2026 ESC Guidelines for the Management of Cardiovascular Disease and Chronic Kidney Disease

Authors, Journal, Affiliations, Type, DOI

• Authors: Damman K, ter Maaten JM, Mayne KJ, et al; chaired by K. Damman and W. G. Herrington
• Journal: European Heart Journal 2026
• Affiliations: ESC Task Force, in collaboration with the European Renal Association; participating bodies include ACNAP, ACVC, EACVI, EAPC, EAPCI, EHRA and the HFA, plus the ESC Councils on Hypertension and Valvular Heart Disease
• Type: Clinical practice guideline — the first dedicated ESC guideline on cardiovascular disease and chronic kidney disease
• DOI: 10.1093/eurheartj/ehag098
• Grading: GRADE-based recommendation tables using the new ESC 2026 levels-of-evidence framework, applied here for the first time

Overview

The guideline reframes CKD as a cardiovascular risk state and cardiovascular disease as a kidney risk state, and organises care around the acronym STAMP on CKD — Screen, Triage and stage, Address CKD risk, Modify CVD management, Plan health services. It mandates eGFR plus spot urine albumin-to-creatinine ratio in every patient with established cardiovascular disease, KDIGO CGA staging, and absolute kidney-failure risk estimation with the Kidney Failure Risk Equation in G3–G5. It then sets out a four-pillar cardiorenal pharmacotherapy stack — ACE inhibitor or ARB, SGLT2 inhibitor, non-steroidal MRA and GLP-1 receptor agonist — with initiation thresholds taken directly from trial eligibility criteria, and applies CKD-specific modifications across heart failure, chronic and acute coronary syndromes, peripheral artery and cerebrovascular disease, venous thromboembolism, atrial fibrillation, valvular disease, acute kidney injury, dialysis and transplantation. Three themes recur: do not delay indicated cardiovascular procedures for fear of contrast-associated AKI; continue foundational drugs through an acute eGFR dip of under 30%; and prefer factor Xa inhibitors over vitamin K antagonists at low eGFR while abandoning conventional stroke and bleeding scores below eGFR 30.

Keywords

Chronic kidney disease; cardiovascular disease; blood pressure; lipids; heart failure; acute coronary syndrome; chronic coronary syndrome; stroke; peripheral arterial disease; venous thromboembolism; atrial fibrillation; anticoagulation; contrast-induced nephropathy; dialysis; transplantation; albuminuria; SGLT2 inhibitors; finerenone; GLP-1 receptor agonists; KFRE

Key Takeaways

Definition, Staging and Screening

• Definition: abnormality of kidney structure or function present for ≥3 months with health implications — in practice eGFR <60 mL/min/1.73 m² or uACR ≥3 mg/mmol (≥30 mg/g).
• Staging is CGA — Cause, GFR, Albuminuria — displayed as the KDIGO heatmap. G5 is persistent eGFR <15 and is termed kidney failure, replacing "end-stage kidney disease". A1 is uACR <3, A2 3–30, A3 >30 mg/mmol.
• Relative kidney-failure risk by heatmap colour: moderate 3–20-fold, high 20–70-fold, very high >70-fold, independent of age and sex.
• Classify by GFR and albuminuria into moderate, high or very high risk: I A. Use creatinine-based eGFR with a validated equation (I A), a spot morning uACR (I A), and two values ≥3 months apart to establish chronicity (I C). Cystatin C-based eGFR is recommended when creatinine is unreliable — extremes of muscle mass, or trimethoprim-like tubular secretion interference (IIa A).
• Equation choice: the 2009 CKD-EPI equation without a race coefficient is described as "an optimal compromise for European populations"; the 2021 US-derived equation overestimates GFR in large parts of Europe.
• Screen every patient with cardiovascular disease — hypertension, CAD, HF, PAD or stroke — with eGFR plus albuminuria (I C). Repeat annually in diabetes or high risk, and within days to weeks when a new or unexpected abnormality appears.
• Nephrology referral triggers: KDIGO very-high risk, eGFR <30, uACR ≥70 mg/mmol, uACR ≥30 mg/mmol with haematuria, a ≥2-fold uACR rise from a baseline ≥30 mg/mmol, KFRE >3%–5% five-year risk, or metabolic complications of severe CKD.
• KFRE in G3–G5 (I A): a >3%–5% five-year risk prompts nephrology referral and a >40% two-year risk prompts dialysis-access planning. The KDIGO heatmap serves population triage; KFRE gives individual absolute risk.
• Bidirectional risk: incident cardiovascular disease raises subsequent kidney replacement therapy risk most in the first three months — 2–4-fold after CAD, stroke or AF, and 45-fold after incident heart failure.

