Abstract
Background: Dialyzer-associated hypersensitivity reactions are rare but potentially life-threatening complications of hemodialysis (HD). Their pathophysiology is heterogeneous. Methods: We report a 49-year-old patient with end-stage chronic kidney disease (CKD G5), severe secondary hyperparathyroidism, poorly controlled arterial hypertension, a long history of heavy smoking, severe coronary and valvular disease, reduced left ventricular ejection fraction, renal anemia, and chronic volume overload. Results: Shortly after initiation of HD with a polysulfone dialyzer (Diacap Pro), she repeatedly developed severe dyspnea, hypoxemia, and marked hypertensive responses. Similar reactions occurred after switching to a cellulose triacetate dialyzer (Sureflux), necessitating temporary conversion to peritoneal dialysis (PD). Progressive PD ultrafiltration failure and loss of residual kidney function eventually required a return to HD. Severe reactions recurred within 15–30 min of treatment despite premedication. During the most severe episode, the patient developed profound hypoxemia (SpO2 55%), severe hypertension (up to 240/130 mmHg), ventricular tachycardia, and cardiac arrest requiring successful cardiopulmonary resuscitation. Immunological evaluation demonstrated normal total IgE (17 U/mL), decreased C3 (0.76 g/L), markedly reduced total hemolytic complement activity (CH50, 18%), and elevated IL-6 (87.5 pg/mL). Chronic HD was successfully reinitiated using an FX CorAL dialyzer with a Helixone® hydro membrane. Since its introduction, no further hypersensitivity reactions have occurred, and corticosteroid, antihistamine, and bronchodilator premedication has been discontinued. This case demonstrates severe recurrent dialyzer-associated hypersensitivity with findings suggestive of complement involvement, complicated by cardiac arrest in a patient with markedly impaired cardiovascular reserve. Conclusions: Successful long-term treatment with a hydrophilic Helixone® dialyzer highlights the importance of individualized dialyzer selection in patients with severe hypersensitivity reactions.
1. Introduction
Dialyzer-associated hypersensitivity reactions were historically closely associated with the use of ethylene oxide (EtO) as a sterilizing agent and poorly biocompatible, unmodified cellulose membranes. Despite major advances in dialysis membrane technology, manufacturing processes, and sterilization methods, acute reactions related to the extracorporeal circuit continue to occur with contemporary dialysis membranes.
Traditionally, these reactions have been classified as type A and type B. Type A reactions typically occur within the first few minutes of hemodialysis (HD) and clinically resemble anaphylaxis, whereas type B reactions generally occur later and have historically been associated with complement activation. However, contemporary evidence suggests that this classification does not fully reflect the mechanistic heterogeneity of dialyzer-associated reactions. Potential mechanisms include IgE-dependent and IgE-independent pathways, mast-cell and basophil activation, contact-system activation, complement activation, inflammatory mediator release, or combinations of these processes [1,2].
Furthermore, reactions may be related not only to the basic membrane polymer but also to membrane surface properties, hydrophilic modifiers such as polyvinylpyrrolidone (PVP), manufacturing-related compounds, sterilization methods, or other components of the extracorporeal circuit [3,4,5].
Identifying a safe dialysis membrane may therefore represent a major clinical challenge, particularly when severe reactions recur with more than one dialyzer type. We describe a patient with recurrent life-threatening reactions to both a polysulfone and a cellulose triacetate dialyzer, culminating in ventricular tachycardia and cardiac arrest. Long-term HD was ultimately successfully established using an FX CorAL dialyzer containing a Helixone® hydro membrane.
2. Case Presentation
A 49-year-old woman was hospitalized with end-stage chronic kidney disease (ESRD) and uremic syndrome. Initial laboratory findings included urea 24.8 mmol/L, serum creatinine 852 µmol/L, hemoglobin 87 g/L, and an estimated glomerular filtration rate of 8 mL/min/1.73 m2.
The patient had an extremely high cardiovascular risk profile, including a long history of heavy smoking, severe and poorly controlled arterial hypertension, and pronounced secondary hyperparathyroidism, with a parathyroid hormone concentration of 95.00 pmol/L and serum phosphate of 2.57 mmol/L.
