Lucan · Conditions

Chronic kidney disease

Australian guidance: Kidney Health Australia CKD Management Handbook (5th ed, 2024)

1. Definition and epidemiology

Chronic kidney disease (CKD) is defined as an estimated or measured glomerular filtration rate (GFR) below 60 mL/min/1.73m² persisting for three months or more, with or without evidence of kidney damage, or evidence of kidney damage regardless of GFR level, persisting for three months or more. Evidence of kidney damage includes albuminuria, haematuria after exclusion of urological causes, structural abnormalities on imaging, or pathological abnormalities on biopsy. In Australia, over 2 million adults live with CKD, affecting approximately 1 in 10 Australians aged 18 years and over, and 1 in 5 First Nations Australians aged 18 years and over; over 31,000 Australians require kidney replacement therapy (dialysis or transplantation). Up to 90% of kidney function can be lost before symptoms appear, and fewer than 10% of those with CKD are aware they have the condition.

2. Pathophysiology

CKD is characterised by progressive loss of nephron mass and compensatory hypertrophy of surviving nephrons, which sustains GFR at the cost of glomerular hyperfiltration and increased intraglomerular pressure (Robbins Ch 20). The resultant mechanical and haemodynamic stress on the glomerular capillary wall promotes mesangial expansion, podocyte injury, and proteinuria. Proteinuria itself is tubulotoxic: filtered albumin and plasma proteins are taken up by proximal tubular cells via endocytosis, activating complement and nuclear factor kappa B (NF-kB) pathways that drive tubulointerstitial inflammation and fibrosis. Activated pericytes differentiate into myofibroblasts, laying down excess extracellular matrix. Ischaemia from afferent arteriolar disease (common in diabetes and hypertension) superimposes tubular atrophy. The net result is progressive interstitial fibrosis and tubular atrophy, which correlates more closely with declining GFR than does glomerular pathology alone (Robbins Ch 20). Diabetic kidney disease, accounting for 40% of Australian kidney failure cases, follows a distinct sequence from glomerular basement membrane thickening through Kimmelstiel-Wilson nodule formation to diffuse mesangial sclerosis.

3. Clinical presentation and diagnostic criteria

CKD is generally asymptomatic in early stages. Symptoms of advancing disease include hypertension, pruritis, nocturia, lethargy, nausea or vomiting, malaise, anorexia, restless legs, haematuria, and dyspnoea. Physical examination may reveal elevated blood pressure, oedema, pallor from anaemia, or reduced skin turgor. Diagnosis requires persistence of findings over at least three months. The three components needed to fully specify a CKD diagnosis are: the kidney function stage (GFR stage G1 to G5 based on eGFR), the albuminuria stage (A1: urine albumin/creatinine ratio (uACR) below 3.0 mg/mmol; A2: 3.0 to 30 mg/mmol; A3: above 30 mg/mmol), and the underlying aetiology (e.g., diabetic kidney disease, hypertensive nephrosclerosis, glomerulonephritis). Fully specifying the diagnosis, for example as CKD stage 3b with microalbuminuria in the setting of type 2 diabetes, guides both prognosis and management.

4. Investigations and AU-specific cutoffs

The Kidney Health Check, the recommended screening tool in Australian primary care, comprises blood pressure measurement, uACR on a first morning void specimen, and eGFR from serum creatinine using the CKD-EPI equation. Australian pathology laboratories routinely report CKD-EPI eGFR for all creatinine requests in persons aged 18 years and over. Albuminuria is confirmed when at least two uACR results are 3.0 mg/mmol or above over a three-month period; a single result is insufficient. If eGFR is below 60 mL/min/1.73m², it should be repeated within seven days to exclude acute kidney injury (AKI), then rechecked at three months. A reduction in eGFR of 20% or more should prompt consideration of AKI and nephrology review. Baseline investigations always indicated include repeat urea/creatinine/eGFR/electrolytes/albumin, urine microscopy for dysmorphic red cells and casts, full blood count, fasting lipids, glucose, HbA1c, uric acid, liver function tests, hsCRP, erythrocyte sedimentation rate, and renal ultrasound at least once. Parathyroid hormone is measured 6 to 12 monthly when eGFR is below 45 mL/min/1.73m². When systemic disease is suspected (rash, arthritis, pulmonary symptoms, or glomerular haematuria), serological testing should include anti-GBM antibody, ANCA, ANA, extractable nuclear antigens, and complement (C3/C4).

5. Management

The overarching goals of CKD management are to slow decline in eGFR, reduce albuminuria by at least 30%, maintain blood pressure below 130/80 mmHg, lower cardiovascular disease (CVD) risk, and avoid further kidney damage.

