Cardiovascular risk in CKD¶
TL;DR — Both lower eGFR and higher albuminuria predict cardiovascular mortality, coronary disease, stroke and heart failure beyond conventional risk factors (Matsushita 2015, PMID 26028594). Statin-based therapy reduced major atherosclerotic events in broad CKD in SHARP, but initiating statins in haemodialysis did not improve primary composite outcomes in 4D or AURORA (Baigent 2011, PMID 21663949) (Wanner 2005, PMID 16034009) (Fellstrom 2009, PMID 19332456). The stage-specific contrast is central: advanced dialysis biology includes calcification, arrhythmia, heart failure and competing non-atherosclerotic mechanisms. SGLT2 inhibitors and finerenone add cardiovascular benefits in eligible CKD populations (EMPA-KIDNEY Collaborative Group 2023, PMID 36331190) (Agarwal 2022, PMID 35023547).
Risk gradient¶
Cardiovascular risk rises continuously across GFR and albuminuria categories; albuminuria adds information even at preserved eGFR (Matsushita 2015, PMID 26028594).
SHARP¶
Simvastatin plus ezetimibe reduced major atherosclerotic events by 17% in 9,270 CKD patients, most not on dialysis at entry (Baigent 2011, PMID 21663949).
Dialysis statin trials¶
4D randomized 1,255 haemodialysis patients with type 2 diabetes to atorvastatin 20 mg; despite a 42% median LDL reduction the primary composite of cardiac death, non-fatal myocardial infarction and stroke was not reduced (RR 0.92, 95% CI 0.77–1.10) over median four years, and fatal stroke was more frequent (RR 2.03, 1.05–3.93) (Wanner 2005, PMID 16034009). AURORA randomized 2,776 haemodialysis patients to rosuvastatin 10 mg; LDL fell 43% but the primary composite was unchanged (9.2 vs 9.5 events per 100 patient-years; HR 0.96, 0.84–1.11), as was all-cause mortality (HR 0.96, 0.86–1.07) (Fellstrom 2009, PMID 19332456).
Mechanism mix¶
Atherosclerosis is only part of CKD cardiovascular disease. Left-ventricular hypertrophy, arterial stiffness, calcification, electrolyte shifts and sudden death become more prominent as GFR falls.
Kidney-directed drugs¶
EMPA-KIDNEY lowered all-cause hospitalization but not its heart-failure/CV-death secondary composite significantly; outcomes should not be generalized beyond trial precision (EMPA-KIDNEY Collaborative Group 2023, PMID 36331190).
Scope border¶
This page owns CKD as a cardiovascular risk state. General lipid and blood-pressure treatment algorithms remain in their home conditions.
Lipid-trial stage contrast¶
| Trial | Population | Primary atherosclerotic result | CKD interpretation |
|---|---|---|---|
| SHARP | 9,270 CKD; 3,023 on dialysis, no prior MI/revascularization | 11.3% vs 13.4%; RR 0.83 (0.74–0.94) | Statin/ezetimibe reduces major atherosclerotic events in broad CKD (Baigent 2011, PMID 21663949) |
| 4D | 1,255 with type 2 diabetes on haemodialysis | RR 0.92 (0.77–1.10) despite 42% LDL reduction; fatal stroke RR 2.03 (1.05–3.93) | Do not extrapolate non-dialysis initiation benefit to dialysis (Wanner 2005, PMID 16034009) |
| AURORA | 2,776 on haemodialysis | 9.2 vs 9.5 events/100 patient-years; HR 0.96 (0.84–1.11); mortality HR 0.96 (0.86–1.07) | Advanced CKD has competing non-atherosclerotic mechanisms (Fellstrom 2009, PMID 19332456) |
| CKD-PC | Individual-participant meta-analysis | eGFR and albuminuria independently predict CV outcomes | Risk association is not a statin-treatment effect (Matsushita 2015, PMID 26028594) |
Lipid lowering: the effect disappears at the dialysis boundary¶
Non-dialysis CKD. SHARP randomized 9,270 patients with CKD (6,247 not on dialysis, 3,023 on dialysis) and no history of myocardial infarction or coronary revascularisation to simvastatin 20 mg plus ezetimibe 10 mg or placebo. An average LDL-cholesterol difference of 0.85 mmol/L (SE 0.02, at about two-thirds compliance) over median 4.9 years produced a 17% proportional reduction in major atherosclerotic events (526 [11.3%] versus 619 [13.4%]; RR 0.83, 95% CI 0.74–0.94; log-rank p = 0.0021), driven by non-haemorrhagic stroke (131 [2.8%] versus 174 [3.8%]; RR 0.75, 0.60–0.94; p = 0.01) and arterial revascularisation (284 [6.1%] versus 352 [7.6%]; RR 0.79, 0.68–0.93; p = 0.0036), while non-fatal MI or coronary death was not significantly reduced (213 [4.6%] versus 230 [5.0%]; RR 0.92, 0.76–1.11; p = 0.37) (Baigent 2011, PMID 21663949).