Initial echocardiographic evaluation demonstrated reduced left ventricular ejection fraction and severe degenerative calcification of the cardiac valves. HD was initiated through a temporary central venous catheter inserted into the right internal jugular vein.
During the first two HD sessions, a Diacap Pro dialyzer (B. Braun Avitum AG, Melsungen, Germany) with a synthetic high-flux polysulfone membrane was used. Within the first hour of treatment, the patient developed reproducible episodes of severe dyspnea, a sensation of pressure in the head, marked restlessness, and substantial oxygen desaturation, with SpO2 decreasing from 86% to 65%.
The symptoms were initially treated with cetirizine, intravenous methylprednisolone 80 mg, and diazepam.
Because dialyzer-associated hypersensitivity was suspected, the dialyzer was changed to Sureflux-17L, containing a cellulose triacetate membrane. However, an almost identical severe clinical reaction occurred following exposure to this alternative dialyzer.
Given the persistence of potentially life-threatening reactions, the patient was switched to peritoneal dialysis (PD) approximately one month after HD initiation. She was initially treated with continuous ambulatory peritoneal dialysis (CAPD) and subsequently with automated peritoneal dialysis (APD). Peritoneal equilibration testing characterized her as a high transporter, and total Kt/V was 2.1.
Despite adequate small-solute clearance, fluid removal progressively became insufficient. The patient was initially oligoanuric and subsequently became completely anuric. Despite the use of hypertonic glucose solutions and icodextrin, ultrafiltration remained severely impaired, generally ranging from approximately 200 to 400 mL over 24 h.
Progressive ultrafiltration failure resulted in persistent volume overload and recurrent episodes of pulmonary edema. Severe renal anemia also persisted, with hemoglobin concentrations of approximately 87 g/L despite erythropoiesis-stimulating therapy and red blood cell transfusions.
After 3.5 years of PD, progressive ultrafiltration failure and declining adequacy of the dialysis modality necessitated a return to hemodialysis.
Following renewed exposure to HD, severe reactions recurred within the first 15–30 min of treatment despite pharmacological premedication. Symptoms included acute dyspnea, profound oxygen desaturation, marked restlessness, and severe hypertensive surges.
Given the severity of the cardiovascular manifestations, an extensive cardiac reassessment was performed. Coronary angiography demonstrated extensive calcification involving the right coronary artery and left main coronary artery, diffuse atherosclerotic remodeling of the left anterior descending artery, and a short circumferential stenosis of approximately 90% involving the left circumflex artery (LCx). A drug-eluting stent was successfully implanted in the LCx.
Despite successful coronary intervention, severe respiratory and cardiovascular reactions continued during subsequent attempts at conventional HD.
The most severe event occurred approximately three weeks after reinitiation of HD. Only 15 min after connection to the extracorporeal circuit, the patient developed severe hypertension, with blood pressure increasing to 220–240/120–130 mmHg, profound hypoxemia with SpO2 decreasing to 55% despite oxygen administration at 15 L/min, and marked hyperventilation.
She subsequently developed ventricular tachycardia with loss of consciousness and pulselessness. Cardiopulmonary resuscitation was immediately initiated and successfully restored spontaneous circulation. The patient was intubated and transferred to the coronary care unit. CT pulmonary angiography excluded pulmonary embolism.
Immunological and biochemical investigations demonstrated a normal total IgE concentration of 17 U/mL, markedly elevated IL-6 of 87.5 pg/mL, decreased serum C3 of 0.76 g/L, and profoundly reduced total hemolytic complement activity (CH50) of 18%. Among other laboratory findings, notable abnormalities included hypoproteinemia (total protein 57 g/L), hypoalbuminemia (albumin 25.9 g/L), elevated C-reactive protein (CRP, 58 mg/L), hyperphosphatemia (phosphate 3.55 mmol/L), markedly elevated parathyroid hormone levels (PTH, 93.60 pmol/L), and increased β2-microglobulin levels (27.90 mg/L). Serum immunoglobulin E (IgE) was 11 U/mL.
On multiple occasions, samples were measured both before and after hemodialysis, with the following results: normal IgE, decreased C3, normal C4 (0.24–0.30 g/L), and low CH50, which was measured once after hemodialysis. These findings raised suspicion of activation of the alternative complement pathway.
These findings were considered suggestive of substantial complement activation and systemic inflammatory activation but were not considered sufficient to establish involvement of a specific complement pathway.
