There is a blood test I now add to almost every routine check I do for Black patients over 40. It is not standard protocol. It is not what the appointment was booked for. But after years of watching people receive serious kidney disease diagnoses that should have been caught five years earlier — caught, and managed, and slowed — I have stopped waiting to be asked.
The test takes 30 seconds to add to a request form. The result comes back in a few days. And in a meaningful number of cases, what it finds is a kidney function that has been quietly declining for years without producing a single symptom the patient noticed.
That is the defining feature of chronic kidney disease in its early stages: silence. Your kidneys continue filtering your blood, regulating your blood pressure, producing hormones — doing everything they are supposed to do — even when functioning at 60%, 50%, 40% of normal capacity. There is no alarm. No pain. No obvious sign. Just a slow, invisible decline.
For Black and African adults, the risk of that silent decline is three times higher than for white adults. This gap shows up consistently across decades of UK and US data, driven by biology, by the disproportionate burden of hypertension and diabetes in our communities, and by a healthcare system that has historically underdiagnosed us.
Why Black patients are disproportionately affected
Hypertension is the leading cause of kidney disease in Black patients — and as we established in our hypertension guide, Black adults develop high blood pressure earlier and more severely. Sustained high blood pressure damages the small blood vessels within the kidneys over years, progressively reducing their filtering capacity.
Diabetes is the second leading cause of kidney failure overall. Given the higher rates of type 2 diabetes in Black communities, this compounds the risk significantly.
APOL1 gene variants — this is specific to people of African ancestry. Two variants of the APOL1 gene (G1 and G2) are present in approximately 13% of African Americans and similar proportions of African-ancestry populations in the UK. People who inherit two copies of these variants have a dramatically elevated risk of kidney disease — independent of blood pressure or diabetes. This genetic factor explains a significant portion of the racial disparity that cannot be accounted for by other risk factors alone.
Healthcare access and late diagnosis — Black patients are more likely to be diagnosed with kidney disease at a later stage, when management options are more limited. This is partly due to the race correction in eGFR calculations (discussed below), and partly due to structural factors in healthcare access.
The eGFR race correction — a controversy you need to know about
For decades, the standard formula used to calculate eGFR (estimated Glomerular Filtration Rate — the key kidney function measure) included a race correction factor. It assumed that Black patients had greater muscle mass on average, producing more creatinine, and therefore applied a multiplier that gave Black patients a higher estimated eGFR than the same creatinine value would give a white patient.
The consequence: Black patients appeared to have better kidney function than they actually did. This meant they were often diagnosed later, referred to specialists later, and placed on transplant waiting lists later.
Following sustained advocacy from kidney specialists and patient groups, most UK laboratories have now removed this race correction. If you are Black and have kidney function results from before 2022, they may have used the old formula — your actual kidney function may have been worse than the numbers suggested.
If you have any concern about this, ask your GP to re-calculate your eGFR without the race correction, or simply order a fresh blood test.
Understanding the stages of CKD
CKD is staged by eGFR:
| Stage | eGFR | What it means |
|---|---|---|
| G1 | 90+ | Normal or high — with evidence of kidney damage |
| G2 | 60–89 | Mildly reduced |
| G3a | 45–59 | Mildly to moderately reduced |
| G3b | 30–44 | Moderately to severely reduced |
| G4 | 15–29 | Severely reduced — prepare for kidney replacement |
| G5 | Below 15 | Kidney failure — dialysis or transplant |
Stages G1 and G2 with no other markers of kidney damage may simply reflect normal ageing. Stages G3 and above require monitoring and management.
Urine albumin-to-creatinine ratio (ACR) is equally important — protein leaking into the urine (proteinuria) is a sign of kidney damage even when eGFR is normal. Always request both tests.
Case study: Emeka's routine check
Emeka, 48, a project manager from Lagos based in Birmingham, came to see me for a repeat prescription for his blood pressure medication. He had been on amlodipine for two years and his blood pressure was reasonably controlled.
I added a kidney function check to his routine bloods — something his previous GP had not done consistently. His results: eGFR 44, ACR 35 mg/mmol (moderately elevated).
He had stage G3b CKD with significant proteinuria. He had no symptoms whatsoever.
I referred him to a nephrologist. Additional investigations revealed that his APOL1 genotype was high risk. His kidney disease was more advanced than his blood pressure control alone would have predicted.
The nephrologist added an SGLT2 inhibitor (empagliflozin) — a medication originally developed for diabetes that has been shown to significantly slow CKD progression regardless of diabetes status. His ACR has reduced by 40% over 18 months. His eGFR has remained stable.
"I had no idea," Emeka told me. "I felt completely fine. If you hadn't checked, I wouldn't have known until it was much worse."
He is right. Without that routine check, he would likely have continued undetected until his eGFR dropped significantly further.
Symptoms of advanced CKD — what to watch for
In early stages, there are typically no symptoms. As CKD progresses:
- Fatigue — the kidneys produce erythropoietin, which stimulates red blood cells. Reduced production causes anaemia and profound tiredness
- Swelling — particularly ankles and feet, as fluid retention increases
- Shortness of breath — from fluid accumulation or anaemia
- Nausea and loss of appetite — from waste product accumulation
- Itching — from urea and other waste products depositing in the skin
- Muscle cramps — from electrolyte imbalances
- Changes in urination — foamy urine (protein), reduced output, or nocturia (waking to urinate at night)
- High blood pressure that is increasingly difficult to control
If you have any of these symptoms and have not had recent kidney function tests, see your GP promptly.
Management — slowing progression
CKD cannot typically be reversed but its progression can be significantly slowed:
Blood pressure control — target below 130/80 for people with CKD. ACE inhibitors and ARBs (despite being less effective as blood pressure agents in Black patients generally) have specific kidney-protective effects in CKD with proteinuria. The decision requires specialist input.
SGLT2 inhibitors — medications like empagliflozin and dapagliflozin are now first-line for CKD protection regardless of diabetes status. They reduce progression and cardiovascular risk simultaneously.
Finerenone — a newer medication with strong evidence for kidney protection in diabetic kidney disease.
Dietary modifications — reducing dietary protein (in advanced CKD), managing potassium and phosphate intake, reducing salt. A renal dietitian referral is essential in G3b and above.
Avoiding nephrotoxins — NSAIDs (ibuprofen, naproxen) should be avoided or used minimally in CKD — they reduce kidney blood flow and accelerate damage. Many over-the-counter painkillers contain NSAIDs. Paracetamol is the preferred painkiller in CKD.
Regular monitoring — eGFR and ACR every 6–12 months in G3, every 3–6 months in G4.
When to ask your GP for a kidney check
Request an eGFR and urine ACR test if you are:
- Black and over 35
- Have hypertension, regardless of how well controlled
- Have type 1 or type 2 diabetes
- Have a family history of kidney disease or kidney failure
- Experience any of the symptoms listed above
- Take regular NSAIDs
This is a simple blood and urine test. It takes one appointment. It can detect kidney disease years before symptoms appear — years in which meaningful intervention is possible.
Sources: NHS England — Equality and Health Inequalities in Kidney Care 2022; Bikbov B et al, The Lancet 2020 (Global CKD Burden); Freedman BI et al, Clinical Journal of the American Society of Nephrology 2021 (APOL1 variants); NICE CKD Guideline NG203 (2021); NKF/ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease 2021; Perkovic V et al, NEJM 2019 (CREDENCE trial — SGLT2 inhibitors in CKD).