Dialysis. AURORA randomized 2,776 haemodialysis patients aged 50–80 to rosuvastatin 10 mg or placebo. LDL fell 43% from a mean baseline of 100 mg/dL, yet over median 3.8 years the primary composite of cardiovascular death, non-fatal MI or non-fatal stroke occurred at 9.2 versus 9.5 events per 100 patient-years (HR 0.96, 95% CI 0.84–1.11; p = 0.59), with no effect on any individual component and none on all-cause mortality (13.5 versus 14.0 per 100 patient-years; HR 0.96, 0.86–1.07; p = 0.51) (Fellström 2009, PMID 19332456).
The pattern is the single most important structural fact about cardiovascular risk in CKD: LDL lowering works while there is atherosclerotic disease to modify and stops working once the dominant mechanisms become arrhythmic, cardiomyopathic and calcific. It also explains why the SHARP effect was carried by stroke and revascularisation rather than by coronary death — the coronary events in advanced CKD are increasingly not atherothrombotic.
Revascularisation does not rescue it either¶
ISCHEMIA-CKD randomized 777 patients with advanced kidney disease and moderate or severe ischaemia on stress testing to an initial invasive strategy (angiography plus revascularisation if appropriate, added to medical therapy) or an initial conservative strategy. At median 2.2 years, the primary composite of death or non-fatal MI occurred in 123 versus 129 patients (estimated 3-year event rate 36.4% versus 36.7%; adjusted HR 1.01, 95% CI 0.79–1.29; p = 0.95), with the key secondary composite similarly flat (38.5% versus 39.7%; HR 1.01, 0.79–1.29). The invasive strategy carried a higher incidence of stroke (HR 3.76, 95% CI 1.52–9.32; p = 0.004) and of death or dialysis initiation (HR 1.48, 1.04–2.11; p = 0.03) (Bangalore 2020, PMID 32227756).
A 3-year event rate of 36–37% in both arms is the number that frames the whole page: in advanced CKD with documented ischaemia, more than a third of patients die or infarct within three years regardless of strategy, and the intervention that helps in the general population adds stroke and dialysis without adding benefit.
The framing that replaced "cardiorenal syndrome"¶
The AHA presidential advisory defines cardiovascular–kidney–metabolic (CKM) syndrome as the interplay of metabolic risk factors, CKD and the cardiovascular system, and sets out a staging framework intended to promote prevention across the life course, prediction algorithms matched to CKM exposures and outcomes, harmonisation across subspecialty guidelines, and explicit incorporation of social determinants and interdisciplinary care models (Ndumele 2023, PMID 37807924). The concrete downstream product is the PREVENT equation family, which places eGFR inside general cardiovascular risk prediction (see risk prediction and prognosis).
Whether CKM staging changes what is done for an individual patient, rather than reorganising how the problem is described, is not yet established by any outcome study.