Drug Dosing and Metabolic Complications

• Use absolute (de-indexed) GFR — eGFR × BSA/1.73 — at very high or very low body surface area; measure directly where precision matters. Cockcroft-Gault and 24-hour collections overestimate GFR through tubular secretion.
• CKD is itself a risk factor for QT prolongation; monitor ECG where relevant.
• Potassium: act above 5.5 mmol/L, a threshold of ~5.7 is often justified in CKD, but avoid ≥6.0. Review co-medication, correct acidosis, consider a loop diuretic and dietary restriction, then potassium binders. Insulin-dextrose does not excrete potassium, so refractory hyperkalaemia with low GFR may need emergency dialysis.
• Anaemia: start an ESA at haemoglobin <9.0–10.0 g/dL and do not correct beyond 11.5 g/dL.
• Metabolic acidosis: oral sodium bicarbonate only when bicarbonate is <18 mmol/L.

Cardiovascular Risk Assessment

• In a meta-analysis of 114 cohorts (~28 million people), eGFR <60 and/or albuminuria independently raised MI, stroke, HF, AF, PAD and cardiovascular mortality, with the highest risk at eGFR <30 and A3.
• "Relatively very high" risk (I B): eGFR <30 with any albuminuria, or eGFR 30–44 with uACR 3–30, or uACR >30 with any eGFR. "Relatively high" (I B): eGFR 30–44 with uACR <3, or eGFR 45–59 with uACR 3–30.
• Use SCORE2 (<70 years) or SCORE2-OP (≥70) with the CKD Add-On in CKD without type 2 diabetes or ASCVD (I B), SCORE2-Diabetes in type 2 diabetes without ASCVD (I B), and SMART2 for recurrent events in established ASCVD (I B). Scores incorporating eGFR and albuminuria are preferred. Do not sum separate ASCVD and heart-failure estimates, and scores are not for kidney failure.

The Four-Pillar Cardiorenal Pharmacotherapy Stack

• SGLT2 inhibitors reduce kidney disease progression by ~40% irrespective of baseline eGFR, with a class effect across agents and ~25% fewer reported AKI events; there is no effect on MI or stroke, and the cardiovascular benefit is largely heart-failure hospitalisation and cardiovascular or sudden death. Glucose lowering is minimal below eGFR 30. Continue long term, and continue below eGFR 20 until dialysis starts.
• Finerenone: FIDELITY kidney composite HR 0.77 (0.67–0.88), cardiovascular composite HR 0.86 (0.78–0.95) driven by heart-failure hospitalisation HR 0.78 (0.66–0.92). Initiate when potassium is ≤5.0 mmol/L; hyperkalaemia occurred in 14.0% versus 6.9% with no fatal events. Nearly 40% of trial patients had eGFR >60 and qualified on albuminuria.
• GLP-1 receptor agonists: FLOW primary kidney composite HR 0.76 (0.66–0.88), eGFR slope reduced by about one third, MACE HR 0.82 (0.68–0.98); pooled across eight trials, kidney failure HR 0.84 (0.72–0.99). Not tested in non-diabetic CKD.
• A <30% eGFR dip on initiation is expected and acceptable. Check eGFR and potassium 1–4 weeks after starting or increasing an ACE inhibitor, ARB or finerenone, but no extra biochemical monitoring is routinely needed for SGLT2 inhibitors or GLP-1 receptor agonists. Stop ACE inhibitor, ARB or finerenone at potassium ≥6.0. Apply sick-day rules during intercurrent illness and restart promptly.
• Glycaemic control: HbA1c at least twice yearly, target <53 mmol/mol (<7.0%) where achievable (I B1). SGLT2 inhibitors and GLP-1 receptor agonists are first-line glucose-lowering agents (I A); metformin may be used at eGFR ≥30 (IIa B1), halved below 45 and stopped below 30.

Blood Pressure and Lipids

• Intensify when confirmed office BP is ≥130/80 and eGFR ≥30 (I A); target SBP 120–129 mmHg if tolerated (I A). Below eGFR 30 the target is individualised (I C), with 120–129 "reasonable for many". SPRINT included 28% with CKD and showed similar cardiovascular benefit, but intensive lowering increased a 30% eGFR fall in non-CKD participants.
• Prioritise ACE inhibitor or ARB and SGLT2 inhibitors; add a dihydropyridine calcium channel blocker and/or diuretic. Thiazides are preferred at eGFR ≥30 and loop diuretics below it. Spironolactone for resistant hypertension is acceptable at eGFR ≥30 and only if not already on finerenone.
• Lipid strategy is "fire-and-forget": an intensive statin-based regimen without routine re-testing unless results would change management. At eGFR <60 and not on kidney replacement therapy, an intensive statin-based regimen irrespective of lipid level is I A — SHARP showed a 17% relative risk reduction in major atherosclerotic events with simvastatin 20 mg plus ezetimibe 10 mg. Benefit attenuates below eGFR 30, and dialysis-dependent patients show no clear effect (RR 0.94, 99% CI 0.79–1.11).
• Routine antiplatelet therapy at eGFR <60 without symptomatic ASCVD is not recommended — III B1.

