📋 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.
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 |
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
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
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.
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
- 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)
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
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 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.
📚 References
- 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. 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. Australian Institute of Health and Welfare. Chronic kidney disease: Australian facts. AIHW Cat. no. PHE 229. Canberra: AIHW; 2023.
- 4. ANZDATA Registry. 46th Annual Report 2023. Adelaide: Australia and New Zealand Dialysis and Transplant Registry; 2023.
- 5. Kidney Health Australia. Chronic Kidney Disease (CKD) Management in Primary Care. 4th ed. Melbourne: Kidney Health Australia; 2020.
- 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. 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. The EMPA-KIDNEY Collaborative Group. Empagliflozin in patients with chronic kidney disease (EMPA-KIDNEY). N Engl J Med. 2023;388(2):117–127.
- 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. SPRINT Research Group. A randomized trial of intensive versus standard blood-pressure control (SPRINT). N Engl J Med. 2015;373(22):2103–2116.
- 11. Royal Australian College of General Practitioners. Management of type 2 diabetes: A handbook for general practice. Melbourne: RACGP; 2020.
- 12. Australian Bureau of Statistics. National Aboriginal and Torres Strait Islander Health Survey 2018–19. ABS Cat. no. 4715.0. Canberra: ABS; 2019.
- 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. Caring for Australasians with Renal Impairment (CARI). CARI Guidelines: Early chronic kidney disease. Sydney: CARI; 2022.
- 15. National Health and Medical Research Council. NHMRC additional levels of evidence and grades for recommendations for developers of guidelines. Canberra: NHMRC; 2009.