Kidney function: 2.7 million Australians have signs of disease, and 9 in 10 don't know.

Kidney function gets measured three ways. eGFR estimates how fast your kidneys filter blood. Cystatin C is a more muscle-independent version of the same estimate. uACR is a urine test that detects albumin leaking through damaged filters. Between them they answer two different questions: how much filtering capacity you have left, and whether the filters themselves are being wrecked. Most Australians have only ever had the first question answered. That's a problem, because kidney damage shows up in the urine before it shows up in the blood.

The numbers, up front

The AIHW's analysis of the ABS National Health Measures Survey found that 14.2% of Australian adults, roughly 2.7 million people, had biomedical signs of chronic kidney disease in 2022–24. Among people aged 75 and over it was about 47%. Only 7.4% of those with biomedical signs said they had the condition, which makes CKD one of the most under-diagnosed chronic diseases in the country.

Kidneys fail quietly. You can lose a large share of filtering capacity with no symptoms at all, and by the time fatigue, swelling or nausea arrive the disease is usually advanced. Albuminuria typically precedes any measurable fall in eGFR, and it predicts death and cardiovascular events independently of filtration rate. None of this used to be very actionable. It is now: three trials since 2020 have shown the rate of kidney decline can be slowed with drugs that are widely available.

The three tests, and what each one actually tells you

eGFR, your filtering capacity

eGFR (estimated glomerular filtration rate) is the headline number on almost every Australian blood result. It isn't measured directly. It's calculated from your serum creatinine, age and sex. KDIGO 2024 staging puts ≥90 mL/min/1.73m² at normal (G1), 60–89 mildly decreased (G2), 45–59 at G3a, and below 45 at G3b to G5.

The word "estimated" is doing a lot of work there. Creatinine is a by-product of muscle metabolism, so the estimate inherits your body composition. eGFR systematically overestimates kidney function in people with low muscle mass, which means older adults, anyone with sarcopenia, anyone on a low-protein diet. It can go the other way in athletes and heavily muscled people. A normal eGFR in a frail 78-year-old is not the same finding as a normal eGFR in a 40-year-old rower, and reading them the same way is a common and consequential error.

One more thing gets missed constantly. CKD requires chronicity. KDIGO defines it as an abnormality persisting at least three months, so a single low eGFR after a bout of dehydration, a hard training block, or a course of anti-inflammatories is not a diagnosis. It's a reason to repeat the test.

Cystatin C, the accuracy check

Cystatin C is a small protein produced by essentially all nucleated cells and cleared by the kidneys. Its production barely depends on muscle mass, which sidesteps creatinine's biggest weakness. HodieLabs interprets it at <0.90 mg/L optimal, 0.90–1.10 borderline, >1.10 elevated.

The evidence behind it is strong. Shlipak and colleagues pooled 11 general-population cohorts totalling 90,750 people plus five CKD cohorts for their 2013 New England Journal of Medicine paper, and found that cystatin C-based eGFR predicted death and end-stage kidney disease more accurately than creatinine-based eGFR. It also reclassified a meaningful share of people into or out of a CKD diagnosis, which matters most for the people sitting right at the threshold. The 2021 CKD-EPI equations from Inker et al. formalised the combined estimate, eGFRcr-cys, now the most accurate routinely available measure of true filtration rate.

KDIGO 2024 does not replace creatinine with cystatin C. It keeps creatinine as the initial assessment and recommends adding cystatin C when greater accuracy would change what you do next. In preventative health, where the whole point is spotting drift years before a threshold is crossed, that condition is met more often than not.

uACR, the damage signal

The urine albumin-to-creatinine ratio is the test that gets skipped, and it's arguably the most informative of the three. Healthy glomeruli hold albumin back. When the filtration barrier is injured by high blood pressure, high blood glucose or inflammation, albumin starts appearing in urine. KDIGO grades it A1 (<3 mg/mmol, normal), A2 (3–30, moderately increased) and A3 (>30, severely increased). It's substantially more reliable than a dipstick protein reading, and because it reflects generalised microvascular injury it carries cardiovascular meaning as well as renal.

