Despite affecting roughly one in seven adults, chronic kidney disease (CKD) often progresses silently until late stages, when the likelihood of requiring dialysis increases.

Recent evidence and new therapeutic options now provide meaningful opportunities to slow progression and improve long-term outcomes, provided CKD is detected early and managed consistently.

The scale and impact of CKD in Australia

An estimated 2.7 million Australians live with CKD, and around three-quarters of adults are at increased risk due to diabetes, hypertension, cardiovascular disease, obesity or age. CKD is more prevalent in rural and remote communities and disproportionately affects First Nations Australians, who have twice the prevalence of CKD and up to nine times the rate of kidney replacement therapy compared with non-Indigenous Australians.

Only around 10% of people with CKD are aware they have the condition. The REVEAL-CKD study found that 90% of Australians with stage 3 CKD had no documented diagnosis, despite clear biochemical evidence of impaired kidney function. This was common even in those with established risk factors such as diabetes and heart failure, where screening should be routine.

Consequences of late diagnosis

Local registry data show that approximately 15% of patients begin dialysis or receive a kidney transplant within just three months of their first nephrology review, highlighting that many referrals are occurring at a very late stage of disease. Delayed recognition is linked to faster disease progression, a higher likelihood of kidney failure, and more major cardiovascular events.

CKD is also a powerful cardiovascular risk factor, and the strongest independent predictor of cardiovascular death. Patients with CKD have up to 20 times greater risk of dying from a cardiovascular event than requiring dialysis or transplantation.

Even small changes in eGFR or increases in urine ACR are associated with a markedly higher risk of cardiovascular mortality.

Encouragingly, early detection is associated with better outcomes. The REVEAL-CKD study demonstrated that once CKD was formally recognised, guideline-recommended therapies were more likely to be prescribed and kidney function declined more slowly.

Diagnosing CKD

CKD is diagnosed when there is a persistent reduction in kidney function, defined as an eGFR below 60 mL/min/1.73 m² for at least three months, or when there is evidence of kidney damage such as albuminuria, even when eGFR is preserved. Because CKD is often silent until its later stages, identification relies on proactive testing rather than symptomatic presentation.

Testing and screening

Accurate diagnosis requires confirming chronicity, assessing kidney function and identifying kidney damage. Urine ACR is the most overlooked test, which contributes significantly to the under-diagnosis and misclassification of CKD. This not only matters for diagnosis and prognosis but also because many newer therapies require albuminuria thresholds for PBS eligibility.

If eGFR is <60, the test should also be repeated within seven days to exclude acute kidney injury before CKD is assumed.A Kidney Health Check, comprising eGFR, urine ACR and blood pressure, is recommended for patients at increased risk of CKD, such as diabetes, hypertension, cardiovascular disease, obesity, older age, family history of kidney failure, prior acute kidney injury and First Nations background.

Practice tip: Always screen for CKD with both eGFR and urine ACR

It’s essential to test both eGFR and urine ACR for accurate CKD detection, staging and risk assessment. Testing just one of these measurements alone risks missing CKD.

Findings from the AusDiab study show that 57% of people with albuminuria had a normal eGFR, while 92% of those with a low eGFR did not have albuminuria. Once abnormal results are identified, they must be repeated after at least three months to confirm CKD.

CKD staging classification

The combined eGFR–ACR staging system integrates kidney function and kidney damage to guide risk stratification, monitoring frequency and management intensity. The full staging table, along with action plans, detection and diagnosis algorithms, and referral pathways, is available in the Kidney Health Australia CKD Management in Primary Care Handbook and CKD-Go app. Patients can also self-assess their risk using the two-minute Kidney Risk Assessment Tool on the Kidney Health Australia website.

When to refer to nephrology

While many patients with CKD can be safely managed in primary care, referral is indicated when any of the following occurs:

• eGFR falls below 30
• albuminuria is significantly elevated (ACR ≥ 30 mg/mmol) and persistent
• when there is a rapid decline in kidney function, defined as a drop of more than 15 mL/min/1.73 m² in a year or a 25% reduction over 12months
• hypertension remains uncontrolled despite the use of three antihypertensive agents

First Nations Australians warrant earlier referral, particularly when eGFR is below 45 or when there is sustained decline exceeding 10 mL/min per year.

Slowing disease progression: updated evidence

The foundation of CKD management remains lifestyle modification, blood pressure control to a target of 130/80 mmHg, lipid management (including statins, with or without ezetimibe, in patients at high cardiovascular risk), and glycaemic control in diabetic patients to an HbA1c target of around 7%. Building on this, a four-pillar pharmacotherapeutic approach is used to help slow disease progression.

