MFI Cutoffs and Organ-Specific Differences

1. Mean Fluorescence Intensity (MFI)

2. Typical MFI Cutoffs

3. Typical MFI Cutoff Ranges and Locus-Specific Cutoffs

• General MFI Ranges: Most labs in the U.S. use an MFI threshold in the low thousands to call an antibody positive. Surveys show a range from ~500 up to 3,000 MFI as cutoffs in different laboratories (). Many centers consider very low-level reactions (<500) to be negative/background, while values above 1,000–2,000 are often treated as true antibodies (). For example, one transplant center uses MFI <2000 as a negative cutoff for kidney candidates (to maximize organ availability despite low-level DSA) (). In practice, MFI <1000 is considered negative at most kidney centers for unsensitized patients (), and MFI ~1000–2000 is a gray zone that some centers may still accept as “low risk” ().
• HLA Locus-Specific Cutoffs: It is common to adjust cutoffs depending on the HLA locus detected. About 37% of labs report using locus-specific thresholds, often setting higher MFI cutoffs for HLA-C, HLA-DQ, and HLA-DP antibodies (). This is because certain antigens (e.g., HLA-C, DQ, DPB1) tend to yield higher MFI on single-antigen bead (SAB) assays relative to their actual expression in vivo (). In other words, these loci are “overrepresented” on beads (more antigen per bead), so an antibody against them may register a higher MFI than an equivalently strong antibody against HLA-A or -DR (). To avoid over-calling such antibodies, labs may require a higher MFI (e.g. +500–1000 more) to count them as positive. For example, a lab might use an MFI cutoff of 1000 for anti-HLA-A but 2000 for anti-DQ. Each lab validates these thresholds internally, so practices vary ().
• ASHI Guidelines/Surveys: The American Society for Histocompatibility and Immunogenetics (ASHI) doesn’t mandate a universal cutoff but expects labs to define and justify their own. A 2024 ASHI virtual crossmatch survey confirmed wide variability: virtually all labs use an MFI cutoff for SAB, but the specific value ranged from 500 up to 3000 (). Most labs clustered in the 1000–3000 range, and many applied higher cutoffs for C, DQ, DP () (consistent with the overexpression issue). Another report noted most US centers list unacceptable antigens (to avoid donor offers) at roughly MFI 3000–5000 or above (), although some use more conservative or liberal values. Ultimately, each center sets its own MFI threshold based on experience, balancing the risk of rejection against the need to avoid turning down too many organs ().