| Intervention | Population | Result | Boundary |
|---|---|---|---|
| Simvastatin + ezetimibe | CKD, 9,270 (2/3 non-dialysis) | Major atherosclerotic events RR 0.83 (0.74–0.94) per 0.85 mmol/L LDL (PMID 21663949) | Coronary death/MI not significant (RR 0.92, 0.76–1.11) |
| Rosuvastatin | Haemodialysis, 2,776 | CV composite HR 0.96 (0.84–1.11) despite 43% LDL fall (PMID 19332456) | No effect on any component or mortality |
| Invasive vs conservative | Advanced CKD + ischaemia, 777 | Death/MI HR 1.01 (0.79–1.29); 3-year rate 36.4% vs 36.7% (PMID 32227756) | Stroke HR 3.76 (1.52–9.32); death or dialysis HR 1.48 (1.04–2.11) |
| CKM staging framework | Population-level | Definition, staging, prediction and care-model guidance (PMID 37807924) | No outcome evidence that staging changes management |
Anticoagulation in advanced CKD: no adequate trial exists¶
The randomized attempt failed on recruitment. RENAL-AF randomized 154 haemodialysis patients with atrial fibrillation and CHA₂DS₂-VASc ≥2 to apixaban 5 mg twice daily (2.5 mg if age ≥80 or weight ≤60 kg) or dose-adjusted warfarin, in a prospective open-label blinded-endpoint design, and stopped prematurely because of enrolment difficulty. One-year major or clinically relevant non-major bleeding was 32% with apixaban versus 26% with warfarin (HR 1.20, 95% CI 0.63–2.30); one-year stroke or systemic embolism was 3.0% versus 3.3%; death was the most common major event in both arms (26% and 18%). Time in therapeutic range for warfarin was 44% (IQR 23–59%), and the pharmacokinetic substudy found a median steady-state 12-hour AUC of 2,475 ng/mL·h (10th–90th percentile 1,342–3,285) for 5 mg twice daily versus 1,269 (615–1,946) for 2.5 mg (Pokorney 2022, PMID 36335914).
Three things are worth extracting. A 32% one-year clinically relevant bleeding rate and a 26% one-year mortality make this a population in which anticoagulation decisions are dominated by competing risk. A warfarin time-in-therapeutic-range of 44% means the comparator was poorly delivered, which is itself the real-world condition. And the pharmacokinetic data show that the reduced dose produces roughly half the exposure, so dose reduction in dialysis is a substantive change in drug exposure rather than a cautionary gesture.
The observational substitute. Propensity-score matching in two nationwide US claims databases compared warfarin with apixaban (12,488 matched patients) and rivaroxaban with apixaban (5,720) in non-dialysis CKD stage 4/5 with non-valvular atrial fibrillation, adjusting for 80 potential confounders. Warfarin carried higher major bleeding than apixaban (HR 1.85, 95% CI 1.59–2.15), including gastrointestinal (1.86, 1.53–2.25) and intracranial bleeding (2.15, 1.42–3.25); rivaroxaban likewise (1.69, 1.33–2.15). All-cause mortality was similar for warfarin (1.08, 0.98–1.18) and rivaroxaban (0.94, 0.81–1.10) versus apixaban, and ischaemic stroke differences were not significant for either — warfarin 1.14 (0.83–1.57), rivaroxaban 0.71 (0.40–1.24) — with wide confidence intervals (Fu 2024, PMID 37839687).
The bleeding difference is large and consistent; the stroke comparison is uninformative in both directions. Practice in this population therefore rests on a terminated 154-patient randomized trial and on claims-based comparisons that cannot establish whether anticoagulation should be used at all — only which agent, if it is.
Coronary calcification: incidence matters more than progression rate¶
Coronary artery calcification progresses faster in CKD than in the general population, and CRIC allows the prognostic value of that progression to be separated from the prognostic value of having calcification at all. Among 1,310 CRIC participants with at least one CAC scan and no prior cardiovascular disease — 545 without and 765 with prevalent CAC at baseline, mean 3.3 years between scans — 177 (32.5%) of those with a baseline score of zero developed incident CAC, and 270 (35.3%) of those with baseline CAC progressed by ≥50 Agatston units per year.
After multivariable adjustment, incident CAC was associated with a 2.42-fold higher rate of atherosclerotic cardiovascular disease (95% CI 1.23–4.79) and a 1.82-fold higher rate of all-cause mortality (1.03–3.22). Progressive CAC of ≥50 units per year was not associated with atherosclerotic cardiovascular disease (HR 1.42, 95% CI 0.85–2.35) but was associated with 1.73-fold higher all-cause mortality (1.31–2.28), and with neither incident heart failure (Tian 2025, PMID 39154888).
