Immunisation (ATAGI). Australian Immunisation Handbook. Australian Government Department of Health; 2024. Available from: immunisationhandbook.health.gov.au.
  7. 7. Rheumatic Heart Disease Australia (RHDAustralia). The 2020 Australian guideline for prevention, diagnosis, and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020.
  8. 8. Pharmaceutical Benefits Scheme (PBS). PBS Schedule. Australian Government Department of Health. Available from: pbs.gov.au. Accessed 2024.
  9. 9. Agarwal S, Cunnington J, Nossent J. Autoimmune disease in Indigenous Australians: a systematic review. Int J Rheum Dis. 2021;24(12):1487–1498.
  10. 10. Pisetsky DS. Antinuclear antibody testing — misunderstood or misused? Clin Immunol. 2023;255:109717.
  11. 11. Bertsias GK, Tektonidou M, Amoura Z, et al. Joint European League Against Rheumatism and European Renal Association–European Dialysis and Transplant Association (EULAR/ERA-EDTA) recommendations for the management of adult and paediatric lupus nephritis. Ann Rheum Dis. 2012;71(11):1771–1782.
  12. 12. Ledingham J, Deighton C; British Society for Rheumatology Standards, Audit and Guidelines Working Group. Update on the British Society for Rheumatology guidelines for prescribing TNFα blockers in adults with rheumatoid arthritis. Rheumatology. 2005;44(2):155–158.
  13. 13. National Health and Medical Research Council (NHMRC). National statement on ethical conduct in human research. Canberra: NHMRC; 2023 (updated).