What the clinical evidence actually shows

• CKD Prognosis Consortium (Matsushita et al. Lancet 2010): the collaborative meta-analysis that established the modern two-axis model of kidney risk. An eGFR below 60 and an ACR at or above roughly 1.1 mg/mmol were each independent predictors of all-cause and cardiovascular mortality. This is the finding that matters most when you read your own results: a normal eGFR does not cancel out a raised uACR. The two must be read together, which is why KDIGO's risk grid is a grid.
• Cystatin C meta-analysis (Shlipak et al. NEJM 2013): across roughly 93,000 participants, cystatin C-based eGFR beat creatinine-based eGFR for predicting death and end-stage kidney disease.
• Kidney Failure Risk Equation (Tangri et al. JAMA 2011): age, sex, eGFR and uACR, four routinely available inputs, predict 2-year and 5-year probability of kidney failure with strong accuracy. Since validated in over 700,000 people across more than 30 countries, including an Australian cohort. Risk here is quantifiable, not a feeling.
• DAPA-CKD (Heerspink et al. NEJM 2020): dapagliflozin cut the composite of ≥50% eGFR decline, end-stage kidney disease or renal death by 44% (HR 0.56, 95% CI 0.45–0.68), with a 31% reduction in all-cause mortality. Benefit was similar in people without type 2 diabetes.
• EMPA-KIDNEY (NEJM 2023): in 6,609 participants across a wide range of kidney function, empagliflozin reduced CKD progression or cardiovascular death by 28% (HR 0.72, 95% CI 0.64–0.82).
• FLOW (Perkovic et al. NEJM 2024): led from Australia by Vlado Perkovic and colleagues, semaglutide in type 2 diabetes with CKD reduced major kidney events by 24% (HR 0.76, 95% CI 0.66–0.88) and death from any cause by 20%.

Where this evidence stops

Two caveats matter, and skating past them would be exactly the thing this library exists to avoid.

The treatment trials were not run in healthy people. DAPA-CKD, EMPA-KIDNEY and FLOW all enrolled participants who already had established kidney disease, most with significant albuminuria. They prove progression can be slowed once disease exists. They say nothing about someone with a mildly reduced eGFR and a normal uACR, and implying otherwise would be dishonest.

Population-wide CKD screening of low-risk adults has also never been shown in a randomised trial to reduce mortality. The case for testing is strongest in people with diabetes, hypertension, cardiovascular disease, obesity, a family history of kidney disease, or age over 60, where guidelines already recommend annual eGFR and uACR. What CKD-PC and the KFRE do establish is that if you measure, the numbers carry real prognostic weight and can be acted on.

There are practical confounders too. uACR rises transiently with vigorous exercise, febrile illness, urinary tract infection and menstruation, so an incidental abnormal result should be confirmed on a first-morning specimen before anyone changes anything. Serum urea, often reported alongside, climbs with dehydration, high protein intake and GI bleeding. It is not specific to kidney disease at all.

Why kidney numbers are also heart numbers

Here is the part that gets under-appreciated most. The likeliest outcome of chronic kidney disease isn't dialysis. It's cardiovascular death. The CKD-PC data show mortality risk climbing steadily as eGFR falls and albuminuria rises, well before anyone approaches kidney failure. So kidney markers belong in the same risk conversation as ApoB, blood pressure and HbA1c, not in a separate renal silo. An abnormal uACR should trigger a full cardiovascular review.

The Australian gap

Australia is unusual in that the blood half of kidney screening is close to universal. Creatinine and eGFR appear on almost every routine panel, so most adults already have a number sitting in a file somewhere. The gap is entirely on the other side. uACR needs a separate urine sample that frequently isn't ordered outside diabetes care, and cystatin C is essentially never included by default. The result is a system that reliably catches kidney disease once filtration has already dropped and reliably misses it while albumin is leaking but function still looks fine, which is precisely the window where intervention does the most good. With 47% of Australians aged 75 and over showing biomedical signs of CKD, and 1.7 million dialysis-related hospitalisations in 2023–24, that gap is expensive in every sense of the word.

How testing works at HodieLabs

We measure eGFR, cystatin C and uACR in every Health Blueprint at our Melbourne Preventative Health & Longevity Clinic, and interpret them against the KDIGO 2024 thresholds above rather than a lab's population reference range. They're read as a cluster, alongside blood pressure, glycaemic markers and the cardiovascular panel. Because members are tested repeatedly, the value isn't only the single reading. It's the trajectory. Someone moving from an eGFR of 96 to 84 over three years is telling you something that a one-off "normal" result never could.

If you have diabetes, high blood pressure, cardiovascular disease or a family history of kidney problems, the highest-yield test available to you right now probably isn't another blood test. It's the urine one nobody ordered.

References

1. Matsushita K, van der Velde M, Astor BC, et al. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. Lancet. 2010;375(9731):2073–2081.
2. Shlipak MG, Matsushita K, Ärnlöv J, et al. Cystatin C versus creatinine in determining risk based on kidney function. N Engl J Med. 2013;369(10):932–943.
3. Inker LA, Eneanya ND, Coresh J, et al. New creatinine- and cystatin C-based equations to estimate GFR without race. N Engl J Med. 2021;385:1737–1749.
4. 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.
5. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553–1559.
6. Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in patients with chronic kidney disease. N Engl J Med. 2020;383:1436–1446.
7. The EMPA-KIDNEY Collaborative Group. Empagliflozin in patients with chronic kidney disease. N Engl J Med. 2023;388:117–127.
8. Perkovic V, Tuttle KR, Rossing P, et al. Effects of semaglutide on chronic kidney disease in patients with type 2 diabetes. N Engl J Med. 2024;391:109–121.
9. Australian Institute of Health and Welfare. Chronic kidney disease: Australian facts. AIHW, Australian Government; 2026.

This article is general information, not medical advice. Speak with your GP about what testing and care is appropriate for you.