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Medical Associates  ·  Department of Nephrology ← Maintenance Hemodialysis module  ·  urinenephrology.org
Clinical Mastery Series  ·  Maintenance Hemodialysis

Cardiometabolic Monitoring in Maintenance Hemodialysis

Lipids and statins, fish oil, glycemic markers, and cardiovascular screening — what to measure, what to stop measuring, and why
Andrew Bland, MD, FACP, FAAP UICOMP · UDPA · Butler COM Reviewed September 2026 19 min read

Bottom Line

Part of the Maintenance Hemodialysis mastery module. This page condenses sections 1, 2, and 8.3 of the full white paper, Screening and Health Maintenance in Maintenance Hemodialysis.

  • Statins: do not start one on dialysis; continue one the patient already takes. KDIGO 2013 is still the operative lipid guidance for people on dialysis, because the KDIGO 2024 CKD guideline excludes them. It recommends against initiating a statin in a patient already on chronic dialysis (2A) and supports continuing a statin the patient was taking when dialysis began (2C).1,2,3
  • Lipids are fire-and-forget. Check a lipid profile once at dialysis initiation. Routine follow-up panels do not change management, because there is no LDL target to titrate toward.1 After an acute coronary syndrome, continue the statin cardiology started.
  • Fish oil should be considered. In PISCES, a 1,228-patient randomized trial, fish oil given as four 1-g capsules daily (2.4 g/day of EPA plus DHA) reduced recurrent serious cardiovascular events (HR 0.57). At least one event occurred in 20.8% of the fish-oil group versus 33.7% of the placebo group: ARR 12.9%, NNT 8 over the trial. All-cause death did not differ significantly.4
  • HbA1c reads low on dialysis, underestimating mean glucose by approximately 25 mg/dL.5 KDIGO 2022 keeps HbA1c as the primary glycemic marker but supports using CGM data when HbA1c does not match measured glucose or symptoms. It does not endorse glycated albumin as superior.6 CGM devices are not FDA-approved for use in dialysis.7
  • Screen the heart, including the right heart. Obtain an echocardiogram at dialysis initiation and every 1–3 years. Every arteriovenous fistula is a left-to-right shunt, and access-related high-output heart failure is underrecognized.8,9,10

1. Lipids and Statins

The uremic lipid phenotype

Statins were not designed for the dyslipidemia of hemodialysis. The uremic pattern combines elevated triglycerides, low HDL cholesterol, and relatively modest LDL elevation. It is driven by reduced lipoprotein lipase and hepatic lipase activity, apolipoprotein C-III enrichment of circulating lipoproteins, and impaired clearance of triglyceride-rich remnant particles.11

The epidemiology also runs backward. Lower total cholesterol in hemodialysis patients is associated with higher mortality. This "reverse epidemiology" reflects confounding by malnutrition, chronic inflammation, and protein-energy wasting. The malnutrition-inflammation-cachexia syndrome lowers cholesterol while it raises cardiovascular risk through pathways a statin does not reach.3,11

What KDIGO recommends

The KDIGO 2024 CKD guideline is not intended for people receiving dialysis. The 2013 KDIGO lipid statements therefore remain the operative KDIGO guidance for this population.1,2,3

KDIGO 2013 statementGrade
Obtain a lipid profile (total cholesterol, LDL, HDL, triglycerides) at CKD diagnosis and at dialysis initiation1C
Do not initiate a statin or statin/ezetimibe in a patient already on chronic dialysis2A
Continue a statin the patient was already taking when dialysis began2C
Follow-up lipid measurement is not routinely required; LDL targets are abandoned in favor of risk-based prescribingNot graded

The three statin trials

Three randomized trials tested LDL lowering in people on dialysis. 4D and AURORA were powered for their primary end points. SHARP included a large dialysis subgroup but was not powered to assess it separately.12

