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MARS molecular absorbent recirculating system liver failure indications

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MARS - Molecular Absorbent Recirculating System (MARS)

What is MARS?

MARS (Molecular Adsorbent Recirculating System) is an extracorporeal hepatic support system that integrates the mechanisms of dialysis, ultrafiltration, and adsorption to remove both albumin-bound and water-soluble toxins from the blood. It is a form of albumin dialysis that serves as a bridge to liver transplantation or spontaneous hepatic recovery.

The system works by passing blood through an albumin-impregnated membrane. Toxins diffuse from the patient's blood into an albumin-containing dialysate circuit, which is then itself cleaned by passing through activated charcoal and anion exchange resin columns. A conventional hemodialysis module removes water-soluble substances simultaneously.

Mechanism of Action

MARS removes the following accumulated toxins relevant to liver failure pathophysiology:

Bilirubin and bile acids - direct hepatotoxins that cause hepatocyte necrosis; their removal halts ongoing hepatic damage
Ammonia and aromatic amino acids - key drivers of hepatic encephalopathy
Pro-inflammatory cytokines (TNF-alpha, interleukin-6) - mediators of systemic inflammation and multi-organ dysfunction
Nitric oxide (NO) and other vasoactive substances - responsible for the hyperdynamic circulation and splanchnic vasodilation seen in liver failure
Water-soluble toxins - cleared simultaneously via the dialysis component

By removing vasoactive agents (NO and inflammatory cytokines), MARS increases systemic vascular resistance and mean arterial pressure, stabilizing the circulation. It also improves renal vascular resistance and the splenic resistance index (a marker of portal resistance), which underlies its benefit in hepatorenal syndrome.

INDICATIONS

MARS is indicated when maximal medical therapy has failed and there is a potentially reversible etiology or a bridge to transplantation is needed.

1. Acute Liver Failure (ALF)

ALF (severe liver injury without prior liver disease, INR >1.5, and hepatic encephalopathy) that fails to resolve with maximal medical management
Etiology must be treatable
Common causes where MARS has been used: acetaminophen toxicity, viral hepatitis, drug-induced liver injury, Wilson's disease crisis, ischemic hepatitis, Budd-Chiari syndrome presenting as ALF
MARS provides time for hepatocyte regeneration and serves as a bridge to transplantation if needed

2. Acute-on-Chronic Liver Failure (AoCLF)

Acute decompensation superimposed on established chronic liver disease
Used for rehabilitation of liver function and as a bridge to transplantation

3. Decompensated End-Stage Liver Disease

Bridge to liver transplantation in patients awaiting an organ
Helps stabilize the patient and may even improve the condition enough to allow reconsidering transplant candidacy

4. Acute Decompensation of the Liver Causing:

Hepatic encephalopathy grade >= 2 refractory to conventional treatment
Hepatorenal syndrome (HRS) type 1 - particularly when Child-Pugh score >= 12 and/or severe encephalopathy (grade >2), when TIPS is contraindicated
- In a small RCT, a mean of 5 MARS treatments improved kidney function and prolonged survival in type 1 HRS patients (mean survival 25 ± 5 days vs. 5 ± 2 days with hemodiafiltration alone)
Refractory HRS type 2 (if TIPS not suitable)

5. Intractable Pruritus Despite Maximal Medical Treatment

Causes include:
- Primary biliary cirrhosis
- Primary sclerosing cholangitis
- Chronic viral hepatitis
- Alcoholic liver disease
- Non-alcoholic hepatitis

6. Post-Transplantation Liver Failure

Primary graft non-function
Small-for-size syndrome after partial liver transplant

7. Liver Failure After Surgery or Trauma

Post-hepatectomy liver failure
Severe mechanical hepatic trauma with resultant liver failure

8. Poisoning with Albumin-Bound Drugs (unrelated to liver failure)

Phenytoin toxicity
Theophylline toxicity
Lamotrigine toxicity
Other highly protein-bound drugs or toxins where conventional dialysis is insufficient