Heart Failure and CKD

• More than 90% of outpatients with severe CKD are already stage B or C of the heart-failure continuum; NT-proBNP ≥500 pg/mL gave 69% sensitivity and 80% specificity for heart failure, and <125 pg/mL retains a high negative predictive value. Natriuretic peptide screening is only IIb C.
• Irrespective of LVEF: loop diuretics I A; SGLT2 inhibitor at eGFR ≥20 I A. Do not initiate an SGLT2 inhibitor below eGFR 20 or on dialysis, but continue if already established and eGFR falls below 20.
• MRA: steroidal MRA in HFrEF at eGFR ≥30 I A; either steroidal or non-steroidal MRA at LVEF ≥40% with eGFR ≥25 IIa B1. The text concedes the MRA effect is smaller at LVEF >40% and smaller again at eGFR <60, and the FINEARTS-HF CKD subgroup HR of 0.91 (0.78–1.07) crosses unity.
• HFrEF: ACE inhibitor, ARNI or ARB at eGFR ≥30 I A; beta-blocker I A at eGFR ≥30; ARNI IIa B1 as an alternative to slow eGFR decline. At eGFR 15–29, ACE inhibitor or ARB and beta-blockers fall to IIb C; there are no data below eGFR 15 or on dialysis.
• Additional therapy: digoxin or digitoxin IIa B1 at eGFR >20 (DIGIT-HF HR 0.82); ivabradine IIa B1 at eGFR ≥20; vericiguat IIb B1 at eGFR ≥30, since the eGFR 15–30 subgroup had a hazard ratio above 1.
• HFpEF: semaglutide or tirzepatide IIa B1 at eGFR ≥15, LVEF ≥45%, with obesity and with or without diabetes (SUMMIT HR 0.62).
• Devices: indications should not differ by CKD stage, though primary-prevention ICD benefit attenuates below eGFR 60 (adjusted HR 0.49 at eGFR ≥60 versus 0.80 at <60, with a confidence interval crossing 1). CRT effect is not modified by CKD, and mitral TEER benefit is preserved.
• Decompensated HF: SGLT2 inhibitor early in admission at eGFR >20 I B1; IV furosemide-equivalent >40 mg in diuretic-naive patients IIa B2; acetazolamide 500 mg IV for three days added to a loop diuretic at eGFR ≥20 in patients on chronic loop therapy is IIa B1 (ADVOR). Assess diuretic response in the first days (IIa B1) — a spot urinary sodium <70 mmol/L at 2 hours should prompt doubling the dose and twice-daily dosing. Continue decongestion despite a creatinine rise up to 50% where the diuretic response is good (I C).
• Advanced HF: heart–kidney transplant team evaluation when eGFR <30 IIa C; durable mechanical support is not recommended with a baseline eGFR <30 that is unlikely to improve and no dual-organ option — III C.

ACS, Chronic Coronary Syndrome and Stroke

• Troponin is frequently elevated and stable in CKD; serial sampling is essential, and no validated CKD-specific threshold exists. The 99th percentile has lower specificity and positive predictive value.
• Do not delay an immediate or early invasive strategy (I C). STEMI: primary PCI with contrast-sparing protocols at eGFR <30. NSTE-ACS: immediate invasive for very-high-risk features irrespective of CKD; early invasive within 24 hours for dynamic ST-T change or GRACE >140.
• Abbreviated DAPT for three months or de-escalation after 1–3 months — IIa B1, with single antiplatelet therapy considered after three months.
• Chronic coronary syndrome: aspirin or clopidogrel I C, with clopidogrel preferred over aspirin at eGFR >30 (IIa B1); DAPT for 1–3 months after elective PCI IIa B2; very-low-dose rivaroxaban 2.5 mg twice daily added to aspirin at eGFR ≥30. PCSK9 inhibitor at eGFR ≥20 with LDL-C ≥1.8 mmol/L is IIa B1, with no recommendation below eGFR 20.
• An initial conservative strategy with optimal medical therapy is I B1 in chronic coronary syndrome — ISCHEMIA-CKD showed no death or MI benefit, no angina benefit, and stroke HR 3.76 and death or dialysis initiation HR 1.48 with an initial invasive strategy. CABG reduces MI by 51% and repeat revascularisation by 86% versus PCI without a survival difference, and is preferred in multivessel or left-main disease (IIb B2). Radial access is IIa C, and radial arteries should be preserved in patients with fistulae or future dialysis need.
• Stroke: antiplatelet therapy after ischaemic stroke including on kidney replacement therapy I B2; statin or ezetimibe I A in non-dialysis patients; SBP 120–129 I C; maximally tolerated ACE inhibitor or ARB first-line I B1. Carotid endarterectomy for symptomatic high-grade stenosis IIa B2, with no routine revascularisation for asymptomatic stenosis (III B2). Full correction of anaemia with ESAs is not recommended — III A, for stroke risk.