The asymmetry is the finding. Crossing from zero to any detectable calcification carries a larger and more specific atherosclerotic signal than accelerating within an already-calcified vasculature — which fits the CKD-MBD picture in which established calcification is a durable structural state rather than an ongoing atherosclerotic process, and it argues that a baseline zero score is the informative measurement rather than serial scanning.
Decision and interpretation matrix¶
| Dimension | Question | Guardrail |
|---|---|---|
| Diagnostic axis | Cause + G category + A category | Avoid treating eGFR as the diagnosis |
| Time axis | Chronicity and trajectory | Separate acute change from persistent disease |
| Risk axis | Kidney failure + cardiovascular events + death | Show competing events |
| Treatment axis | Eligibility, absolute benefit, harm, burden | Do not rank drugs by relative effect alone |
| Measurement axis | Assay, equation, repeatability | State what was actually measured |
| Equity axis | Testing, referral, access, affordability | Audit downstream care, not labels only |
| Patient axis | Symptoms, function, life participation | Include outcomes patients prioritize |
| Evidence axis | RCT, cohort, model, guideline | Do not collapse designs |
Evidence ledger¶
This ledger makes the page’s evidentiary mix inspectable. It does not imply that every source answers every question.
| PMID | Record used | Role and boundary |
|---|---|---|
| 26028594 | eGFR and albuminuria for prediction of cardiovascular outcomes: individual-participant meta-analysis. (Matsushita 2015, PMID 26028594) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 21663949 | The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease: SHARP. (Baigent 2011, PMID 21663949) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 16034009 | Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. (Wanner 2005, PMID 16034009) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 19332456 | Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. (Fellstrom 2009, PMID 19332456) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 36331190 | Empagliflozin in Patients with Chronic Kidney Disease. (EMPA-KIDNEY Collaborative Group 2023, PMID 36331190) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 35023547 | Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. (Agarwal 2022, PMID 35023547) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 38490803 | KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. (KDIGO CKD Work Group 2024, PMID 38490803) | Guideline or commentary; recommendation evidence depends on its review. |
| 38519239 | Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. (Levin 2024, PMID 38519239) | Guideline or commentary; recommendation evidence depends on its review. |
| 32061315 | Global, regional, and national burden of chronic kidney disease, 1990-2017. (GBD CKD Collaboration 2020, PMID 32061315) | Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up. |
| 22038337 | A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. (Cirillo 2012, PMID 22038337) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 23243116 | Cohort profile: the chronic kidney disease prognosis consortium. (Matsushita 2013, PMID 23243116) | Observational or conceptual evidence; association is not treatment effect. |
| 37787795 | Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. (CKD Prognosis Consortium 2023, PMID 37787795) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 30348535 | Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. (Inker 2019, PMID 30348535) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 34554658 | New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. (Inker 2021, PMID 34554658) | Observational or conceptual evidence; association is not treatment effect. |
| 34563581 | A Unifying Approach for GFR Estimation: Recommendations of the NKF-ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease. (Delgado 2022, PMID 34563581) | Guideline or commentary; recommendation evidence depends on its review. |
| 26757465 | Multinational assessment of equations predicting kidney failure. (Tangri 2016, PMID 26757465) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 36857500 | Kidney Failure Risk Equation evaluation with novel inputs in 59 cohorts. (Grams 2023, PMID 36857500) | Observational or conceptual evidence; association is not treatment effect. |
| 23121374 | Effect of cinacalcet on cardiovascular disease in patients undergoing dialysis. (EVOLVE Trial Investigators 2012, PMID 23121374) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 28646995 | Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder Guideline Update. (Ketteler 2017, PMID 28646995) | Guideline or commentary; recommendation evidence depends on its review. |