Colour-coded action plans guide intensity of follow-up: Yellow (eGFR 45 to 59 with normoalbuminuria or eGFR at or above 60 with microalbuminuria) requires review every 12 months; Orange (eGFR 30 to 59 with microalbuminuria or 30 to 44 with normoalbuminuria) every 3 to 6 months; Red (macroalbuminuria at any eGFR, or eGFR below 30 at any albuminuria stage) every 1 to 3 months with nephrology referral and preparation for kidney replacement therapy where appropriate.

Lifestyle targets include salt intake below 5 g per day, BMI below 25 kg/m² (below 23 kg/m² in Asian populations), waist circumference below 94 cm in men (below 90 cm in Asian men) or below 80 cm in women, smoking cessation, no more than 10 standard alcoholic drinks per week, and at least 2.5 to 5 hours of moderate-intensity physical activity weekly. Glycaemic control targets are fasting blood glucose 6 to 8 mmol/L and HbA1c at or below 53 mmol/mol (7%), individualised to the patient's circumstances. Patients should be educated to hold SADMANS medications (Sulfonylureas, ACE inhibitors, Diuretics, Metformin, ARBs, NSAIDs, SGLT2 inhibitors) during acute illness involving dehydration or hypotension.

Vaccination is recommended for all CKD patients aged 18 and over: annual influenza, 5-yearly pneumococcal, COVID-19, and Herpes Zoster (funded through the National Immunisation Program for eligible groups).

6. Pharmacology and AU PBS notes

ACE inhibitors or angiotensin receptor blockers (ARBs) are first-line pharmacological therapy for all people with CKD, up-titrated to the maximum tolerated dose to reduce albuminuria and slow decline in kidney function. A reversible drop in eGFR of up to 25% is expected on initiation; if eGFR falls more than 25% below baseline within two weeks, cease and consider nephrology referral.

SGLT2 inhibitors (e.g., dapagliflozin, empagliflozin) are recommended as add-on therapy for people with CKD and proteinuria, with or without diabetes, to reduce the risk of progressive kidney function decline. They should not be initiated if eGFR is below 25 mL/min/1.73m². An initial dip in eGFR is expected that rebounds after four weeks; specific retesting at that interval is not required. On the PBS, dapagliflozin (Forxiga) carries a streamlined authority for CKD with albuminuria in patients with type 2 diabetes.

Non-steroidal mineralocorticoid receptor antagonists (ns-MRA; finerenone) are indicated for people with CKD and albuminuria associated with type 2 diabetes when ACE inhibitor or ARB therapy is already in place; finerenone should not be initiated if eGFR is below 25 mL/min/1.73m² or potassium is above 5.0 mmol/L.

Statin therapy (with or without ezetimibe) is indicated to reduce CVD events and death when eGFR is at or above 15 mL/min/1.73m² and 10-year CVD risk is at or above 10%, or when the patient is a First Nations Australian with CKD and CVD risk at or above 5%. GLP-1 receptor agonists are indicated for people with CKD who also have concomitant type 2 diabetes, but are not recommended in kidney failure.

Medications requiring dose reduction or cessation as eGFR falls below 60 mL/min/1.73m² include metformin, gabapentin, pregabalin, most anti-infectives (famciclovir, valaciclovir, ciprofloxacin, trimethoprim, nitrofurantoin), and direct oral anticoagulants (apixaban, dabigatran, rivaroxaban). NSAIDs, aminoglycosides, and the "triple whammy" combination of RAS blockade plus diuretic plus NSAID should be avoided given the heightened risk of AKI.

7. Complications and monitoring

Key complications include cardiovascular disease (people with CKD are up to 20 times more likely to die from premature CVD than to reach kidney failure), anaemia of CKD (monitor full blood count; iron studies before commencing erythropoiesis-stimulating agents), CKD-mineral bone disorder (monitor calcium, phosphate, and parathyroid hormone 6 to 12 monthly from stage 3b onward), hyperkalaemia (target potassium at or below 6.0 mmol/L), and AKI susceptibility (all CKD stage 3 to 5 patients carry elevated AKI risk). Other monitored complications include acidosis, hyperuricaemia, cognitive decline, depression, malnutrition, oedema, pruritus, restless legs, and uraemia.

Monitoring schedule by stage: Yellow plan annually; Orange plan every 3 to 6 months (parathyroid hormone and iron studies added from stage 3b); Red plan every 1 to 3 months with nephrology co-management. Advance care planning and discussion of kidney replacement therapy modalities (haemodialysis, peritoneal dialysis, transplantation, comprehensive conservative care) should be initiated proactively in stage 4 to 5 disease.

Written for Australian practice and grounded in the guidance named above. Study material only — not medical advice. Always check against current guidelines.