4. Organ-Specific MFI Criteria (Kidney vs. Heart vs. Lung vs. Liver)

• Kidney Transplant: Kidneys are sensitive to DSA, but because dialysis is an alternative, centers sometimes tolerate low-to-moderate DSA with desensitization. Many kidney programs treat any DSA >1000 MFI as potentially significant, but not all will exclude a donor for that. A common approach is to avoid donors with strong DSA (e.g. >3000) and proceed with caution (or therapy) if DSA is in the 1000–3000 range (). One center’s practice: MFI <2000 considered negative, acknowledging some DSA might be missed to improve patient access (). Generally, kidney programs use MFI thresholds ~1000–2000 for unacceptable antigens in unsensitized patients (), and up to ~3000 for highly sensitized (to avoid unnecessary donor refusals). Data support that even “weak” pre-transplant DSA (<3000 MFI) often have no major impact on immediate graft outcomes (), especially if properly managed, so kidney transplant candidates can sometimes be transplanted successfully despite low-level DSA.
• Heart Transplant: Heart recipients are at high risk from any DSA because hyperacute rejection of a heart is usually fatal. Thus, heart transplant centers tend to be more stringent – many aim for zero DSA if possible. In practice, some heart programs list any antibody >1000 MFI as unacceptable (), essentially avoiding donors that would trigger even moderate DSA. Others may use a higher cutoff (like 3000 or 5000) to balance waiting time (). An American Heart Association statement noted MFI cutoffs for unacceptable antigens in heart transplant listing vary by center, commonly >1000 (very risk-averse centers) or >5000 (more risk-tolerant) (). For example, one heart transplant center defined >1000 MFI as “high DSA” (500–1000 considered low-level) and would perform desensitization for those patients (). Overall, heart programs are cautious: any DSA above minimal levels is a red flag due to the threat of acute antibody-mediated rejection (AMR) and cardiac allograft vasculopathy.
• Lung Transplant: Lung transplant candidates also fare poorly with DSA, which can cause primary graft dysfunction or chronic lung allograft dysfunction. However, due to organ scarcity, lung programs may be slightly more permissive than heart. A study of lung transplant candidates found those with high-strength antibodies (MFI >3000) had significantly lower transplant rates and higher post-transplant AMR, whereas those with only moderate antibodies (1000–3000 MFI) often received transplants without immediate AMR () (). Many lung centers use ~2000–3000 MFI as a threshold to avoid a donor: e.g., using >3000 as “unacceptable” cutoff improved management of waitlist and post-transplant outcomes (). In practice, lung candidates with antibodies <3000 MFI may still be transplanted (with close monitoring or peri-operative treatment), while >3000 is considered high risk for AMR (). Antibodies at very low levels (<1000) are often ignored in lung allocation, similar to kidney.
• Liver Transplant: Historically, liver transplants have been considered more tolerant to HLA antibodies. The liver can sometimes absorb or clear antibodies, and liver grafts are less prone to hyperacute rejection from DSA. Indeed, human liver allografts are “more resilient to antibody-mediated damage” compared to heart or kidney allografts (). Thus, many liver transplant centers do not routinely perform virtual crossmatching or may not exclude donors based on HLA DSA alone () (). A positive crossmatch or DSA presence was long thought to be clinically irrelevant in liver transplantation, though recent studies show DSA can contribute to fibrosis or rejection in some cases (). There are no universally adopted MFI cutoffs for liver – in fact, some programs will proceed with a liver transplant despite high DSA, especially in urgent cases, whereas such DSA would preclude kidney or heart transplant. The liver’s unique immunology (e.g. high clearance of antibody and induction of tolerance) means that even strong DSA might not cause hyperacute rejection of a liver. That said, very high DSA (e.g. MFI >10,000 or complement-fixing DSA) have been linked to early liver graft loss in some reports () (). In summary, liver transplants rarely use strict MFI cutoffs; they often rely on clinical judgment, considering DSA only if the patient has a history of rejection or if multiple organs (liver+kidney) are involved.

5. Clinical Outcomes and Transplant Success Relative to MFI

• Impact on Rejection and Graft Survival: Higher DSA MFI correlates with higher risk of antibody-mediated rejection (AMR) and graft loss in most organs. For kidneys, even low-level DSA (MFI 500–1000) can increase the incidence of subclinical AMR, though they may not significantly affect short-term graft survival (). In a large kidney study, any pre-transplant DSA >1000 MFI led to worse long-term graft survival compared to no DSA () (). Patients with very high DSA (cumulative MFI >5000) had the poorest outcomes, experiencing more rejection and faster graft function decline (). Conversely, “weak” DSA below ~1000 had minimal impact on graft longevity (). These data suggest that using a cutoff that labels antibodies below 1000 as “negative” is generally safe (their presence didn’t impair survival) (), but ignoring antibodies above 1000 could jeopardize the graft. Similarly, in heart transplants, pre-formed DSA (especially Class II DSA with high MFI) are associated with increased risk of AMR, early cellular rejection, and chronic vasculopathy () (), which can reduce graft survival. Lung transplant recipients with pre-transplant antibodies >3000 MFI had higher rates of AMR post-transplant (20% vs ~6% in those without antibodies) (). In liver transplants, high-strength DSA that persist post-operatively have been linked to graft fibrosis and failure, although many DSA-positive liver recipients still do well, reflecting the liver’s partial resistance to AMR () ().
• Transplant Access vs. Risk: There is a trade-off between avoiding all DSA and getting the patient transplanted sooner. A lower MFI threshold (strict cutoff) – for example, considering anything >500 MFI as unacceptable – maximizes safety but can dramatically limit organ offers for sensitized patients, prolonging wait times. A study modeling kidney allocation showed the most “stringent” virtual crossmatch (requiring DSA MFI <500) yielded the lowest risk of rejection but also significantly reduced transplant opportunities () (). On the other hand, a higher cutoff (e.g. 5000) will allow more transplants but at the cost of more frequent positive crossmatches or post-transplant rejections (). Each center strikes a balance: for kidney patients, avoiding all DSA might keep them on dialysis indefinitely, which has its own mortality risk () (). Therefore, many programs accept some “weak DSA” to improve access to transplant, using treatments (IVIG, plasmapheresis, etc.) around the time of transplant to mitigate risk. Published evidence supports this approach: kidney recipients with pre-transplant DSA in the 800–3000 MFI range often have comparable outcomes to those without DSA when properly managed () (). In one series, patients with weak DSA had similar graft survival to DSA-negative patients despite being higher immunologic risk overall (). This suggests that strict cutoffs may overestimate risk in some cases.
• Organ-Specific Outcomes: Because hearts and lungs have little backup treatment if rejection occurs, even moderate DSA can be deadly, hence the cautious approach and historically poorer outcomes when DSA is present. For hearts, pre-transplant DSA (especially complement-fixing ones) significantly increase 1-year rejection rates and contribute to cardiac allograft vasculopathy, impacting long-term survival () (). Desensitization therapies in heart transplant have shown some success in allowing transplantation despite DSA, but such patients require intensive monitoring and still face higher rejection risk () (). In lung transplants, patients with high MFI antibodies had longer waits and some were not transplanted at all due to positive virtual crossmatches () (). Those who were transplanted with high-DSA had more AMR and likely worse lung function down the line. Liver transplant outcomes seem less tightly linked to DSA strength – many DSA-positive liver recipients do fine, and some studies show preformed DSA often disappear after liver transplant with no intervention (). Still, liver recipients who do suffer AMR (rare) often had very strong DSA that persisted, indicating that beyond a certain MFI threshold, even the liver’s resilience can be overcome ().

