I had a blood test and my eGFR was 55 — does that mean I have kidney disease?

Possibly, but one result is not a diagnosis. CKD requires the abnormality to be present for at least 3 months, so a repeat eGFR and a urine albumin-creatinine ratio (UACR) on a first-morning urine sample are needed. eGFR can also be temporarily low from dehydration, certain medicines (including trimethoprim, fenofibrate, some HIV antivirals), heavy creatine supplementation, or after a recent illness. If the eGFR stays in the 45–59 range across two readings 3 months apart, that meets criteria for CKD stage 3a — most of which is stable and managed well in general practice.

Why is the urine test (UACR) as important as the blood test (eGFR)?

Because albumin leaking into the urine is one of the earliest signs the filtering units of the kidney are under stress, and it independently predicts both kidney decline and heart attack and stroke risk. Two people with the same eGFR but different UACRs sit in very different risk categories. UACR also drives treatment — Australian PBS access to dapagliflozin for non-diabetic CKD, for example, requires a UACR above a threshold. A first-morning urine sample is preferred; very heavy exercise, a urinary tract infection, or menstruation in the prior 24 hours can produce a falsely high result, so a confirmation on a second sample is standard.

I've been told to take an ACE inhibitor and my creatinine went up a bit — should I stop?

Usually not. A rise in creatinine of up to about 25% after starting an ACE inhibitor or ARB is expected and reflects the medicine doing its job — reducing pressure inside the filtering units (glomeruli) to protect them long-term. Per RACGP and Australian Medicines Handbook guidance, this is checked with a blood test at 1–2 weeks. The medicine is typically continued unless the creatinine rises more than 25%, potassium rises above about 5.5 mmol/L without correction, or symptoms (dizziness, very low blood pressure) develop. Stopping the medicine because of a small expected change can lose you the long-term benefit on kidney and heart outcomes.

What are SGLT2 inhibitors and why are they being used in people without diabetes?

SGLT2 inhibitors (dapagliflozin/Forxiga, empagliflozin/Jardiance) were developed for type 2 diabetes but were shown in the DAPA-CKD (2020) and EMPA-KIDNEY (2023) trials to slow kidney decline and reduce cardiovascular events in people with CKD regardless of whether they have diabetes. They work by easing the abnormal pressure inside the filtering units and reducing inflammation. PBS access in Australia covers CKD with albuminuria above defined thresholds at eGFR ≥25 (dapagliflozin) or ≥20 (empagliflozin). The main practical things to know: a small expected dip in eGFR after starting, increased thrush/urinary thrush, the need to pause the medicine during vomiting or diarrhoea (sick-day rules), and a rare but serious risk of diabetic ketoacidosis even at near-normal sugar levels.

Do I need to avoid Nurofen or other anti-inflammatories?

Yes, where reasonable. Non-steroidal anti-inflammatory drugs (NSAIDs) — ibuprofen (Nurofen), diclofenac (Voltaren), naproxen, and prescription cousins like celecoxib — reduce blood flow inside the kidney and can both accelerate CKD progression and trigger acute kidney injury, especially when combined with an ACE inhibitor or ARB plus a diuretic (the 'triple whammy'). Paracetamol is the safer first-line for most musculoskeletal pain in CKD. Topical NSAID gels carry less risk than oral, and short courses can be discussed with your GP. The same caution applies to high-dose vitamin C above 500 mg/day, certain Chinese herbal preparations (aristolochic acid contamination), and avoidable IV contrast scans.

My eGFR is dropping — am I heading for dialysis?

For most Australians with CKD the answer is no. The trajectory depends on the cause, the rate of decline, the UACR, and how much of the four-pillar treatment is already in place. The Kidney Failure Risk Equation (KFRE) gives a personalised 2-year and 5-year risk of needing dialysis or transplant from your eGFR, UACR, age, and sex. Most people with stage 3 CKD never progress to dialysis — they die of (or with) cardiovascular disease, which is why blood pressure, cholesterol, smoking, and diabetes control matter as much as the kidneys themselves. For people who do approach kidney failure, options include transplant (often pre-emptive, before dialysis), home or in-centre dialysis, or conservative non-dialysis care — particularly relevant for frail older adults where dialysis may add little quality-adjusted survival. These conversations should start early, not at the last minute.