NT-proBNP was markedly elevated at 46,118 pg/mL, consistent with severe cardiac wall stress in the setting of kidney failure, structural heart disease, and chronic volume overload (see Table 1).
Table 1.
Immunological and biochemical profile of the patient during the acute event.
A more detailed analysis of individual complement components and complement activation products, together with genetic analysis of the complement system, is currently underway to further characterize the underlying mechanism and investigate a possible susceptibility related to complement regulation.
Following the cardiac arrest, a temporary return to PD was attempted. However, PD had to be permanently discontinued three months later because of fungal peritonitis caused by Candida parapsilosis, requiring removal of the PD catheter.
The patient subsequently presented with severe pulmonary edema and was transitioned to continuous venovenous hemodiafiltration (CVVHDF; Prismaflex M100 system, AN69 membrane, Gambro Industries, Meyzieu, France (Baxter group). The current legal manufacturer is listed as Vantive Health GmbH, Glattpark, Switzerland), with intravenous methylprednisolone 80 mg administered during treatment.
After three days and clinical stabilization, she was transitioned to chronic HD using an FX CorAL dialyzer (Fresenius Medical Care Deutschland GmbH, Bad Homburg, Germany) containing a Helixone® hydro polysulfone-based membrane sterilized using INLINE steam (A proprietary steam sterilization technology developed by Fresenius Medical Care, Germany).
Since the introduction of the FX CorAL dialyzer, the patient has tolerated regular HD sessions without recurrence of respiratory, hypersensitivity, or hemodynamic manifestations. Corticosteroid, antihistamine, and bronchodilator premedication was subsequently completely discontinued, and dialysis sessions have remained clinically stable.
It is important to note that the patient was not receiving angiotensin-converting enzyme (ACE) inhibitors. Furthermore, all other components of the extracorporeal circuit and dialysis procedure, including blood tubing, dialysis needles, ultrapure dialysate composition, and anticoagulation, remained unchanged across all treatment sessions associated with hypersensitivity reactions. The type of dialyzer was therefore the only variable modified between these sessions.
At the most recent follow-up assessment, after six months of treatment with online hemodiafiltration (OL-HDF), laboratory findings showed an erythrocyte count of 3.88 × 1012/L, mildly reduced hemoglobin levels (118 g/L), and slightly decreased total protein levels (65 g/L), while serum albumin was within the normal range (42.4 g/L). Inflammatory markers were low, with a C-reactive protein (CRP) level of 0.6 mg/L, although interleukin-6 (IL-6) remained mildly elevated at 8.8 pg/mL. Serum phosphate (1.55 mmol/L) and parathyroid hormone (PTH, 25.40 pmol/L) levels remained elevated, while β2-microglobulin was 7 mg/L.
3. Discussion
During extracorporeal dialysis, patients’ blood is exposed to various non-physiological surfaces, particularly the dialysis membrane, potentially triggering a range of biological responses, including complement activation, inflammatory processes, and hypersensitivity reactions. These reactions may involve both IgE-mediated and non IgE-mediated mechanisms, with complement activation playing an important role in certain cases. Despite substantial advances in dialysis membrane biocompatibility, manufacturing technologies, and sterilization methods, clinically significant adverse reactions continue to occur. Individual susceptibility to specific membrane materials, their chemical constituents, and other components of the extracorporeal circuit may vary considerably, making the selection of an appropriate dialysis membrane particularly challenging in susceptible patients. Although modern dialysis technologies have improved treatment safety and tolerability, reliable predictors of membrane-associated hypersensitivity reactions remain limited, and universally applicable preventive strategies have yet to be established [1,2].
This case describes severe, recurrent dialyzer-associated hypersensitivity occurring with two different dialysis membranes and ultimately culminating in ventricular tachycardia and cardiac arrest. The close temporal relationship between initiation of HD and symptom onset, reproducibility of the reactions upon re-exposure, and complete resolution after transition to the FX CorAL dialyzer strongly support an extracorporeal circuit-related hypersensitivity reaction.