6. Virtual Crossmatch Interpretation Considerations

6.1 HLA Expression Discrepancies: Test Cells vs. Organ Tissue

• Cells Used for Crossmatch: For a physical crossmatch, the donor’s lymphocytes (T and B cells, usually from peripheral blood, spleen, or lymph node) are used. T cells express HLA Class I (A, B, C) but little to no Class II (unless activated), whereas B cells express both Class I and Class II (DR, DQ, DP). In a flow crossmatch, T-cell positivity indicates class I DSA; B-cell positivity can indicate class I or class II DSA. Importantly, the level of HLA on these cells can be affected by donor factors. For example, living donors often have normal baseline HLA expression, but a deceased donor (especially brain-dead) may have upregulated certain HLAs (discussed more below). Additionally, donors on certain medications like statins or steroids can have reduced HLA expression on their lymphocytes (). Lower HLA density on test cells might cause a weak or negative crossmatch even if antibodies are present (a false-negative). For instance, a patient’s serum with DSA of MFI ~2500 might not produce a positive flow crossmatch if the donor T cells have downregulated HLA levels (). Labs mitigate this by treating cells (e.g. with pronase) to improve detection or by interpreting virtual crossmatch data alongside.
• HLA on Organ Tissue: The transplanted organ’s cells (e.g. endothelium of a kidney, heart, lung, liver) have different HLA expression patterns. Class I (HLA-A, B, C) is expressed on almost all nucleated cells, including endothelium, so any Class I DSA can target the organ immediately. Class II (HLA-DR, DQ, DP) is normally expressed only on antigen-presenting cells (like B cells, dendritic cells). However, in transplanted organs, Class II can be induced on endothelial and other cells by inflammation. Notably, organs from brain-dead donors often already have Class II upregulation due to the cytokine “storm” of brain death () (). For example, one study showed that within hours of brain death, donor kidneys began expressing MHC class II on endothelial and tubular cells, whereas virtually no class II was present in living-donor controls (). This means a recipient with Class II DSA (say anti-DQ) could experience immediate injury in a deceased-donor transplant (because the antigen is present on the graft), whereas the same DSA in a living-donor transplant might not cause hyperacute rejection since class II is minimally expressed at implantation. Virtual crossmatch interpretations must account for donor type: a borderline DSA, which might be deemed “acceptable” for a living donor, could be riskier with a deceased donor. If a donor was given high-dose steroids (common in brain-dead donors), their lymphocytes used in crossmatch may have lower HLA levels (), potentially yielding a negative crossmatch even though the organ’s tissue (especially after reperfusion) expresses the antigen robustly – this discrepancy can affect clinical decisions. Transplant teams sometimes err on the side of caution: e.g., if the virtual crossmatch indicates a DSA of concern but the flow crossmatch is negative, they consider whether low HLA expression could be the reason. Close communication between lab and clinicians is vital ().
• Beads vs Cells: In a virtual crossmatch, we rely on solid-phase assays (like SAB on Luminex beads) rather than actual donor cells. As mentioned, bead assays often use recombinant HLA coated at high density. This can lead to overestimation of antibody strength for certain loci (C, DQ, DP) (). Therefore, an antibody that is 3000 MFI to an HLA-DP on beads might not actually find much DP antigen on the transplanted organ (if the organ’s cells barely express DP). Such a DSA might never cause harm, yet the virtual crossmatch flags it. Labs mitigate this by raising the cutoff for those loci or by performing a cell-based crossmatch if there’s uncertainty. Conversely, antibodies to antigens that are not represented on beads will be missed by virtual crossmatch (though this is rare, since modern panels cover most common alleles). Overall, understanding these expression differences helps avoid false assurance or overreaction to the virtual crossmatch. As a rule of thumb, Class I DSA correlate well between SAB MFI and actual risk (since Class I is always present on graft), while Class II DSA need careful consideration of donor condition (living vs deceased) and timing, as their targets may or may not be immediately present on the graft.

