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Kidney Health

Blood Tests for Kidney Disease

eGFR, creatinine, urine ACR, and CKD staging explained in plain English — with Australian reference ranges and the GP-to-specialist pathway.

The Quick Answer

Chronic kidney disease (CKD) affects over 1.7 million Australians and is largely silent in its early stages. The two most important tests are eGFR(a blood test estimating how well the kidneys filter) and urine ACR(albumin-creatinine ratio in urine — detecting protein leakage). CKD is diagnosed when either or both are abnormal for at least 3 months.

The urine ACR is critically important and often missed. eGFR can be normal even when the kidneys are already being damaged — the ACR catches this early protein leakage before eGFR starts to fall. Both tests together are required for a complete kidney health picture.

eGFR: kidney filtration capacity
Urine ACR: early damage signal
Both tests needed — not just eGFR

Who Should Be Tested — The Kidney Health Check

Kidney Health Australia recommends a Kidney Health Check (eGFR + urine ACR + blood pressure) for all Australians in higher-risk groups. Most people with CKD have NO symptoms until it is quite advanced — only testing detects it early.

Type 2 diabetes
Annual urine ACR and eGFR from diagnosis

Highest risk — diabetic nephropathy is the leading cause of CKD in Australia

High blood pressure (hypertension)
Annual eGFR and urine ACR

Second most common cause of CKD — sustained BP elevation damages glomeruli

Obesity (BMI > 30)
Every 2 years or annually if other risk factors

Insulin resistance and inflammation damage renal vasculature

Family history of kidney disease
Discuss screening frequency with GP

Multiple inherited kidney conditions (ADPKD, IgA nephropathy, Alport syndrome)

Aboriginal and Torres Strait Islander peoples
Annual Kidney Health Check from age 18

CKD is 3-4× more prevalent; often detected at a younger age and progresses faster

Age > 60
Every 2 years if no other risk factors

eGFR naturally declines with age; important to distinguish aging from pathological CKD

The Tests — What Each One Measures

A complete CKD assessment includes kidney filtration markers, damage markers (urine ACR), electrolytes, bone-mineral markers, and a blood count. Here is what each test shows and why it matters.

eGFR (Estimated Glomerular Filtration Rate)
Normal: ≥ 60 mL/min/1.73m² (normal filtration); ≥ 90 = optimal
CKD pattern: < 60 for ≥ 3 months = CKD diagnosis

Calculated from serum creatinine, age, and sex (CKD-EPI equation). Declines naturally with age (~1 mL/min/year after 40). A single low eGFR may reflect dehydration — always confirm over at least 3 months.

Serum Creatinine
Normal: Men: 60–110 µmol/L; Women: 45–90 µmol/L
CKD pattern: Elevated; rises as eGFR falls

A byproduct of muscle metabolism, cleared by the kidneys. Higher muscle mass = higher creatinine (misleading in bodybuilders). Lower muscle mass = lower creatinine (misleading in frail elderly — may hide moderate CKD). eGFR is a better measure than creatinine alone.

Urine ACR (Albumin-Creatinine Ratio)
Normal: Men: < 2.5 mg/mmol; Women: < 3.5 mg/mmol
CKD pattern: A1: < 3; A2: 3–30; A3: > 30 mg/mmol

THE MOST IMPORTANT test for early kidney damage — often abnormal before eGFR falls. A first morning urine sample is preferred. A single elevated result should be confirmed on two further samples over 3 months (transient elevation possible with heavy exercise, infection, fever).

Electrolytes (Sodium, Potassium, Bicarbonate)
Normal: Na: 136–145 mmol/L; K: 3.5–5.0 mmol/L; HCO3: 22–30 mmol/L
CKD pattern: High potassium (hyperkalaemia), low bicarbonate (metabolic acidosis) in advanced CKD

Hyperkalaemia (high potassium) is the most dangerous CKD electrolyte complication — it can cause cardiac arrhythmias. Metabolic acidosis accelerates CKD progression and bone loss. Both become more common as eGFR drops below 30.