Chronic kidney disease

Chronic kidney disease: the four-pillar AU primary-care approach

By Dr HB Lo, FACRRM Reviewed 18 May 2026 12 min read

Chronic kidney disease (CKD) is abnormality of kidney structure or function lasting ≥3 months, classified by eGFR and urine albumin-creatinine ratio (UACR). Roughly 1 in 10 Australian adults has it; ~80% is unrecognised. CKD is also a cardiovascular risk equivalent — heart, not kidneys, is the leading cause of death.

Four-pillar AU framework (RACGP, KHA-CARI, eTG, KDIGO 2024): ACE inhibitor or ARB; SGLT2 inhibitor where eligible; finerenone in T2DM with albuminuria; statin plus CV risk. Salt restriction, nephrotoxin avoidance, sick-day rules underneath.

Refer nephrology at eGFR <30, UACR >70, rapid decline, or unclear cause.

What CKD actually is

Chronic kidney disease is an abnormality of kidney structure or function — usually measured by reduced filtering rate (eGFR) or protein leaking into the urine (UACR) — present for at least three months. It affects roughly 1 in 10 Australian adults (AIHW CKD), and the most striking feature is that around 80% of cases are unrecognised at the general practice level. The kidneys can lose more than half their function with no symptoms at all. The first hint is often a routine blood and urine test ordered for something else.

The other thing worth saying clearly: CKD is not just a kidney problem. It’s a cardiovascular risk condition — the leading cause of death in CKD is heart attack and stroke, not kidney failure (Heart Foundation 2023). That changes the whole framing of treatment. The same medicines that protect the kidneys also protect the heart, and that is no coincidence.

A common pattern in clinic: someone in their 50s or 60s comes in saying “my bloods were normal so it’s fine.” On a closer look the eGFR has been quietly dropping for years, the UACR has never been measured, and the blood pressure target is set for someone without CKD. None of this is the patient’s fault — the test has simply never been requested. The aim of this page is to make the framework clear enough that you can ask better questions of your own GP.

A. Core clinical — the AU primary-care framework

How CKD is diagnosed and staged

Kidney Health Australia / KHA-CARI and KDIGO 2024 use a combined system based on two numbers:

eGFR (estimated glomerular filtration rate) — how fast the filtering units (glomeruli) are working. Reported automatically with most blood tests using the CKD-EPI 2021 equation.
- Stage 1: eGFR ≥90 with other kidney damage
- Stage 2: eGFR 60–89 with other kidney damage
- Stage 3a: eGFR 45–59
- Stage 3b: eGFR 30–44
- Stage 4: eGFR 15–29
- Stage 5: eGFR <15 or on dialysis
UACR (urine albumin-creatinine ratio) — measured on a first-morning urine sample.
- A1: normal (men <2.5, women <3.5 mg/mmol)
- A2: moderately increased — 3–30 mg/mmol
- A3: severely increased — >30 mg/mmol

The two together (for example, G3aA2) drive risk stratification on the KDIGO heat map and decide how often you should be reviewed.

Who should be screened

RACGP CKD Handbook and KHA-CARI recommend annual eGFR plus UACR in:

Type 1 diabetes for at least 5 years, or type 2 diabetes from diagnosis
High blood pressure
Established cardiovascular disease (heart attack, stroke, peripheral vascular disease, heart failure)
Family history of advanced CKD or inherited kidney disease
Aboriginal and Torres Strait Islander adults from age 18 — prevalence is 2–3 times the general population (AIHW Indigenous CKD)
Age 60 and over
Obesity (BMI ≥30) or current smokers
Previous acute kidney injury
Long-term nephrotoxic medications (chronic NSAIDs, lithium, calcineurin inhibitors)

If you fit one of these groups and have not had a UACR done, that is a reasonable thing to raise at your next GP appointment.

What a workup involves

If the screening tests are abnormal, the next layer typically includes a renal ultrasound to check kidney size and rule out obstruction, a fuller blood panel (electrolytes, calcium, phosphate, full blood count, iron studies, parathyroid hormone where eGFR is below 45), and cause-finding immunology (ANA, ANCA, complement, paraprotein screen) in selected cases per eTG nephrology. The aim is to identify a treatable cause early — diabetes, hypertension, glomerulonephritis, polycystic kidney disease, or drug-induced injury are the most common.