Placement in the Therapeutic Algorithm (HRS Context)

Per the Comprehensive Clinical Nephrology algorithm for type 1 HRS:

All patients - vasoconstrictor (terlipressin IV or norepinephrine) + albumin infusion
If Child-Pugh < 12 and HE grade ≤ 2 - consider TIPS
If Child-Pugh ≥ 12 and/or HE grade > 2 - consider MARS/FPSA
Critically ill with advancing kidney failure - CVVH (continuous venovenous hemofiltration), may be combined with MARS

CONTRAINDICATIONS

Absolute Contraindications

None are universally absolute, but the following are considered prohibitions to use in practice:

Uncontrolled sepsis - systemic infection that is not being adequately controlled
Uncontrolled hemorrhage - active life-threatening bleeding that cannot be controlled

Relative Contraindications

Coagulopathy risk - specifically:
- Platelets < 50,000/microlitre
- INR > 2.3
- Disseminated intravascular coagulation (DIC)
Hemodynamic instability severe enough to preclude extracorporeal circulation
Severe cardiovascular disease that contraindicates the extracorporeal circuit
Liver failure with no potential for recovery and no transplant candidacy - if there is no bridge-to-recovery or bridge-to-transplantation goal, the risk-benefit ratio does not favor MARS
Active intracranial hemorrhage (relevant in ALF with coagulopathy)

Adverse Effects and Safety Concerns

Thrombocytopenia (platelet consumption by the circuit)
Hypotension during the procedure
Bleeding - worsened by anticoagulation needed for the extracorporeal circuit
Electrolyte disturbances
Hypothermia
Air embolism
Line sepsis (central venous access complications)
Removal of beneficial albumin-bound substances (e.g., certain drugs)

Limitations and Current Evidence

Meta-analyses show MARS achieves significant reduction in serum bilirubin and improvement in hepatic encephalopathy grade relative to standard medical therapy, but has not demonstrated a consistent survival benefit in large randomized trials - Brenner and Rector's The Kidney
Current guidelines recommend MARS primarily as a bridge to transplantation rather than definitive therapy
Effect on survival in pure AoCLF remains unclear; one landmark study showed safety and efficacy in ALF but did not improve survival in acute-on-chronic liver failure specifically - Current Surgical Therapy 14e
A 2026 meta-analysis (PMID 42214012) examined MARS specifically for hepatic encephalopathy in liver failure and confirmed improved encephalopathy grades
The Prometheus system (FPSA) and single-pass albumin dialysis (SPAD) are alternatives with overlapping but distinct indications

Summary Table

Category	Details
Device type	Extracorporeal albumin dialysis + hemofiltration
Primary role	Bridge to transplantation or hepatic recovery
Key indications	ALF, AoCLF, HRS type 1/2, HE grade ≥2, post-transplant failure, intractable pruritus, albumin-bound drug toxicity
MARS preferred over TIPS when	Child-Pugh ≥ 12 and/or HE grade > 2
Absolute contraindications	Uncontrolled sepsis, uncontrolled hemorrhage
Relative contraindications	Platelets <50k, INR >2.3, DIC
Toxins removed	Bilirubin, bile acids, ammonia, NO, cytokines, aromatic amino acids
Survival benefit	Not consistently demonstrated; improves encephalopathy grade and bilirubin

Sources: - Comprehensive Clinical Nephrology 7th ed., p. 1044-1045 | - Brenner and Rector's The Kidney, p. 616 | - Current Surgical Therapy 14e, p. 493 | - StatPearls: MARS

Do mars remove albumin

No, MARS does not remove albumin from the patient. That's actually the key design principle of the system.

Here's why:

The MARS membrane is albumin-impregnated and albumin-impermeable. The patient's blood flows on one side of this membrane. Toxins that are bound to the patient's own albumin diffuse across the membrane (because of the concentration gradient) into the dialysate circuit - but the albumin molecules themselves are too large to pass through the pores.