Phosphate
Normal: 0.75–1.50 mmol/L
CKD pattern: Elevated (hyperphosphataemia) in CKD G4-G5

Failing kidneys cannot excrete phosphate efficiently. High phosphate binds calcium, lowering serum calcium and stimulating PTH (secondary hyperparathyroidism), causing bone disease and vascular calcification. Dietary phosphate restriction and phosphate binders are used in advanced CKD.

Calcium
Normal: Total: 2.10–2.60 mmol/L; Corrected (for albumin): 2.15–2.65 mmol/L
CKD pattern: Low-normal or low (hypocalcaemia) in advanced CKD

CKD reduces vitamin D activation (1,25-dihydroxyvitamin D), lowering calcium absorption. Always correct for albumin — low albumin (common in CKD) artificially lowers measured total calcium.

PTH (Parathyroid Hormone)
Normal: 1.6–7.2 pmol/L
CKD pattern: Elevated (secondary hyperparathyroidism) in CKD G3b-G5

The kidney-bone axis response to low calcium and high phosphate. Chronically elevated PTH causes renal osteodystrophy (weakened bones) and cardiovascular calcification. Treated with vitamin D analogues, phosphate binders, and cinacalcet.

FBC (Haemoglobin)
Normal: Men: 130–180 g/L; Women: 115–160 g/L
CKD pattern: Normocytic anaemia in CKD G3-G5

The kidneys produce erythropoietin (EPO), which stimulates red cell production. CKD reduces EPO production, causing normocytic anaemia. Treated with iron supplementation and erythropoiesis-stimulating agents (ESAs) when Hb falls below 100-110 g/L in CKD.

CKD Staging — What the KDIGO G-Categories Mean

The KDIGO (Kidney Disease: Improving Global Outcomes) staging system classifies CKD into G1-G5 based on eGFR, and A1-A3 based on urine ACR (albumin category). Together, these determine prognosis and guide monitoring frequency. Australian guidelines align with KDIGO.

G1
Normal or high filtration (with kidney damage markers)
eGFR ≥ 90 mL/min/1.73m²

Treat underlying cause, control BP and glucose, annual monitoring

G2
Mildly reduced filtration (with kidney damage markers)
eGFR 60–89 mL/min/1.73m²

As above; identify and manage risk factors

G3a
Mildly to moderately reduced filtration
eGFR 45–59 mL/min/1.73m²

GP monitoring every 6 months; consider endocrinology/nephrology input

G3b
Moderately to severely reduced filtration
eGFR 30–44 mL/min/1.73m²

More frequent monitoring; assess for CKD complications; consider nephrology referral

G4
Severely reduced filtration
eGFR 15–29 mL/min/1.73m²

Nephrology referral; prepare for kidney replacement therapy; intensive monitoring

G5
Kidney failure
eGFR < 15 mL/min/1.73m²

Specialist care; dialysis or transplant planning; palliative pathway if applicable

Red Flags — When to Act Urgently

eGFR < 30 (CKD G4)

Nephrology referral is recommended. Preparation for kidney replacement therapy should begin even if dialysis is not yet needed. Complications (anaemia, bone disease, acidosis) become more frequent.

Rapid eGFR decline (> 5 mL/min/year)

Faster than expected decline suggests an acute or reversible process on top of CKD. Causes include dehydration, NSAIDs, contrast dye, ACE inhibitor/ARB in the setting of renal artery stenosis, or urinary obstruction. Urgent review.

Urine ACR > 70 mg/mmol

High-grade albuminuria significantly accelerates CKD progression and cardiovascular risk. Specialist referral is recommended regardless of eGFR stage.

Serum potassium > 6.0 mmol/L

Severe hyperkalaemia can cause fatal cardiac arrhythmias. This requires urgent management — often same-day or emergency presentation. Common in CKD patients on ACE inhibitors, ARBs, potassium-sparing diuretics, or NSAIDs.

Haematuria (blood in urine) plus proteinuria

This combination (the "nephritic-nephrotic" picture) suggests a glomerulonephritis that needs urgent renal biopsy and immunosuppressive treatment. Refer to nephrology promptly.

Sudden drop in eGFR in a hospitalised patient

Acute kidney injury (AKI) superimposed on CKD is common and often preventable. Identify and remove triggers: nephrotoxic drugs (NSAIDs, aminoglycosides, contrast), dehydration, hypotension, urinary obstruction.