A note on eGFR pitfalls: the number is unreliable in extremes of muscle mass (very low in cachexia, falsely low in heavy bodybuilders), in pregnancy, and during acute illness. Some medicines (trimethoprim, fenofibrate, cobicistat, dolutegravir) inhibit tubular creatinine secretion and produce a “fake” eGFR drop without true kidney damage. The clinical picture and a trend over time matter more than any single number.

The four-pillar treatment hierarchy

This is the part that has changed most in the last 5 years and is worth understanding clearly. The current Australian and international framework (RACGP, KHA-CARI, eTG, KDIGO 2024) sits on four evidence-led pillars for albuminuric CKD:

Maximally tolerated ACE inhibitor or ARB. Examples: ramipril, perindopril, irbesartan, candesartan (AMH). Titrated upward as blood pressure and potassium allow. An expected up-to-25% rise in creatinine and a modest potassium rise are part of the medicine working, not reasons to stop. Combination of ACE inhibitor plus ARB is avoided — the ONTARGET 2008 trial showed more acute kidney injury and hyperkalaemia without survival benefit.
SGLT2 inhibitor — dapagliflozin (Forxiga) 10 mg daily for CKD with albuminuria at eGFR ≥25, or empagliflozin (Jardiance) 10 mg daily down to eGFR ≥20. Both have PBS Authority (Streamlined) listing for CKD with albuminuria, regardless of diabetes status. The evidence — DAPA-CKD 2020 (44% reduction in composite kidney decline and death) and EMPA-KIDNEY 2023 (28% reduction) — is some of the strongest in modern nephrology.
Finerenone (Kerendia) 10–20 mg daily — a non-steroidal selective mineralocorticoid receptor antagonist with anti-fibrotic and anti-inflammatory effect. PBS Authority for type 2 diabetes plus CKD with UACR ≥3, potassium ≤4.8 mmol/L, and eGFR ≥25, on top of maximally tolerated ACE inhibitor or ARB. Evidence: FIDELIO-DKD and FIGARO-DKD.
Statin plus broader cardiovascular risk management — atorvastatin 20–40 mg or rosuvastatin 10–20 mg per Heart Foundation 2023. Aspirin is reserved for established cardiovascular disease, not primary prevention. Smoking cessation via Quitline 13 78 48 is high-leverage.

Lifestyle sits underneath all four: blood pressure target <130/80 mmHg where albuminuria or diabetes are present (otherwise <140/90 and individualised in frail older adults), salt under 5 g/day, a Mediterranean or DASH-style eating pattern, weight optimisation, at least 150 minutes of moderate exercise per week, and sick-day rules (NPS) — temporarily holding ACE inhibitor or ARB, SGLT2 inhibitor, diuretics, metformin, and NSAIDs during vomiting, diarrhoea, fever, or dehydration, then restarting when eating and drinking normally.

If you have CKD with albuminuria and only one or two of those four pillars is in place, that is a conversation to have with your GP. The likelihood of slowing decline and reducing heart events is high when the full stack is part of your picture.

B. Evidence appraisal — what the trials actually show

A few areas where the evidence is worth understanding rather than just accepted:

SGLT2 inhibitors in non-diabetic CKD. The historical assumption was that SGLT2 inhibitors were diabetes drugs. DAPA-CKD and EMPA-KIDNEY deliberately enrolled non-diabetic CKD and showed the same magnitude of benefit. The mechanism (restoring normal feedback inside the filtering unit and reducing intraglomerular pressure) is not diabetes-specific. Trade-offs: an expected small dip in eGFR after starting, increased genital thrush, volume depletion in older or thin patients, rare euglycaemic ketoacidosis (a reason for sick-day pausing), and a very rare risk of Fournier’s gangrene. For most people with CKD plus albuminuria, the kidney and heart benefit outweighs these.

Aspirin in primary prevention. Three large trials — ASCEND 2018, ARRIVE 2018, and ASPREE 2018 (the latter Australian-led in older adults) — showed that the bleeding risk of low-dose aspirin outweighs cardiovascular benefit when used for primary prevention, including in CKD subgroups. Aspirin is continued in people with established cardiovascular disease and not used routinely for primary prevention.