Atrial Fibrillation and Anticoagulation

• AF risk is ~50% higher at eGFR 30–59 and 2.4-fold at eGFR <30; prevalence on kidney replacement therapy is 11.6% (range 4.5%–27%).
• Existing ischaemic stroke risk scores are not recommended below eGFR 30 — III B. Existing bleeding scores are not recommended below eGFR 30 — III C, with c-statistics of 0.49–0.68. Such patients should be regarded as high risk for both stroke and bleeding, and are systematically undertreated.
• DOAC over VKA at eGFR ≥30 — I A (network meta-analysis of 170,059 patients: 14% fewer thromboembolic and 19% fewer bleeding events). Factor Xa inhibitor preferred at eGFR 15–29 (IIa B1).
• Below eGFR 15 the decision is individualised (IIa C). If anticoagulating: VKA or apixaban 2.5 mg twice daily below eGFR 15 off dialysis (IIb C); low-dose factor Xa inhibitor on dialysis (IIb C).
• AAD choice must account for structural disease, QT prolongation and electrolytes (I C); rhythm control is an alternative to rate control IIa C; catheter ablation for dialysis patients with AF and intradialytic haemodynamic instability is IIa C. Only ~20% of haemodialysis patients are AF-free at five years after ablation versus ~60% without CKD.
• VTE: DOAC over LMWH plus VKA at eGFR ≥30 I B2 (EINSTEIN major bleeding HR 0.54); factor Xa inhibitor at eGFR 15–29 IIb C; factor Xa inhibitor on dialysis IIb C.

Valvular Disease, AKI and Dialysis

• Valvular disease risk is 1.2–1.8-fold higher in CKD, with aortic valve area declining 0.1–0.2 cm²/year at eGFR <15 versus 0.05–0.1 in the general population. TTE for suspected valve disease irrespective of symptoms — I C; clinical and echo review every 6–9 months for moderate-to-severe AS with eGFR <45 (IIa C). TAVI over surgical replacement in severe AS at age ≥70 is IIa C. No pharmacological therapy slows calcific AS.
• AKI uses the KDIGO definition; the 26.5 µmol/L delta should not define AKI in CKD because of the exponential creatinine–GFR relationship. Contrast-associated AKI: pooled across 37 RCTs and 12,166 patients, AKI occurred in 9.5% and dialysis was needed in only 1.1%, usually temporarily; permanent harm is rare.
• Never delay a contrast procedure — I C; iso-osmolar or low-osmolar contrast with contrast-sparing protocols at eGFR <30 I A; group 2 or 3 gadolinium agents at eGFR <30 I B2; peri-procedural IV hydration at eGFR <30 IIb C; prophylactic haemodialysis is not recommended — III B2.
• Dialysis: cardiovascular mortality is 5–10-fold higher than in the age- and sex-matched population, vascular calcification affects ~85%, and long interdialytic intervals cluster MI, stroke, decompensated HF and sudden death. Sudden cardiac death accounts for >40% of dialysis deaths, and loop-recorder data suggest bradyarrhythmias dominate.
• Proactive high-dose IV iron in maintenance haemodialysis unless ferritin >700 µg/L or TSAT ≥40% — I B1 (PIVOTAL: 400 mg monthly versus reactive, 15% reduction in the composite of non-fatal MI, stroke, heart-failure hospitalisation or death, HR 0.85). Haemoglobin target <11.5 g/dL.
• Routine MRAs on dialysis are not recommended — III A. Routine ICD for primary prevention at LVEF ≥35% on haemodialysis is not recommended — III C (ICD2, n=200, no benefit at five years). Antibiotic envelopes at CIED implantation are IIb C; subcutaneous ICDs IIb C.
• Transplantation is intermediate-risk surgery (1%–5% 30-day MACE). Diagnostic screening is not recommended in low-probability candidates (III C) because of the risk of delaying listing; screening is stratified by risk, with myocardial perfusion imaging or CCTA in high-risk asymptomatic candidates (IIa B).