What Happens After Abnormal Results — The GP Pathway

1
Confirm the results

A single abnormal eGFR or urine ACR should be repeated over 3 months. Transient causes (dehydration, heavy exercise, urinary infection, fever) can temporarily worsen both results. Only when abnormal on at least two of three tests over 3 months is CKD confirmed.

2
Identify the underlying cause

Common causes: diabetic kidney disease (most common), hypertensive nephrosclerosis, IgA nephropathy, polycystic kidney disease. Your GP will order additional tests: hepatitis serology, ANA, complement (C3, C4), urine protein electrophoresis, renal ultrasound.

3
Optimise blood pressure

Target blood pressure in CKD is below 130/80 mmHg. ACE inhibitors (ramipril, perindopril) or ARBs (irbesartan, losartan) are first-line — they reduce proteinuria and slow CKD progression beyond their BP-lowering effect. Monitor potassium and creatinine 1-2 weeks after starting or up-titrating.

4
Treat diabetes aggressively

Target HbA1c below 53 mmol/mol (7%) in most patients with CKD and diabetes. SGLT2 inhibitors (empagliflozin, dapagliflozin, canagliflozin) have strong evidence for reducing CKD progression and cardiovascular events — now first-line in diabetic kidney disease regardless of baseline HbA1c.

5
Monitor for CKD complications

As eGFR falls, check for: anaemia (FBC), secondary hyperparathyroidism (calcium, phosphate, PTH, vitamin D), metabolic acidosis (bicarbonate), hyperkalaemia (potassium), and dyslipidaemia. Each complication has specific management.

6
Nephrology referral

Recommended at eGFR < 30, rapid decline, high ACR, or uncertain diagnosis. A nephrologist will perform a detailed assessment, optimise management, and plan for kidney replacement therapy if needed. Early referral (before kidney failure) leads to better outcomes.

Slowing CKD Progression — What Works

Blood pressure control

The single most important modifiable factor. Target below 130/80 mmHg. ACE inhibitors or ARBs are preferred in proteinuric CKD (urine ACR > 3 mg/mmol) — they reduce intraglomerular pressure independently of systemic BP reduction. Avoid both an ACE inhibitor AND an ARB simultaneously (dual blockade increases hyperkalaemia and AKI risk).

SGLT2 inhibitors (game-changing new evidence)

Empagliflozin, dapagliflozin, and canagliflozin reduce CKD progression and cardiovascular events in patients with CKD and type 2 diabetes, and increasingly in non-diabetic CKD. PBS-listed in Australia for eligible patients. They reduce urine ACR, slow eGFR decline, and may even cause a modest initial eGFR dip (expected and not a reason to stop).

Lifestyle modification

Aim for a healthy weight, limit sodium intake (less than 2 g/day, roughly 5 g of salt) to reduce blood pressure and proteinuria, moderate protein intake (0.8 g/kg/day — very low protein diets are no longer recommended), avoid NSAIDs (ibuprofen, naproxen, diclofenac — all worsen CKD), quit smoking, and limit alcohol.

Costs and Medicare — Kidney Tests in Australia

eGFR / creatinine / electrolytes
Fully Medicare-rebatable with GP referral

Bulk-billed at most collection centres

Urine ACR (albumin-creatinine ratio)
Fully Medicare-rebatable with GP referral

First morning urine sample — can be self-collected at home

Calcium, phosphate, PTH, vitamin D
Medicare-rebatable with clinical indication

Required from CKD G3b onwards

Renal ultrasound
Medicare-rebatable with GP referral

Checks kidney size, structure, obstruction, and cysts

SGLT2 inhibitor (empagliflozin, dapagliflozin)
PBS-subsidised for eligible CKD patients

Criteria include eGFR threshold and urine ACR — ask your GP

Nephrology consultation
Specialist rebate via Medicare

GP referral required; gap fees may apply privately


See What Your Kidney Results Mean

Upload your blood test and SmarterBlood will explain your eGFR, creatinine, electrolytes, and other kidney markers in plain English — with Australian reference ranges.

This page provides general educational information about chronic kidney disease (CKD) and the blood tests used to detect and monitor it. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your GP or nephrologist about kidney function results. SmarterBlood does not provide medical care.