Blood pressure target. SPRINT 2015 showed lower mortality at systolic blood pressure below 120 mmHg in non-diabetic CKD, but used unattended automated readings — which run lower than clinic readings. Heart Foundation 2023 sits on <130/80 in proteinuric CKD or diabetes, individualised upward in frail older adults where orthostatic drops and falls are real concerns.

GLP-1 receptor agonists (semaglutide / Ozempic, dulaglutide / Trulicity). The FLOW 2024 trial showed a 24% reduction in major kidney and cardiovascular events in type 2 diabetes plus CKD with semaglutide on top of a four-pillar regimen. PBS access is via type 2 diabetes (HbA1c ≥7% on metformin) — the cardiorenal indication continues to evolve. Non-diabetic CKD evidence is emerging and not yet practice-changing in Australia.

Statins after dialysis starts. SHARP 2011 showed simvastatin plus ezetimibe reduces major events pre-dialysis. The 4D and AURORA trials showed no benefit of initiating a statin once already on dialysis — so the pre-dialysis vs dialysis distinction matters. Existing statin therapy is continued; new starts in dialysis-only populations are not routine.

Sodium bicarbonate for low blood bicarbonate. de Brito-Ashurst 2009 showed benefit when bicarbonate was kept ≥22 mmol/L, but the more recent BiCARB 2020 trial in older adults found no functional benefit and concerns about sodium load. Reasonable when bicarbonate is below 22, weighed against blood pressure and fluid status.

Things that look reasonable but the trials don’t support. N-acetylcysteine before contrast scans (PRESERVE 2018 showed no benefit — saline hydration is what works). High-dose vitamin C (oxalate nephropathy risk). Astragalus and other Chinese herbal preparations marketed for kidney function — historical aristolochic-acid contamination has been associated with rapidly progressive CKD and urothelial cancer (NEJM 2000). Generic “kidney detox” supplements have no evidence base and a non-zero harm signal.

C. Australian operations — how access actually works

PBS access to the kidney-protective medicines (PBS Schedule, verified via web search 2026-05-12):

ACE inhibitors and ARBs — general schedule, no Authority needed.
Dapagliflozin (Forxiga) 10 mg — PBS Authority Required (Streamlined) for CKD with albuminuria above the listed threshold at eGFR ≥25, separate codes for type 2 diabetes and heart failure.
Empagliflozin (Jardiance) 10 mg — PBS Authority Required (Streamlined), CKD listing at eGFR ≥20 with albuminuria.
Finerenone (Kerendia) 10/20 mg — PBS Authority (Telephone/Online) for type 2 diabetes plus CKD plus UACR ≥3 plus potassium ≤4.8 plus eGFR ≥25, on maximally tolerated ACE inhibitor or ARB.
Semaglutide / dulaglutide — PBS Streamlined for type 2 diabetes with HbA1c ≥7% on metformin.
Statins — general schedule when cardiovascular risk criteria are met.
Phosphate binders, active vitamin D, erythropoiesis-stimulating agents — kidney-specialist initiated under Authority or Section 100 listings.

GP chronic condition management — under the 1 July 2025 reform, CKD is an eligible chronic condition for a GP Chronic Condition Management Plan (GPCCMP). Preparation (MBS 965) and review (MBS 967, recommended every 3 months and mandatory within 18 months to keep allied-health continuity) provide access to a renal accredited practising dietitian, exercise physiologist, and podiatrist if diabetic.

Specialist screening / risk-assessment items. Heart Health Check (MBS 699) — for ages 45–79 (or 30+ for Aboriginal and Torres Strait Islander Australians) — uses the Heart Foundation 2023 calculator which treats CKD as a risk modifier. The annual ATSI Health Assessment (MBS 715) is the central platform for CKD screening in Aboriginal and Torres Strait Islander populations.

Pathology. Bulk-billed under General Practice Pathology when ordered under CKD-screening criteria: serum creatinine / eGFR (item 66500) and UACR (66509 / 66512).

Telehealth. Video and phone consultations are available under standard MBS rules including the 12-month existing-relationship requirement, with exemptions for Aboriginal and Torres Strait Islander Australians, under-7s, and people experiencing homelessness (MBS telehealth factsheet).

Vaccinations. The Australian Immunisation Handbook lists annual influenza, COVID-19 boosters, pneumococcal (PCV13 then PPSV23), high-dose hepatitis B schedule at eGFR <30 (especially pre-transplant), and RSV per current schedule.