6.2 Cold Ischemia Time and HLA Upregulation

• HLA Upregulation: Ischemia-reperfusion injury triggers inflammation in the graft. Studies have shown that various “danger signals” and cytokines from ischemia can increase HLA expression on graft endothelial cells (). For instance, after reperfusion of a cold-stored kidney, you may see higher Class I and Class II expression than pre-harvest. This means a DSA that was borderline might find more targets to bind on a cold-ischemic, injured organ than on a fresh one. Brain death itself (often accompanied by some warm ischemia during shock or hypotension episodes) already induces HLA Class II as noted. Additional cold storage exacerbates this. The combination of donor brain death + extended cold ischemia can thus markedly increase the risk that any pre-existing DSA will cause damage, because the graft is “primed” for immune recognition.
• Outcomes by CIT: Large cohort analyses in kidney transplants show that prolonged CIT worsens outcomes in the presence of DSA. In DSA-positive kidney transplants, extended cold time was associated with significantly higher rates of AMR and graft loss compared to short cold time () (). One study noted that among deceased donor kidneys, the combination of pre-transplant DSA plus longer CIT conferred a “very large risk” for AMR, much greater than either risk factor alone (). Even in DSA-negative patients, longer cold time slightly increased rejection, but DSA-positive patients were affected far more () (). For living donor transplants (minimal cold time), even DSA-positive cases had lower rejection rates, presumably because the lack of significant ischemia kept the graft less immunogenic (). Heart and lung transplants typically have short CIT (4–6 hours), but even within that window, any delay can impact primary graft function. It’s less documented for HLA specifically, but given that heart and lung donors are all brain-dead (in most cases), those organs already have maximal immune activation; thus keeping CIT short is crucial to avoid compounding the issue. Liver transplants can sometimes tolerate longer CIT (up to 12+ hours), but extended CIT in liver is known to increase early graft dysfunction. While liver grafts are tolerant, a long cold ischemia combined with high DSA might tip the balance toward AMR or early loss (some liver studies show higher DSA-mediated complications with longer cold times, though data are limited).
• Implication for VXM: When interpreting a virtual crossmatch, it’s worth considering how soon the organ will be implanted. If a kidney is coming from across the country (hence likely >20 hours CIT), the team might be more wary of even moderate DSA because the prolonged cold time could heighten the risk of that DSA causing rejection. Conversely, a local kidney with 6 hours CIT might do fine with the same level of DSA. While this level of nuance is not always explicitly factored into crossmatch reports, experienced clinicians recognize that DSA risk is not static – it is amplified by longer cold ischemia (and by donor inflammation). Thus, some centers use more aggressive immunosuppression or desensitization for DSA-positive transplants with long CIT, or they may decline a marginal organ if the patient has DSA and the transport time is long.