RAS inhibitors

ACE inhibitors and ARBs are central to CKD care due to their renoprotective and antiproteinuric effects. A stable decline in eGFR of up to 25% is expected and acceptable. Potassium should be monitored, and if elevated, may be addressed through dietary modifications, diuretics, sodium bicarbonate, potassium binders or dose adjustments.

The evidence clearly shows that stopping RAS inhibitors because of hyperkalaemia leads to worse outcomes, including increased hospitalisation due to worsening CKD and heart failure. Managing potassium is therefore strongly preferred over discontinuing therapy.

SGLT2 inhibitors

The DAPA-CKD and EMPA-KIDNEY trials demonstrated that SGLT2 inhibitors significantly reduce kidney failure, slow eGFR decline and offer cardiovascular protection, even in patients without diabetes. An initial eGFR dip is expected but transient. Importantly, the SMART Consortium meta-analysis found a 23% reduction in acute kidney injury, despite the mild diuretic effect of SGLT2 inhibitors.

SGLT2 inhibitors are now PBS-listed for patients with proteinuric CKD who have an eGFR between 25–75 mL/min/1.73 m² and a urine ACR between 22.6–565 mg/mmol, and who are stabilised on the maximum tolerated dose of a RAS inhibitor. Recent PBS changes have extended SGLT2 inhibitor access to select, non-proteinuric CKD populations with lower eGFR. They are also PBS-listed for people with diabetes and CKD regardless of HbA1c, who are taking metformin (unless contraindicated) and have established cardiovascular disease, are at high cardiovascular risk or are of First Nations Australian background. An eGFR 30 mg/mmol qualifies as predetermined high cardiovascular risk, thus expanding their eligibility.

SGLT2 inhibitors can cause osmotic diuresis, so dose reductions of diuretics may be required. In diabetes, a mild increase in genital infections and ketoacidosis risk exists, but, overall, these agents are well tolerated.

Finerenone

Finerenone, a selective non-steroidal mineralocorticoid receptor antagonist, has shown clear benefits when added to RAS inhibitors (and SGLT2 inhibitors where possible), improving both kidney and cardiovascular outcomes. It is PBS-listed for people with diabetic CKD who meet albuminuria and eGFR thresholds (eGFR >25 mL/min/1.73 m² and ACR >22.6 mg/mmol) and are already established on a RAS inhibitor and, where not contraindicated or intolerant, an SGLT2 inhibitor. Its benefits appear independent of SGLT2 inhibitor therapy whilst co-administration with an SGLT2 inhibitor is also associated with a reduced incidence of hyperkalaemia.

GLP-1 receptor agonists

Emerging evidence from the FLOW trial demonstrated that semaglutide improves renal endpoints, major cardiovascular events and all-cause mortality in people with diabetic CKD, while also slowing eGFR decline. The study reported a 24% reduction in the primary kidney composite outcome, an 18% reduction in major adverse cardiovascular events and a 20% reduction in all-cause mortality, with a less steep annual eGFR decline compared with placebo.

Medication stewardship and sick-day management

Effective drug stewardship is critical in the management of CKD. This includes regular medication review, appropriate dose adjustment for reduced kidney function, planned temporary discontinuation where clinically appropriate, and avoidance of potential nephrotoxins. Sick-day plans are particularly important, as acute illness increases the risk of dehydration and acute kidney injury.

Practice tip: the SADMANS mnemonic is a practical tool to identify medicines that should be temporarily paused during episodes of acute illness:

Sulfonylureas
ACE inhibitors
Diuretics
Metformin
ARBs
NSAIDs
SGLT2 inhibitors

These medicines should be restarted once the patient has recovered, and timely re-initiation is essential. While temporary discontinuation is sometimes necessary it must not become prolonged. In one study, SGLT2 inhibitors and GLP-1 receptor agonists were discontinued in almost half of patients with CKD, often for more than 180 days, and this was associated with higher risks of death, heart failure hospitalisation, myocardial infarction and stroke.

A sick-day plan should not only guide temporary medication cessation, but also serve as a prompt that disease-modifying therapies should be restarted promptly once the acute illness has resolved.

Key takeaways

• Early CKD detection relies on targeted, risk-based, screening and measurement of both eGFR and urine ACR
• Confirming chronicity through repeat testing ensures accurate diagnosis and staging
• Most CKD can be managed in primary care, supported by clear criteria for timely nephrology referral
• Slowing progression is now supported by a four-pillar therapy approach: RAS inhibitors, SGLT2 inhibitors, finerenone and GLP-1 receptor agonists
• Medication optimisation includes using the SADMANS mnemonic for sick-day management and ensuring paused medicines are restarted once the patient has recovered