So what happens is:

The toxins detach from the patient's albumin and bind to the albumin in the dialysate
The patient's own albumin stays in circulation, now "cleaned" of its toxic cargo
The dialysate albumin (loaded with toxins) is then regenerated by passing through activated charcoal and anion exchange resin columns, and recirculated - hence the name Recirculating System

This is a critical distinction from plasma exchange, which does remove albumin (along with the plasma). MARS selectively removes albumin-bound toxins (bilirubin, bile acids, aromatic amino acids, NO, cytokines) while preserving and recycling the patient's albumin.

The only caveat is that some albumin-bound substances that are beneficial (certain drugs, hormones) may also be partially removed as a side effect - but the albumin protein itself stays in the patient.

Do hemodialysis remove albumin

No, conventional hemodialysis does not remove albumin - and this is by design.

Why Not

Standard hemodialysis membranes have a molecular weight cutoff of approximately 15,000-20,000 daltons (for low-flux membranes) or up to ~50,000 daltons (for high-flux membranes).

Albumin has a molecular weight of ~66,000 daltons - far too large to pass through these pores under normal conditions.

So albumin stays in the blood circuit and is returned to the patient.

What Hemodialysis Does Remove

Substance	MW	Removed?
Urea	60 Da	Yes
Creatinine	113 Da	Yes
Potassium, phosphate	Small ions	Yes
Beta-2 microglobulin	11,800 Da	Partially (high-flux)
Albumin	66,000 Da	No
Albumin-bound toxins	Large complexes	No

The Clinical Problem This Creates

Because albumin-bound toxins (bilirubin, bile acids, ammonia complexes, inflammatory cytokines) travel bound to albumin, conventional hemodialysis cannot clear them. This is precisely the gap that MARS fills - it removes albumin-bound toxins using its specialized membrane, something ordinary hemodialysis cannot do.

Exception Worth Knowing

In high-cut-off (HCO) dialysis membranes (cutoff ~60,000-100,000 Da), there is measurable albumin loss into the dialysate - this is an intentional trade-off used in conditions like myeloma cast nephropathy to remove free light chains. But this is a specialized, non-standard modality, not conventional HD.

Do albumin removed by High flux dialyzer

Technically yes, but only in tiny, clinically insignificant amounts under normal conditions.

The Numbers

Dialyzer Type	Membrane Cutoff	Albumin Loss per Session
Low-flux	~15,000 Da	Essentially zero
High-flux	~30,000–50,000 Da	~1–3 g per session (trace)
High-cut-off (HCO)	~60,000–100,000 Da	5–20 g per session (significant)

Albumin = 66,000 Da, so:

Low-flux membranes: pores are far too small - no passage
High-flux membranes: pores approach but don't consistently exceed albumin's size - a small amount leaks through, especially early in a session before the membrane becomes partially fouled/coated with proteins
HCO membranes: deliberately sized to allow albumin passage

Why High-Flux Albumin Loss is Minimal in Practice

Protein fouling - within minutes of starting dialysis, a protein layer coats the membrane pores, effectively reducing the functional pore size and blocking further albumin passage
Back-filtration effect - in high-flux dialyzers, convective back-flow from dialysate to blood in parts of the circuit can actually return some albumin
The 1-3 g lost is small compared to the body's albumin pool (~120-140 g total) and daily synthesis (~12-15 g/day)

When It Becomes Clinically Relevant

High-flux albumin loss matters in:

Malnourished patients with already low albumin - cumulative loss over frequent sessions can worsen hypoalbuminemia
Daily HD or prolonged sessions - losses add up
Patients with chronic inflammation - where albumin synthesis is already suppressed

Bottom Line

High-flux dialyzers remove albumin in trace amounts (1-3 g/session) - not clinically significant for most patients. Meaningful albumin removal requires a high-cut-off (HCO) dialyzer, which is a separate specialized category. This is why neither conventional low-flux nor high-flux HD can remove albumin-bound toxins the way MARS does.

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