| 35232774 | Interventions To Attenuate Vascular Calcification Progression in Chronic Kidney Disease: A Systematic Review of Clinical Trials. (Xu 2022, PMID 35232774) | Synthesis; heterogeneity and included-study definitions constrain transport. |
| 26564024 | Cinacalcet, dialysate calcium concentration, and cardiovascular events in the EVOLVE trial. (Pun 2016, PMID 26564024) | Intervention study; eligibility, comparator, endpoint and follow-up bound inference. |
| 32753447 | Cost-effectiveness analysis of cinacalcet for haemodialysis patients with secondary hyperparathyroidism based on EVOLVE. (Liu 2020, PMID 32753447) | Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up. |
| 26265359 | Cinacalcet and Clinical Outcomes in Dialysis. (Komaba 2015, PMID 26265359) | Observational or conceptual evidence; association is not treatment effect. |
| 26686794 | Economic Evaluation of Cinacalcet in the United States: The EVOLVE Trial. (Belozeroff 2015, PMID 26686794) | Modelled projection; the estimate follows from the model inputs and assumptions, not from observed randomized follow-up. |
| 30675420 | KDIGO 2017 Clinical Practice Guideline Update for CKD-MBD. (KDIGO CKD-MBD Update Work Group 2017, PMID 30675420) | Guideline or commentary; recommendation evidence depends on its review. |
| 39864017 | Chronic kidney disease-mineral and bone disorder: conclusions from a KDIGO Controversies Conference. (Ketteler 2025, PMID 39864017) | Guideline or commentary; recommendation evidence depends on its review. |
| 30236082 | Renal Association commentary on the KDIGO 2017 CKD-MBD guideline update. (Burton 2018, PMID 30236082) | Guideline or commentary; recommendation evidence depends on its review. |
| 30150095 | Overview of the 2017 KDIGO CKD-MBD Update: Practice Implications for Adult Hemodialysis Patients. (Beto 2019, PMID 30150095) | Guideline or commentary; recommendation evidence depends on its review. |
| 31890994 | KDIGO CKD-MBD Guideline Update Implementation: Asia Summit Conference Report. (Wang 2019, PMID 31890994) | Guideline or commentary; recommendation evidence depends on its review. |
| 28941764 | KDOQI US Commentary on the 2017 KDIGO CKD-MBD Guideline Update. (Isakova 2017, PMID 28941764) | Guideline or commentary; recommendation evidence depends on its review. |
What can and cannot be concluded¶
- Risk associations do not by themselves establish that changing the marker changes risk.
- A relative effect must be paired with baseline risk, follow-up and the exact endpoint.
- Albuminuria, acute eGFR change, chronic eGFR slope and kidney failure are not interchangeable.
- Subgroup consistency is not evidence that every subgroup had adequate power.
- Guideline recommendations combine evidence with values, feasibility, cost and service capacity.
- Older adults require competing-mortality and treatment-burden framing.
- Dialysis and transplantation comparisons are vulnerable to eligibility and immortal-time bias.
- Modelled lifetime benefit is not a randomized observed benefit.
- A biochemical response without a patient-important outcome remains a surrogate result.
- This page is research synthesis, not individualized medical advice.
Research-design checklist¶
- Define CKD cause, G category, A category and chronicity at baseline.
- Report the creatinine or cystatin C equation and laboratory calibration.
- Prespecify acute and chronic eGFR slopes when haemodynamic effects are expected.
- Keep sustained GFR decline, kidney failure and replacement therapy separable.
- Report absolute event risks, follow-up and confidence intervals with relative effects.
- Treat death as a competing event where it can preclude kidney failure.
- Measure hyperkalaemia, acute kidney injury and treatment discontinuation consistently.
- Include symptoms, function, life participation and treatment burden.
- Describe background RAS, SGLT2, MRA and GLP-1 therapy explicitly.
- Prespecify albuminuria and cause strata without over-reading underpowered interactions.
- Record screening, prescribing, persistence and monitoring as separate implementation steps.
- Report representation, access and affordability variables needed for equity analysis.
Open questions¶
- Why did statin initiation fail in prevalent haemodialysis (4D, AURORA) while succeeding across broad CKD (SHARP)? Competing non-atherosclerotic mechanisms are the usual explanation but have not been tested as a mediator (Wanner 2005, PMID 16034009) (Fellstrom 2009, PMID 19332456) (Baigent 2011, PMID 21663949).
- Do patients already established on a statin before dialysis benefit from continuation? All three trials tested initiation, not continuation.
- How much of the residual cardiovascular risk at low eGFR is sudden arrhythmic death, and what modifies it?
-
Does albuminuria-guided treatment intensification improve cardiovascular outcomes, given that albuminuria predicts them independently (Matsushita 2015, PMID 26028594)?