6.3 Antibody Spreading and Shared Epitopes

• Shared Epitope Dilution: Patients often develop antibodies against public epitopes (shared by multiple HLA alleles) – for example, the Bw4 epitope is present on many HLA-B antigens. It was hypothesized that if a patient has a finite amount of antibody against Bw4, and the SAB kit has many different beads each carrying a Bw4-positive antigen, the antibody could bind across all those beads. Each bead would then show a moderate MFI instead of one bead showing a very high MFI. In theory, this could make a strong antibody appear “weak” because its signal is split. This raised concern that using a strict per-bead MFI cutoff might miss a significant antibody. However, recent research by Claisse et al. specifically tested this “MFI dilution” hypothesis. They isolated beads with single alleles containing certain common eplets and compared reactivity (). Their results found no evidence of clinically significant MFI dilution for the epitopes studied (). In other words, a strong antibody still gave strong MFI readings, and the notion of dilution across beads did not materially mask any dangerous DSA in their analysis. Thus, while the concept of antibody spreading across shared epitopes is biologically plausible, current evidence suggests it’s unlikely to cause a truly strong DSA to slip under the radar of SAB testing (). That said, this was one study – it would be valuable to test other epitopes and different kits to fully lay the issue to rest ().
• Epitope Coverage and Missed Detections: Another aspect is if an antibody’s target epitope isn’t represented on the bead panel properly. Modern panels cover most polymorphic epitopes, but if a patient’s antibody is against a rare epitope or an epitope that only appears in combination on an allele not included, the SAB may miss it (). This scenario is rare but possible; for instance, a patient could react to a peculiar HLA-DQ heterodimer epitope not mirrored on any single antigen bead. In practice, labs sometimes see patients with clear crossmatch positivity but no corresponding SAB specificity – raising suspicion of an antibody against an unrepresented epitope or denatured antigen (see below). Another scenario of “antibody spreading” is epitope spreading over time – a patient sensitized to one mismatched antigen can develop new antibodies to related epitopes after transplant (broadening the DSA profile). This is more relevant post-transplant (de novo DSA evolution) and underscores why a single MFI cutoff isn’t a complete assessment of risk – the qualitative specificity matters too (e.g., a patient with multiple moderate DSAs might be at higher risk than one with a single moderate DSA).
• Clinical Decision Impact: Because of these considerations, some centers prefer epitope-level analysis in tricky cases. If a virtual crossmatch is positive only for low-level antibodies to several antigens sharing a public epitope, clinicians might infer the patient has one antibody causing all those and gauge the overall strength collectively rather than per bead. The crossmatch review literature encourages performing an epitope analysis of SAB results to better understand the immune risk (). For now, most studies indicate that the standard approach of looking at the highest single-bead MFI is sufficient, and true “antibody spreading” causing false negatives is not a common problem (). Nonetheless, awareness of shared epitope effects is important, especially if a patient’s serum has many low-level reactions that form a pattern.

6.4 Allele-Specific Antibodies and SAB Pitfalls

• Detection and Interpretation: If SAB testing shows reactivity to, say, HLA-B44:02 bead but not to B44:03, the patient may have an allele-specific antibody targeting an epitope unique to B44:02. In traditional serologic terms, both are “B44”; a virtual crossmatch that only considers antigen-level might call it anti-B44. But if a donor has B44:03, perhaps the antibody wouldn’t bind at all. Studies indicate allele-specific anti-HLA reactivity is not uncommon – one analysis found ~15% of sensitized patients had potential allele-specific antibodies identified by discordant bead reactions () (). Crucially, if we list the broad antigen as unacceptable in these cases, we could unnecessarily exclude patients from donors that express the non-reactive allele. One recent study estimated up to 10% of highly sensitized candidates were unnecessarily prevented from receiving certain organ offers due to over-calling unacceptable antigens when their antibodies were actually allele-specific () (). They even confirmed some allele-specific patterns with actual crossmatch results, showing that considering the allele nuance could safely expand donor options () ().
• Policy and Practice: Current UNOS policy for listing unacceptable antigens works at the antigen (serologic) level, not allele level. Therefore, most centers err on the side of caution and list the broad antigen if any allele of that antigen is reactive. However, sophisticated centers, in consultation with their HLA lab, might make a clinical decision to accept an organ if the donor’s allele is known and the patient’s antibody is believed to be allele-specific not targeting that allele. For example, if a patient only has anti-A68:01 (and not A68:02) and a donor offers has A*68:02, the center might choose to proceed. This is delicate and requires high-resolution typing and confidence in the antibody assessment.
• Multiple Bead Reactivity Rule: A practical rule some labs use is to require multiple bead reactivities to call an antibody positive at the antigen level. If only one out of several beads for an antigen is positive (especially if it’s a lower MFI), they suspect an allele-specific or artifactual reaction. True broad antibodies usually hit all alleles of that antigen to some extent. Thus, seeing concordant reactivity on multiple beads (for the same antigen) strengthens the case that a real antibody exists. If reactivity is discordant, further investigation is done. This might include testing the serum on a different manufacturer’s kit (different allele representations) or performing a cell-based crossmatch against a target with the specific allele in question.
• Allele vs Antigen Pitfalls: Another pitfall is that SAB kits might lack certain alleles – if a patient’s donor has a rare allele not on the panel, an antibody could be missed or misassigned. For instance, the panel might have B15:01 and B15:02, but the donor is B15:10. If the patient’s antibody is specific to an epitope on B15:10 not shared by 01/02, the virtual crossmatch could be falsely negative. Conversely, if the patient has antibody to B*15:01 (bead positive) but the donor’s B15 allele is different and maybe not recognized by that antibody, the virtual crossmatch might appear positive even though the actual transplant might be fine. These scenarios are complex, but awareness is growing. Manufacturers are continuously updating bead alleles to improve coverage ().