Driving. Austroads “Assessing Fitness to Drive 2022” — dialysis patients do not drive for at least 4 hours after a haemodialysis session; uraemic encephalopathy precludes driving until corrected; the driver licensing authority is notified where the condition affects safe driving.

Advance care planning. Advance Care Planning Australia is the AU resource. The Australian recommendation is to start the conversation well before eGFR drops below 15 — discussing transplant, dialysis, and conservative non-dialysis pathways — rather than at the point of crisis.

D. Special populations

Aboriginal and Torres Strait Islander Australians. CKD prevalence is 2–3 times the general population and end-stage kidney disease rates are markedly higher (AIHW Indigenous CKD). Annual eGFR plus UACR from age 18 is standard, typically delivered through the MBS 715 Health Assessment. Cultural safety in transplant assessment, the “off-country” issue for dialysis access in regional areas, and family-centred decision-making sit within KHA-CARI’s specific guidance.

Older adults and frailty. Blood pressure targets are individualised — a <130/80 target in a robust 70-year-old looks different from a frail 88-year-old where the priority is preventing falls and orthostatic syncope. SGLT2 inhibitor benefit is preserved in older patients in EMPA-KIDNEY, but volume depletion needs more attention. Conservative non-dialysis care is a valid pathway for frail older adults where dialysis adds little quality-adjusted survival — work by Murtagh and others has shown survival differences narrow with rising frailty.

Type 2 diabetes. Diabetes is the single largest cause of end-stage kidney disease in Australia. All four pillars apply with extra emphasis on finerenone (PBS-listed specifically for this group) and GLP-1 receptor agonists where HbA1c remains above 7% on metformin. Glycaemic targets are individualised — HbA1c around 7% is reasonable in younger fitter patients, more relaxed (7.5–8%) in older or frail patients to avoid hypoglycaemia.

Pregnancy. ACE inhibitors, ARBs, finerenone, and SGLT2 inhibitors are not used in pregnancy. Pre-conception planning is important — switching to pregnancy-compatible antihypertensives (labetalol, methyldopa, nifedipine), tightening blood pressure, ensuring adequate folate, and arranging joint obstetric–nephrology care. A history of pre-eclampsia or gestational hypertension itself is a reason for annual eGFR plus UACR in later years.

When to escalate / refer nephrology

Per KHA-CARI and RACGP, referral is indicated when:

Routine kidney specialist review: eGFR <30, UACR >70 mg/mmol, eGFR falling more than 5 mL/min/year, persistent blood plus protein in urine, resistant high blood pressure on three or more agents, suspected inherited kidney disease, CKD diagnosed under age 40, recurrent kidney stones.
Semi-urgent: new nephrotic-range proteinuria, suspected glomerulonephritis or vasculitis (rapidly progressive picture with falling eGFR and active urine sediment), pregnancy with CKD.
Urgent / emergency department: acute kidney injury with eGFR <15, potassium >6.5 not correctable, fluid overload not responding to diuretics, uraemic symptoms (confusion, vomiting, pericarditis), suspected rapidly progressive glomerulonephritis with deteriorating function, malignant hypertension with acute kidney injury.

What goes with the referral: a trended graph of eGFR, UACR and blood pressure, the full medication list (especially nephrotoxins), urinalysis, renal ultrasound, any immunology that has been run, and a list of comorbidities (diabetes, heart failure, cardiovascular disease).

What this article is and is not

This is general health information drawn from current Australian primary-care guidelines — RACGP CKD resources, Kidney Health Australia / KHA-CARI, Therapeutic Guidelines, Australian Medicines Handbook, NPS MedicineWise, Heart Foundation 2023 — together with the major modern kidney trials (DAPA-CKD, EMPA-KIDNEY, FIDELIO-DKD, FIGARO-DKD, FLOW). It is not personal medical advice and does not create a doctor–patient relationship. Decisions about specific medicines, doses, and referral are made with your own GP and treating clinicians based on your full clinical picture.

For Australian consumer-friendly sources: Kidney Health Australia, HealthDirect — Chronic kidney disease, Better Health Channel — Kidney disease, NPS MedicineWise consumer.