Trial (design)AgentPopulationPrimary outcomeResult
4D (2005, RCT)Atorvastatin 20 mg1,255 hemodialysis patients with type 2 diabetesCardiac death, MI, strokeRR 0.92 (95% CI 0.77–1.10); p = 0.37. No benefit.13
AURORA (2009, RCT)Rosuvastatin 10 mg2,776 hemodialysis patients aged 50–80CV death, MI, strokeHR 0.96 (95% CI 0.84–1.11); p = 0.59. No benefit.14
SHARP (2011, RCT)Simvastatin 20 mg + ezetimibe 10 mg9,270 CKD patients, 3,023 on dialysisMajor atherosclerotic eventsOverall RR 0.83 (95% CI 0.74–0.94); ARR 2.1%, NNT 48 over 4.9 years. No statistically significant benefit in the dialysis subgroup (heterogeneity vs non-dialysis p = 0.25).12

Across these three trials and more than 7,000 dialysis patients, the answer is consistent. LDL lowering reduces events in earlier CKD. It has not reduced cardiovascular events once patients reach dialysis.

Clinical Pearl

On dialysis, the cardiovascular phenotype shifts away from atherosclerotic plaque rupture, where statins help, toward vascular calcification, myocardial fibrosis, volume-mediated cardiomyopathy, arrhythmia, and sudden cardiac death. Statins do not address these processes.13,14 4D is the instructive trial. It enrolled only hemodialysis patients with diabetes, the group expected to gain the most from a statin, and it found no benefit.

Primary versus secondary prevention

The KDIGO recommendation against starting a statin on dialysis (2A) makes no distinction between primary and secondary prevention. The trials support that position. 4D enrolled a high-risk population with diabetes, AURORA enrolled patients with substantial baseline cardiovascular disease, and neither showed benefit in subgroups with prior cardiovascular events.13,14 Practice diverges from the guideline in one predictable place.

ScenarioKDIGO 2013Real-world practice
Primary prevention (no prior cardiovascular event)Do not initiate (2A)Generally followed
Secondary prevention (prior MI, stroke, or revascularization)Do not initiate (2A)Frequently overridden by cardiology
Already taking a statin at dialysis initiationContinue (2C)Followed

The gap reflects two bodies of evidence. The nephrology trials (4D, AURORA, and the SHARP dialysis subgroup) are negative. General cardiology guidelines recommend high-intensity statin therapy for clinical atherosclerotic disease without a dialysis exception, so most cardiologists start a statin after an acute MI as part of standard post-ACS care.

Clinical Pearl — after an acute coronary syndrome

When a dialysis patient has an acute coronary event, the cardiology team usually starts the statin, and the KDIGO guideline supports continuing it from that point. Nephrologists should not initiate statins for primary prevention in prevalent hemodialysis patients, but they need not fight to discontinue a statin cardiology started for a legitimate secondary-prevention indication, even though the dialysis-specific evidence is weak.

Warning

Do not reflexively stop a statin at dialysis initiation. KDIGO distinguishes initiation, which it does not recommend, from continuation, which it supports. Stopping carries a theoretical risk of rebound events that has not been rigorously studied in dialysis.1

Lipid monitoring: fire-and-forget

KDIGO abandoned LDL targets in CKD, including dialysis. With no LDL goal to titrate toward, the same approach applies whether the statin is for primary or secondary prevention.1

Clinical contextCheck lipids?Rationale
New hemodialysis patient, baseline assessmentYes, onceRule out secondary causes; document a baseline
Stable patient on a statin, routine follow-upNoNo LDL target; fire-and-forget
Post-ACS, statin started by cardiologyNo (from the nephrology side)Cardiology may monitor under its own guidelines
Suspected medication non-adherenceConsiderAdherence assessment
New nephrotic syndrome, hypothyroidism, or liver diseaseYesEvaluate secondary dyslipidemia
Transplant evaluationYesMany transplant centers require a recent lipid panel
Low-value care

A routine lipid panel in a stable hemodialysis patient on a statin will not change management. Nobody titrates the dose, switches agents, or stops the drug because of the LDL number. Resist ordering one "because it has been a while."