-
Why does LDL lowering lose all effect at the dialysis boundary? SHARP shows benefit in predominantly non-dialysis CKD (RR 0.83, 0.74–0.94) (PMID 21663949) while AURORA shows none on dialysis despite a 43% LDL reduction (PMID 19332456) — competing arrhythmic and calcific mechanisms are the usual explanation but have not been tested as such.
- What should be offered to the third of advanced-CKD patients with ischaemia who die or infarct within 3 years, given that an invasive strategy adds stroke (HR 3.76, 1.52–9.32) and dialysis initiation (HR 1.48, 1.04–2.11) without benefit (Bangalore 2020, PMID 32227756)?
-
Does CKM staging change management or only description? No outcome study has tested the framework itself (Ndumele 2023, PMID 37807924).
-
Should patients on dialysis with atrial fibrillation be anticoagulated at all? The only randomized trial stopped early at 154 patients with one-year bleeding of 32% versus 26% and mortality of 26% versus 18% (Pokorney 2022, PMID 36335914); no trial has compared anticoagulation with none.
- Is the halved apixaban exposure with dose reduction in dialysis (AUC 1,269 vs 2,475 ng/mL·h) therapeutically adequate (Pokorney 2022, PMID 36335914)?
-
Does the consistent bleeding advantage of apixaban over warfarin and rivaroxaban in CKD stage 4/5 (HR 1.85 and 1.69 against it) survive unmeasured confounding in claims data, given that the stroke comparisons remain uninformative (Fu 2024, PMID 37839687)?
-
Why does incident coronary calcification predict atherosclerotic events (HR 2.42, 1.23–4.79) while progression within already-calcified arteries does not (HR 1.42, 0.85–2.35), even though both predict mortality (Tian 2025, PMID 39154888)? If confirmed, serial CAC scanning in CKD would have limited value beyond an initial zero-versus-non-zero determination.
Related pages¶
- mineral and bone disorder — complementary CKD evidence and decision context.
- causes and aetiology — complementary CKD evidence and decision context.
- definition staging and measurement — complementary CKD evidence and decision context.
- epidemiology and burden — complementary CKD evidence and decision context.
- guidelines — complementary CKD evidence and decision context.
- overview — complementary CKD evidence and decision context.
References¶
- Matsushita et al. eGFR and albuminuria for prediction of cardiovascular outcomes: individual-participant meta-analysis. Lancet Diabetes Endocrinol. 2015;3(7):514-525. PMID 26028594
- Baigent et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease: SHARP. Lancet. 2011;377(9784):2181-2192. PMID 21663949
- Wanner et al. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248. PMID 16034009
- Fellstrom et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009;360(14):1395-1407. PMID 19332456
- EMPA-KIDNEY Collaborative Group et al. Empagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2023;388(2):117-127. PMID 36331190
- Agarwal et al. Cardiovascular and kidney outcomes with finerenone in patients with type 2 diabetes and chronic kidney disease: the FIDELITY pooled analysis. Eur Heart J. 2022;43(6):474-484. PMID 35023547
- KDIGO CKD Work Group et al. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117-S314. PMID 38490803
- Levin et al. Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns. Kidney Int. 2024;105(4):684-701. PMID 38519239
- GBD CKD Collaboration et al. Global, regional, and national burden of chronic kidney disease, 1990-2017. Lancet. 2020;395(10225):709-733. PMID 32061315
- Cirillo et al. A population-based approach for the definition of chronic kidney disease: CKD Prognosis Consortium. J Nephrol. 2012;25(1):7-12. PMID 22038337
- Matsushita et al. Cohort profile: the chronic kidney disease prognosis consortium. Int J Epidemiol. 2013;42(6):1660-1668. PMID 23243116
