Chronic kidney disease (CKD) affects hundreds of millions of people worldwide and is projected to become a leading cause of death by mid-century. Simple laboratory tests allow early detection and staging, yet many individuals experience cardiovascular events or disability before kidney failure develops. Since 2019, large trials have expanded effective treatment options that slow loss of kidney function and reduce cardiovascular risk, while updated international guidance encourages coordinated action across specialties and health systems. Implementing straightforward, evidence-based interventions alongside routine monitoring can lessen the global burden of complications and delay progression to kidney failure in diverse clinical settings.
Global Burden and Simple Detection
CKD is defined by persistent abnormalities in kidney structure or function for at least 3 months with implications for health. Global prevalence is estimated in the hundreds of millions, with millions already receiving kidney replacement therapy. Mortality attributable to CKD is rising and is projected to rank among the top causes of death worldwide by 2050, with marked inequities in access to dialysis and transplantation across regions. A 2025 resolution highlights prevention, early detection and equitable care as priorities, including expanded transplantation capacity where feasible.
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Early identification relies on routine tests available in most settings. Glomerular filtration rate (GFR) reflects the volume of filtrate produced per minute and is commonly estimated from serum creatinine, with additional cystatin C recommended when precision is required. Albuminuria, quantified by urine albumin-to-creatinine ratio (uACR), is a key marker that often precedes GFR decline and signals higher risk even when estimated GFR (eGFR) is preserved. First-morning samples improve reliability, though random spot tests are practical and informative. Screening is advised for people at increased risk, including older adults and those with obesity, diabetes, high blood pressure, cardiovascular disease, structural abnormalities, family history or incidental haematuria.
Staging and Risk Stratification
International guidance recommends the CGA system, combining primary Cause with GFR categories (G1–G5) and albuminuria categories (A1–A3). Both eGFR and uACR should be measured to complete staging because each independently predicts outcomes, including kidney failure and cardiovascular disease. The staging framework aligns with a heat map that categorises risk as moderate, high or very high relative to the general population without CKD.
Absolute risk estimates refine decisions beyond categorical staging. The kidney failure risk equation uses age, sex, eGFR and uACR to calculate 2- or 5-year risk and can be integrated into electronic records when recent values are available. Higher predicted risk prompts closer monitoring, faster initiation of risk-modifying therapy and timely referral. Referral to nephrology is recommended when the 5-year risk exceeds 3–5%, when the primary cause is unclear or when complications require specialist management. Initial evaluation should include blood pressure, glycated haemoglobin, uACR, urine dipstick and renal ultrasound, with additional serological, imaging, genetic testing or biopsy if indicated.
Evidence-Based Interventions Across Settings
A core set of treatments reduces kidney failure and cardiovascular events across a broad CKD population. Sodium-glucose co-transporter-2 (SGLT2) inhibitors reduce kidney failure risk by approximately one-third and heart failure risk by approximately two-fifths, with benefits seen irrespective of diabetes status or primary cause and sustained at low eGFR. Renin-angiotensin system (RAS) inhibition with a single angiotensin-converting enzyme inhibitor or angiotensin-II receptor blocker lowers progression risk in albuminuric disease, though combining two RAS agents is not advised. Intensive blood pressure control to below 130/80 mm Hg, and to below 120 mm Hg systolic when tolerated and measured appropriately, reduces major cardiovascular events. Statin-based regimens, initiated early and used as a fire-and-forget strategy for eligible adults, mitigate atherosclerotic risk and are widely applicable, including primary prevention in many patients.
For CKD with type 2 diabetes, additional therapies further reduce risk. The non-steroidal mineralocorticoid receptor antagonist finerenone lowers kidney failure by about a quarter and reduces heart failure hospitalisation by about a fifth, with potassium monitoring required. Glucagon-like peptide-1 (GLP-1) receptor agonists, notably subcutaneous semaglutide at the anti-diabetic dose, reduce a composite of major kidney outcomes by about a quarter and improve cardiovascular outcomes, with an initiation titration to mitigate gastrointestinal effects. Glycaemic targets should be individualised, prioritising agents that confer kidney or cardiovascular benefit and adjusting metformin dosing at lower eGFR with discontinuation below specified thresholds.
Broader care includes lifestyle advice, vaccination against common infections where relevant, review of nephrotoxic medications, dose adjustments by kidney function and guidance on sick-day rules to prevent acute kidney injury. Diagnostic or interventional imaging should not be delayed solely due to CKD, permanent harm attributable to modern iodinated contrast is uncommon, and risk can be mitigated by minimising contrast volume and using low- or iso-osmolar agents.
CKD can be detected and staged with routine tests, and risk can be estimated with simple variables to guide timely, effective care. Core pharmacological strategies—SGLT2 inhibition, RAS blockade, statin-based regimens and intensive blood pressure targets—combine with lifestyle measures to slow progression and reduce cardiovascular events. In CKD with type 2 diabetes, finerenone and GLP-1 receptor agonists provide additional protection. Consistent application of these interventions, aligned with updated guidance and embedded risk stratification, enables clinicians across specialties to attenuate CKD complications and delay kidney failure without adding complexity to everyday practice.
Source: The Lancet
Image Credit: iStock