2. Fish Oil: The PISCES Trial

After three negative statin trials, PISCES (Lok et al., N Engl J Med 2026) was the first large placebo-controlled trial to reduce cardiovascular events in people on dialysis. It randomized 1,228 maintenance hemodialysis patients at 26 sites in Canada and Australia to fish oil, given as four 1-g capsules daily that provide 2.4 g/day of EPA plus DHA (1.6 g EPA and 0.8 g DHA), or a corn-oil placebo. Patients were followed for up to 3.5 years (2,776 patient-years). The primary end point counted every serious cardiovascular event, including recurrences: cardiac death, fatal and nonfatal MI, fatal and nonfatal stroke, and peripheral vascular disease leading to amputation.4

PISCES outcome (RCT)Fish oil vs placebo
All serious cardiovascular events, recurrences counted (primary)HR 0.57 (95% CI 0.47–0.70), p < 0.001; 0.31 vs 0.61 events per 1,000 patient-days
Patients with at least one event20.8% vs 33.7%. ARR 12.9%, NNT 8 over the trial (mean follow-up approximately 2.3 years)
Patients without prior cardiovascular diseaseHR 0.55 (95% CI 0.40–0.76)
All-cause death175 vs 195 deaths; HR 0.89. Not statistically significant
Serious bleeding4.8% vs 7.6%

Placing PISCES accurately matters. It was the first large placebo-controlled trial to show cardiovascular event reduction in the dialysis population. A smaller placebo-controlled trial of carvedilol in 114 dialysis patients with dilated cardiomyopathy preceded it.4,15 UpToDate now suggests fish oil supplements for patients on maintenance dialysis to prevent new and recurrent cardiovascular events (Grade 2B; topic updated November 2025), while noting that confirmatory trials are warranted. The KDOQI 2020 nutrition guideline predates PISCES and suggests not routinely prescribing long-chain omega-3 fatty acids to lower mortality (2C) or cardiovascular events (2B) in hemodialysis.16 On the strength of PISCES, fish oil supplementation should be considered for patients on maintenance hemodialysis.4

Clinical Pearl

Fish oil is thought to act through mechanisms other than LDL lowering. The proposed pathways are anti-inflammatory, anti-arrhythmic, and triglyceride-lowering, and PISCES did not establish which one operates.4 Those pathways fit the dialysis cardiovascular phenotype (arrhythmia, inflammation, vascular calcification) better than plaque stabilization does. The inflammation side of this story is developed further in Inflammation and fish oil (PISCES) in HD.

3. Glycemic Monitoring: Why HbA1c Misleads

Why HbA1c fails on hemodialysis

HbA1c reflects average glucose over the 90–120 day erythrocyte lifespan. On hemodialysis that lifespan shortens to 60–90 days, and several other factors distort the result.5,17,18

FactorEffect on HbA1cMechanism
Shortened red-cell lifespan (uremia)Falsely lowLess time for hemoglobin glycation
ESA therapyFalsely lowMore reticulocytes: young, less-glycated red cells
Untreated iron deficiencyFalsely highAn older red-cell population predominates
IV iron or transfusionFalsely lowRapid red-cell turnover
Carbamylated hemoglobinVariableUrea-derived carbamylation interferes with some assays
Metabolic acidosisVariableMay alter hemoglobin-glucose binding kinetics
Hemoglobin variantsVariableAssay-specific interference

The net effect is usually underestimation. In a study that compared HbA1c against long-term continuous glucose monitoring, HbA1c underestimated mean glucose in hemodialysis patients by approximately 1.4 mmol/L (25 mg/dL).5 That is a clinically meaningful gap, and it produces false reassurance.

What the guidelines say, and where they diverge

  • KDIGO 2022 (diabetes in CKD). Keeps HbA1c as the primary glycemic biomarker, even on dialysis. It suggests monitoring twice yearly in stable patients meeting goals and quarterly after therapy changes or when targets are unmet. KDIGO acknowledges that accuracy declines in advanced CKD, but states that glycated albumin and fructosamine offer no known advantage over HbA1c and are biased by hypoalbuminemia.6
  • ADA/KDIGO 2022 consensus. Emphasizes adding CGM when HbA1c may be inaccurate or when hypoglycemia risk needs assessment. It notes that neither glycated albumin nor fructosamine is free of limitations and does not replace HbA1c as the primary marker.19
  • Consensus report on CGM in CKD (Rhee et al., 2025). Takes a more assertive position. In ESKD and "burnt-out" diabetes, CGM detects occult hyperglycemia and hypoglycemia that HbA1c misses, and the report calls for greater CGM use in CKD and dialysis. It also notes that CGM devices are not FDA-approved for patients on dialysis.7
  • Zelnick et al., 2026 (prospective CGM study in maintenance dialysis). Both HbA1c and glycated albumin correlated strongly with CGM mean glucose (r = 0.85 and 0.87). Each carried substantial bias from clinical characteristics. ESA dose, hemoglobin, serum albumin, and BMI biased HbA1c. Dialysis modality, vintage, residual kidney function, and BMI biased glycated albumin.20

No single laboratory marker is reliable on its own in this population.