Sources cited

Frequently asked questions

I had a blood test and my eGFR was 55 — does that mean I have kidney disease?

Possibly, but one result is not a diagnosis. CKD requires the abnormality to be present for at least 3 months, so a repeat eGFR and a urine albumin-creatinine ratio (UACR) on a first-morning urine sample are needed. eGFR can also be temporarily low from dehydration, certain medicines (including trimethoprim, fenofibrate, some HIV antivirals), heavy creatine supplementation, or after a recent illness. If the eGFR stays in the 45–59 range across two readings 3 months apart, that meets criteria for CKD stage 3a — most of which is stable and managed well in general practice.
Why is the urine test (UACR) as important as the blood test (eGFR)?

Because albumin leaking into the urine is one of the earliest signs the filtering units of the kidney are under stress, and it independently predicts both kidney decline and heart attack and stroke risk. Two people with the same eGFR but different UACRs sit in very different risk categories. UACR also drives treatment — Australian PBS access to dapagliflozin for non-diabetic CKD, for example, requires a UACR above a threshold. A first-morning urine sample is preferred; very heavy exercise, a urinary tract infection, or menstruation in the prior 24 hours can produce a falsely high result, so a confirmation on a second sample is standard.
I've been told to take an ACE inhibitor and my creatinine went up a bit — should I stop?

Usually not. A rise in creatinine of up to about 25% after starting an ACE inhibitor or ARB is expected and reflects the medicine doing its job — reducing pressure inside the filtering units (glomeruli) to protect them long-term. Per RACGP and Australian Medicines Handbook guidance, this is checked with a blood test at 1–2 weeks. The medicine is typically continued unless the creatinine rises more than 25%, potassium rises above about 5.5 mmol/L without correction, or symptoms (dizziness, very low blood pressure) develop. Stopping the medicine because of a small expected change can lose you the long-term benefit on kidney and heart outcomes.
What are SGLT2 inhibitors and why are they being used in people without diabetes?

SGLT2 inhibitors (dapagliflozin/Forxiga, empagliflozin/Jardiance) were developed for type 2 diabetes but were shown in the DAPA-CKD (2020) and EMPA-KIDNEY (2023) trials to slow kidney decline and reduce cardiovascular events in people with CKD regardless of whether they have diabetes. They work by easing the abnormal pressure inside the filtering units and reducing inflammation. PBS access in Australia covers CKD with albuminuria above defined thresholds at eGFR ≥25 (dapagliflozin) or ≥20 (empagliflozin). The main practical things to know: a small expected dip in eGFR after starting, increased thrush/urinary thrush, the need to pause the medicine during vomiting or diarrhoea (sick-day rules), and a rare but serious risk of diabetic ketoacidosis even at near-normal sugar levels.
Do I need to avoid Nurofen or other anti-inflammatories?

Yes, where reasonable. Non-steroidal anti-inflammatory drugs (NSAIDs) — ibuprofen (Nurofen), diclofenac (Voltaren), naproxen, and prescription cousins like celecoxib — reduce blood flow inside the kidney and can both accelerate CKD progression and trigger acute kidney injury, especially when combined with an ACE inhibitor or ARB plus a diuretic (the 'triple whammy'). Paracetamol is the safer first-line for most musculoskeletal pain in CKD. Topical NSAID gels carry less risk than oral, and short courses can be discussed with your GP. The same caution applies to high-dose vitamin C above 500 mg/day, certain Chinese herbal preparations (aristolochic acid contamination), and avoidable IV contrast scans.
My eGFR is dropping — am I heading for dialysis?

For most Australians with CKD the answer is no. The trajectory depends on the cause, the rate of decline, the UACR, and how much of the four-pillar treatment is already in place. The Kidney Failure Risk Equation (KFRE) gives a personalised 2-year and 5-year risk of needing dialysis or transplant from your eGFR, UACR, age, and sex. Most people with stage 3 CKD never progress to dialysis — they die of (or with) cardiovascular disease, which is why blood pressure, cholesterol, smoking, and diabetes control matter as much as the kidneys themselves. For people who do approach kidney failure, options include transplant (often pre-emptive, before dialysis), home or in-centre dialysis, or conservative non-dialysis care — particularly relevant for frail older adults where dialysis may add little quality-adjusted survival. These conversations should start early, not at the last minute.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.