6.5 Other Pitfalls: Denatured Antigens and Prozone

• Antibodies to Denatured Antigens: SAB assays use purified HLA antigens, and some may be partially denatured (misfolded) on the beads. Patients can have antibodies that bind these denatured epitopes which do not exist on native cell-surface HLA. These can yield positive virtual crossmatches that don’t actually pose a risk to the graft. For instance, certain anti-HLA antibodies found in non-alloimmunized males were later attributed to artifacts of denatured antigens on beads (). If such an antibody is detected, a physical crossmatch might be negative (since the antibody won’t bind the native HLA on cells) (). Traditionally, many labs ignored antibodies to denatured antigens as clinically irrelevant (). However, recent data complicate this, showing some sera with “denatured-only” antibody reactivity could also bind native antigens under certain conditions (). This area is evolving. Generally, if a patient’s antibody reactivity pattern suggests it’s only targeting cryptic epitopes (e.g., reacts with a heavy chain-only bead but not the intact antigen beads), labs will annotate that and often not count it as a positive DSA. Noting these patterns is important so that a virtual crossmatch isn’t over-interpreted. Each case should be examined for consistency – e.g., do the positive beads share an epitope that could be denatured? Are they all from a single manufacturer lot? This level of analysis goes beyond simple MFI cutoff and requires HLA lab expertise ().
• Prozone and Blocking Factors: Sometimes very high titers of antibody can paradoxically produce lower apparent MFI due to prozone effect or complement interference. Some sera have C1 complement components that bind the beads and prevent the detection reagent from binding, thus lowering MFI. Labs commonly treat sera with EDTA or DTT to eliminate complement and IgM, which can otherwise mask true IgG antibody strength () (). Most labs (89% in one survey) use treatments like EDTA to avoid this interference () (). If not addressed, a prozone effect could cause a dangerous antibody to register an MFI of, say, 1000 when it’s actually much stronger – leading to a false sense of security in the virtual crossmatch. This is why sample handling and dilution protocols are an important part of virtual crossmatch practice, though it’s a technical detail often handled behind the scenes.

7. Conclusion

1. Tinckam K, et al. “Interpreting Anti-HLA Antibody Testing Data: A Practical Guide for Physicians.” Am J Transplant. 2016. – Discusses MFI cutoff differences by organ and a pragmatic approach ().
2. ASHI 2024 Virtual Crossmatch Educational Challenge Summary. – Survey of U.S. labs’ practices: MFI cutoff range 500–3000; higher thresholds for HLA-C/DQ/DP by many labs ().
3. Claisse et al., Transplantation. 2021. – Investigated the “MFI dilution” hypothesis for shared epitopes; found no significant dilution effect ().
4. Aubert O, et al., J Am Soc Nephrol. 2022 (Swiss Transplant Cohort). – Demonstrated that kidney grafts with DSA MFI >1000 had worse survival; >5000 had highest risk () ().
5. Valenzuela NM, et al. “Understanding solid-phase HLA antibody assays and the value of MFI.” Hum Immunol. 2017. – Review of SAB pitfalls: denatured antigens, prozone, variability, etc. () ().
6. Lung Transplant study (Ajrccm, 2014). – Showed lung candidates with antibodies >3000 MFI had lower transplant rates and higher post-transplant AMR ().
7. ESC Press Release 2017 (Coutance). – Heart transplant desensitization program; defined >1000 MFI as high DSA, with outcomes ().
8. Zeevi A, et al. “Donor-specific HLA antibodies in solid organ transplantation: clinical relevance and debates.” 2019. – Discusses impact of preformed DSA on outcomes in various organs (notes liver historically considered more tolerant) ().
9. Tambur AR, et al. “The presence of allele-specific HLA antibodies: to worry or not to worry?” (BWH study, 2023). – Found allele-specific DSAs can exclude patients unnecessarily; up to 10% of sensitized candidates impacted ().
10. Cruzado LM, et al. “Virtual Crossmatch in Kidney Transplantation.” Front Immunol. 2023. – Explores integration of virtual crossmatch with donor types (living vs DCD), showing prolonged CIT heightens DSA risk () ().