"Burnt-out" diabetes

Approximately 20% of patients with diabetes and ESKD have an HbA1c below 6.5% after more than 6 months without antidiabetic therapy, a pattern called "burnt-out diabetes." In a small CGM study (n = 40), these patients had significantly higher mean daily glucose than nondiabetic ESKD controls, more excursions above 180 mg/dL, and greater glycemic variability.21 The apparent remission is largely an artifact of HbA1c in ESKD. These patients are undertreated, not cured.

Clinical Pearl

A "normal" HbA1c in a dialysis patient with a history of diabetes is not reassuring. The most dangerous glycemic pattern on dialysis, wide swings between hypoglycemia and hyperglycemia, is invisible to HbA1c. Stop checking and you stop treating.

Alternative glycemic markers

MarkerWhat it reflectsStrengthsLimitations
Glycated albuminAverage glucose over 2–3 weeks (albumin half-life approximately 20 days)Unaffected by red-cell lifespan, ESA use, or hemoglobin variants. A meta-analysis in CKD stages 4–5 including dialysis found a pooled correlation with average glucose of R = 0.57, versus 0.49 for HbA1c.22 It outperformed HbA1c against CGM in the small burnt-out-diabetes study.21Altered by conditions that change albumin metabolism (nephrotic syndrome, cirrhosis, peritoneal protein loss, severe malnutrition). In the larger 2026 cohort it correlated with CGM no better than HbA1c and was biased by modality, vintage, residual function, and BMI.20
FructosamineGlycation of all serum proteins, mostly albumin; 2–3 weeksA shorter window (2–3 weeks) than HbA1cLess specific than glycated albumin; affected by albumin level and protein turnover. Not superior to HbA1c in ESKD.21
Continuous glucose monitoringReal-time glucose; time in range, above range, and below range; variabilityCaptures hypoglycemia, variability, and occult hyperglycemia that no single laboratory marker detectsNot FDA-approved for dialysis; device labeling states use in dialysis has not been validated.7 Insurance coverage is inconsistent for patients not on intensive insulin therapy.

Glycemic targets

KDIGO 2022 recommends an individualized HbA1c target, generally 6.5–8.0%, while acknowledging that HbA1c may not reflect glycemia accurately in this population. The ADA/KDIGO consensus suggests relaxing targets when hypoglycemia risk is high, life expectancy is limited, or comorbidity is significant.6,19 For CGM, the 2025 consensus report extrapolates the international targets for high-risk patients and notes that they have not been validated in CKD.7

CGM metricTarget
Time in range (70–180 mg/dL)> 50%
Time below range (< 70 mg/dL)< 1%
Time above range (> 180 mg/dL)< 50%
Time above range (> 250 mg/dL)< 10%
Warning — do not act on HbA1c alone

KDIGO 2022 keeps HbA1c as the primary glycemic marker but states that its accuracy is low in dialysis, and it supports using CGM data when HbA1c does not match measured glucose or symptoms. It does not endorse glycated albumin or fructosamine as superior.6 The ADA/KDIGO consensus favors adding CGM when HbA1c may be inaccurate.19 The 2026 prospective data show that glycated albumin also carries bias, which leaves CGM as the most direct glycemic tool in this population, even though it is not FDA-approved for dialysis.7,20

4. Cardiovascular Screening

Cardiovascular disease accounts for most deaths in ESKD. Structured assessment rests on three tools.