- CKD Prognosis Consortium et al. Estimated GFR, Albuminuria, and Adverse Outcomes: individual-participant data meta-analysis. JAMA. 2023;330(13):1266-1277. PMID 37787795
- Inker et al. Relationship of Estimated GFR and Albuminuria to Concurrent Laboratory Abnormalities. Am J Kidney Dis. 2019;73(2):206-217. PMID 30348535
- Inker et al. New Creatinine- and Cystatin C-Based Equations to Estimate GFR without Race. N Engl J Med. 2021;385(19):1737-1749. PMID 34554658
- Delgado et al. A Unifying Approach for GFR Estimation: Recommendations of the NKF-ASN Task Force on Reassessing the Inclusion of Race in Diagnosing Kidney Disease. Am J Kidney Dis. 2022;79(2):268-288.e1. PMID 34563581
- Tangri et al. Multinational assessment of equations predicting kidney failure. JAMA. 2016;315(2):164-174. PMID 26757465
- Grams et al. Kidney Failure Risk Equation evaluation with novel inputs in 59 cohorts. J Am Soc Nephrol. 2023;34(3):482-494. PMID 36857500
- EVOLVE Trial Investigators et al. Effect of cinacalcet on cardiovascular disease in patients undergoing dialysis. N Engl J Med. 2012;367(26):2482-2494. PMID 23121374
- Ketteler et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder Guideline Update. Kidney Int. 2017;92(1):26-36. PMID 28646995
- Xu et al. Interventions To Attenuate Vascular Calcification Progression in Chronic Kidney Disease: A Systematic Review of Clinical Trials. J Am Soc Nephrol. 2022;33(5):1011-1032. PMID 35232774
- Pun et al. Cinacalcet, dialysate calcium concentration, and cardiovascular events in the EVOLVE trial. Hemodial Int. 2016;20(3):421-431. PMID 26564024
- Liu et al. Cost-effectiveness analysis of cinacalcet for haemodialysis patients with secondary hyperparathyroidism based on EVOLVE. BMJ Open. 2020;10(8):e034123. PMID 32753447
- Komaba et al. Cinacalcet and Clinical Outcomes in Dialysis. Semin Dial. 2015;28(6):594-603. PMID 26265359
- Belozeroff et al. Economic Evaluation of Cinacalcet in the United States: The EVOLVE Trial. Value Health. 2015;18(8):1079-1087. PMID 26686794
- KDIGO CKD-MBD Update Work Group et al. KDIGO 2017 Clinical Practice Guideline Update for CKD-MBD. Kidney Int Suppl (2011). 2017;7(1):1-59. PMID 30675420
- Ketteler et al. Chronic kidney disease-mineral and bone disorder: conclusions from a KDIGO Controversies Conference. Kidney Int. 2025;107(3):405-423. PMID 39864017
- Burton et al. Renal Association commentary on the KDIGO 2017 CKD-MBD guideline update. BMC Nephrol. 2018;19(1):240. PMID 30236082
- Beto et al. Overview of the 2017 KDIGO CKD-MBD Update: Practice Implications for Adult Hemodialysis Patients. J Ren Nutr. 2019;29(1):2-15. PMID 30150095
- Wang et al. KDIGO CKD-MBD Guideline Update Implementation: Asia Summit Conference Report. Kidney Int Rep. 2019;4(11):1523-1537. PMID 31890994
- Isakova et al. KDOQI US Commentary on the 2017 KDIGO CKD-MBD Guideline Update. Am J Kidney Dis. 2017;70(6):737-751. PMID 28941764
- Bangalore S, et al. Management of Coronary Disease in Patients with Advanced Kidney Disease. N Engl J Med. 2020;382(17):1608-1618. PMID 32227756
- Ndumele CE, et al. Cardiovascular-Kidney-Metabolic Health: A Presidential Advisory From the American Heart Association. Circulation. 2023;148(20):1606-1635. PMID 37807924
- Pokorney SD, et al. Apixaban for Patients With Atrial Fibrillation on Hemodialysis: A Multicenter Randomized Controlled Trial. Circulation. 2022;146(23):1735-1745. PMID 36335914
- Fu EL, et al. Comparative Safety and Effectiveness of Warfarin or Rivaroxaban Versus Apixaban in Patients With Advanced CKD and Atrial Fibrillation: Nationwide US Cohort Study. Am J Kidney Dis. 2024;83(3):293-305.e1. PMID 37839687
- Tian L, et al. Progression of Coronary Artery Calcification and Risk of Clinical Events in CKD: The Chronic Renal Insufficiency Cohort Study. Am J Kidney Dis. 2025;85(1):67-77.e1. PMID 39154888