Limitations of the document

• The evidence is thinnest exactly where the decisions are hardest. Most recommendations in the dialysis, transplant, valvular, stroke and device sections are Class IIa, IIb or III with level C, resting on post-hoc subgroup analyses or observational data with residual confounding.
• Trial-eligibility thresholds are presented as treatment thresholds. The eGFR and uACR cut-offs reflect enrolment criteria and health-economic analyses rather than biological boundaries, and the guideline concedes that within-person variability can misclassify patients without offering a firm rule.
• Internal text–table discordance: the narrative recommends GLP-1 receptor agonists for eGFR 25–89 with uACR ≥10 while the recommendation table specifies narrower bands; the key messages call it "reasonable" to start SGLT2 inhibitors below eGFR 20 while the recommendation table and heart-failure section decline to.
• Apixaban dosing is internally inconsistent — 2.5 mg twice daily is advised below eGFR 15 off dialysis, but 5 mg twice daily on dialysis, a higher dose in more profound kidney failure and one that omits the serum-creatinine limb of the standard dose-reduction criteria.
• The HFpEF MRA grade rests on a subgroup that crossed unity (FINEARTS-HF CKD HR 0.91, 0.78–1.07).
• No drug-dosing reference by design — doses are only those used in trials, and the reader is redirected to product labels and KDIGO.
• The population is European, adult and predominantly non-dialysis. The rejection of the 2021 CKD-EPI equation will not translate to US practice; paediatric, pregnancy and rare-cause CKD are out of scope.
• The new levels-of-evidence framework is used for the first time here, so B1 and B2 grading is not directly comparable with earlier ESC documents.
• Evidence tables are online-only, so several recommendations cannot be traced to individual trials from the document alone.

Key Concepts Mentioned

• CKD as a CGA-staged KDIGO heatmap state; G5 as kidney failure
• uACR as the preferred albuminuria metric, with dipstick limitations
• Bidirectional cardiorenal risk: CKD to CVD, and CVD to kidney failure
• Two-tier risk stratification — population heatmap versus individual absolute risk (KFRE, SCORE2 with CKD Add-On)
• The four-pillar cardiorenal pharmacotherapy stack and its initiation thresholds
• The haemodynamic eGFR dip as an expected pharmacological effect
• The "fire-and-forget" lipid strategy
• Diuretic resistance and natriuresis-guided decongestion
• Contrast-associated AKI versus AKI from multiple causes
• Proactive IV iron in haemodialysis
• The STAMP on CKD implementation framework

Key Entities Mentioned

• concepts/Chronic-Kidney-Disease · concepts/Cardiorenal-Syndrome · concepts/SGLT2-Inhibitors-in-CKD
• entities/Finerenone · concepts/GLP-1-Receptor-Agonists
• entities/Heart-Failure · entities/HFrEF · entities/HFpEF
• entities/Acute-Coronary-Syndrome · entities/Chronic-Coronary-Disease
• entities/Atrial-Fibrillation · concepts/NOAC-AF-Management
• concepts/Aortic-Stenosis · entities/Peripheral-Artery-Disease
• concepts/Dyslipidemia · entities/Hypertension
• Trials cited: SHARP, CREDENCE, DAPA-CKD, EMPA-KIDNEY, FIDELITY, FLOW, SOUL, SELECT, EMPEROR-Reduced/Preserved, DAPA-HF, DELIVER, RALES, EMPHASIS-HF, FINEARTS-HF, DIGIT-HF, SUMMIT, ADVOR, DOSE, CLOROTIC, ISCHEMIA-CKD, COMPASS, EINSTEIN, PIVOTAL, ICD2, WRAP-IT, ALERT, SPRINT, PROGRESS, CARSK

Wiki Pages Updated

• wiki/sources/CVD-CKD-ESC-2026.md — created
• wiki/concepts/Chronic-Kidney-Disease.md — rebuilt around CGA staging, KFRE, the four-pillar stack and the eGFR-dip rule
• wiki/concepts/NOAC-AF-Management.md — CKD-specific anticoagulation, including the abandonment of risk scores below eGFR 30
• wiki/entities/Heart-Failure.md — HF with CKD thresholds and drug classes
• wiki/sourceindex.md — new row
• wiki/wikiindex.md — new row