Echocardiography, ECG, and stress testing

  • Echocardiography at dialysis initiation establishes LV function, chamber dimensions, valvular calcification, and pericardial disease. Repeat every 1–3 years to follow LV hypertrophy (present in most hemodialysis patients), diastolic dysfunction, and valvular calcification. A study performed the day after dialysis, when the patient is closest to dry weight, gives the most accurate read of LV function. Track LV mass index, ejection fraction, mitral and aortic valve calcification, pericardial effusion, and RV systolic pressure.
  • ECG at initiation and periodically, mainly to detect electrolyte-driven arrhythmias (hyperkalemia, hypocalcemia), QTc prolongation, and conduction disease. Sudden cardiac death is the leading cause of cardiovascular death in ESKD, driven by rapid electrolyte shifts during and immediately after dialysis. Potassium management is covered in Hyperkalemia on HD. Atrial fibrillation and anticoagulation decisions are covered in Atrial fibrillation and anticoagulation in HD.
  • Stress testing belongs to transplant candidacy evaluation under institutional protocols. It is not routinely recommended for asymptomatic patients who are not transplant candidates, and its accuracy falls in ESKD because of LV hypertrophy, baseline ECG abnormalities, and chronotropic incompetence.
Clinical Pearl — pulmonary hypertension

Pulmonary hypertension is common on hemodialysis, reported in 20–60% of patients depending on the study and definition, and is independently associated with mortality.23 Most of it is postcapillary (group 2), related to volume overload and left heart disease, and fistula flow can contribute. Optimize volume and assess the access before considering pulmonary-hypertension-specific therapy.

The right heart and access-related high-output failure

Every arteriovenous fistula is a left-to-right shunt. A functioning fistula diverts 400–2,000+ mL/min of arterial blood straight into the venous circulation, and the heart must raise its output to keep the "effective" cardiac output (total output minus access flow) perfusing the organs.24 When access flow exceeds 1.5–2.0 L/min or consumes more than 25–30% of cardiac output, the burden is strongly associated with LV hypertrophy, high-output heart failure, and pulmonary hypertension.23 In one single-center cohort, 29.4% (10 of 34) of fistula patients who underwent right heart catheterization met criteria for high-output failure.10 The problem is underrecognized and underreported.8,9

The right ventricle is the weak link. Chronic volume overload produces RV dilation, tricuspid regurgitation, elevated right atrial pressure, hepatic congestion, and, in severe cases, ascites that can masquerade as dialysis fluid overload.25

FindingStudy (design)
RV dilation after fistula or graft creation independently associated with mortality: HR 3.9 (95% CI 1.7–9.2)Reddy 2017 (retrospective echocardiographic cohort, n = 137)26
RV end-diastolic volume index rose from 80 ± 15 to 91 ± 18 mL/m² within approximately 8 months of fistula creationFornazarič 2025 (prospective echocardiographic study)27
Qa/CO ≥ 20%: 100% sensitivity, 74.7% specificity for high-output failure. Qa ≥ 2.0 L/min: 89% sensitivity, 100% specificityBasile 2008 (observational)28
Upper-arm access: OR 8.1 (95% CI 1.8–35.7) for Qa/CO > 0.3 versus forearm. Baseline Qa of approximately 1.4 L/min identified Qa/CO > 0.3 (AUC 0.97)Kim 2025 (prospective study)29

The clinical signals are easy to misattribute:

  • Dyspnea blamed on volume or anemia, when the cause is high output and elevated pulmonary pressure.
  • Peripheral edema blamed on missed ultrafiltration targets, when it reflects right heart failure.
  • Ascites blamed on liver or peritoneal disease, when it is hepatic congestion from RV failure.25
  • Intradialytic hypotension blamed on ultrafiltration rate, when a high-flow access is producing coronary steal, particularly after bypass grafting with an internal mammary artery.30

What to add to the echocardiogram

Expand the standard hemodialysis echocardiogram to include a structured right-heart assessment at baseline and at each surveillance study.

ParameterWhat it tells youThreshold for concern
RV basal diameterRV volume overload> 41 mm
TAPSERV systolic function< 17 mm
RV S′ (tissue Doppler)RV longitudinal function< 9.5 cm/s
RVSP (from TR jet)Pulmonary artery pressure> 35 mmHg elevated; > 50 mmHg severe
TR severityConsequence of RV and annular dilationModerate or greater: investigate access flow
RA areaRV filling pressure> 18 cm²
E/e′LV filling pressure> 14
Cardiac outputTotal output> 7 L/min: measure access flow
Height-indexed access flow (Qa/height2.7)Body-size-adjusted shunt burden≥ 603 mL/min/m2.7 (100% sensitivity, 60% specificity for high-output failure in 29 patients with Qa ≥ 2,000 mL/min)31
IVC diameter and collapseVolume status and RA pressure> 21 mm with < 50% collapse

Obtain a baseline echocardiogram before any access is created, especially in patients with any cardiac history. The findings bear directly on which access to create and whether shunt physiology is safe at all. When the echocardiogram shows elevated RVSP, RV dilation, or unexpectedly high output, measure access flow and calculate the access-flow-to-cardiac-output ratio. A Qa/CO above 25–30% identifies patients at high risk of progressive cardiac remodeling.23,29

Clinical Pearl — the occlusion test

Temporarily compress the fistula, manually or with a cuff proximal to the anastomosis, and watch the hemodynamics. A fall in heart rate (the Branham sign) and a rise in blood pressure show that the access is driving the high-output state. In one reported patient with 3 L/min fistula flow, elevated RVSP resolved on echocardiography during occlusion, proving reversibility and supporting intervention.32

Access choice when the heart is the constraint

Current access guidance favors individualized planning within a patient life-plan that accounts for cardiac comorbidity, life expectancy, vessel mapping, and preference.8,9 Forearm fistulas carry less flow than upper-arm fistulas (mean approximately 948 versus 1,580 mL/min),28 so a forearm-first strategy limits the hemodynamic insult in patients with reduced ejection fraction or RV dysfunction. In patients with symptomatic heart disease, a catheter showed non-inferior major-adverse-event-free survival compared with a fistula, and more fistula patients deteriorated in heart-failure status (35 of 57 versus 10 of 42).33 Grafts carry their own cost: among patients with heart failure, primary-assisted patency at one year was 39% for grafts versus 87% for fistulas.34 The decision is which failure mode the individual patient can least afford. Access examination and cannulation are covered in Examining and cannulating the AVF/AVG, and access selection in older patients in Vascular Access Selection in Older Patients Starting Hemodialysis.

Warning — the internal mammary artery trap

In a patient with a left internal mammary artery bypass graft, an ipsilateral upper-extremity fistula creates a low-resistance steal pathway that can divert flow from the graft and produce coronary ischemia despite patent grafts. A reported case of post-angioplasty hypotension from this mechanism resolved with fistula banding.30 Avoid ipsilateral fistula creation in these patients.

5. Evidence Gaps

  • Statin withdrawal on dialysis has not been rigorously studied. The rebound risk that argues for continuation is theoretical.1
  • Statin initiation for secondary prevention on dialysis has no dedicated trial. The only evidence is subgroup data from 4D and AURORA, and it is negative.13,14
  • PISCES is a single trial. Its mechanism is unknown, all-cause mortality did not fall significantly, and the KDOQI 2020 guidance on omega-3 fatty acids predates it.4,16
  • Glycemic monitoring lacks a validated standard. CGM is not FDA-approved or validated for dialysis, its targets are extrapolated rather than validated in CKD, and glycated albumin carries its own biases.7,20
  • Access-related high-output failure is described mainly in small single-center, retrospective, and observational cohorts, and the Qa/CO thresholds come from small studies.10,26,28,29

6. At the Chair

For the dialysis team
  • A stable patient on a statin does not need repeat lipid panels. The question to ask is whether a statin the patient took before dialysis is still on the medication list.
  • A normal HbA1c in a patient with a history of diabetes does not rule out high or low blood sugars. Report symptoms of hypoglycemia, or glucose readings that do not fit the HbA1c.
  • In a patient with a fistula, report new or worsening shortness of breath, leg swelling, or abdominal swelling. These can be signs of high-output heart failure from the access rather than simple fluid overload.

Chair-side reference: Nursing card N9 — Monthly labs: what they mean and what to report.

References

Claims and references on this page are drawn from the source white paper (Screening and Health Maintenance in Maintenance Hemodialysis), whose reference list was re-verified against PubMed on 2026-09-26. References are renumbered for this page.

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