The mechanisms of contemporary dialyzer-associated hypersensitivity are heterogeneous and may involve IgE dependent and IgE-independent pathways, mast-cell and basophil activation, the contact system, complement activation, and inflammatory mediator release. Blood–membrane interaction is a recognized trigger of complement activation during HD, and the magnitude of this response varies according to membrane composition and surface characteristics [1,2,6]. In our patient, decreased C3 (0.76 g/L), markedly reduced CH50 activity (18%), and elevated IL-6 (87.5 pg/mL) support an important complement-mediated and inflammatory component. However, these findings do not establish activation of the alternative complement pathway specifically, while normal total IgE does not exclude other immunologically mediated mechanisms. Detailed analysis of individual complement components and activation products, together with genetic analysis of the complement system, is currently underway. A limitation of this case report is the inability to measure serum tryptase levels and to perform CH50 measurements more frequently.
The recurrence of almost identical reactions with both a polysulfone (Diacap Pro) and a cellulose triacetate (Sureflux) dialyzer argues against hypersensitivity to a single membrane polymer. PVP, differences in membrane surface properties, manufacturing-related compounds, and sterilization methods have all been proposed as potential contributors to biological responses associated with contemporary dialysis membranes, although a specific causative factor is frequently not identified [3,4,5]. Particularly noteworthy in our patient was the subsequent complete tolerance of FX CorAL, which also contains a polysulfone/PVP-based membrane. This observation further suggests that polysulfone itself was unlikely to represent the sole trigger.
FX CorAL uses a Helixone® hydro membrane with a PVP-enriched blood-contacting surface stabilized by α tocopherol and is sterilized using INLINE steam. Experimental and clinical studies have demonstrated favorable hemocompatibility characteristics of this membrane design, including relatively low complement activation and favorable blood–membrane interactions [3,6,7,8]. Furthermore, a recent retrospective study of 31 patients with previous hypersensitivity reactions to synthetic dialysis membranes reported no further symptoms in 28 patients (90.3%) after transition to hydrophilic Helixone dialyzers [9]. Nevertheless, the present case cannot determine whether membrane hydrophilicity, PVP stabilization, α-tocopherol, sterilization method, or another characteristic of the dialyzer was responsible for successful tolerance.
To further contextualize the present findings, Table 2 summarizes the clinical characteristics and principal findings of the present case alongside those of published studies investigating the hemocompatibility and performance of polysulfone dialyzers, including FX CorAL. This comparison highlights the complementary contributions of individual clinical observations and controlled studies to the understanding of dialyzer-associated reactions and membrane hemocompatibility [8,10].
Table 2.
Comparison of the present case with published studies on the hemocompatibility and performance of hemodialyzers.
The exceptional severity of the reaction was likely amplified by the patient’s markedly impaired cardiovascular reserve. She had extensive coronary and valvular disease, left ventricular dysfunction, severe CKD-MBD, persistent volume overload due to peritoneal ultrafiltration failure, and severe renal anemia. Disturbances in mineral metabolism are associated with increased morbidity and mortality in maintenance HD patients [11], while anemia, kidney failure, and cardiac dysfunction may interact to further compromise cardiovascular reserve [12]. Her coronary artery disease was clearly multifactorial and cannot be attributed directly to secondary hyperparathyroidism.
Against this highly vulnerable cardiovascular background, the acute dialyzer-associated reaction likely acted as a proximate trigger rather than the sole cause of cardiac arrest. Profound hypoxemia, severe hypertension, abrupt hemodynamic changes, sympathetic activation, and increased myocardial oxygen demand may have promoted myocardial ischemia and electrical instability, ultimately resulting in ventricular tachycardia and cardiac arrest.
Following the transition to a better-tolerated dialysis membrane and the initiation of online hemodiafiltration (OL-HDF), the patient demonstrated substantial clinical improvement, with no further hypersensitivity reactions observed. OL-HDF combines diffusive and convective solute removal, potentially enhancing the clearance of middle-molecular-weight uremic toxins and certain inflammatory mediators compared with conventional hemodialysis. At the six-month follow-up, laboratory findings demonstrated a marked reduction in inflammatory markers, with C-reactive protein (CRP) decreasing to 0.6 mg/L and interleukin-6 (IL-6) to 8.8 pg/mL. Improvements in mineral metabolism parameters were also observed, with serum phosphate decreasing to 1.55 mmol/L and parathyroid hormone (PTH) to 25.40 pmol/L, although both remained mildly elevated. Furthermore, β2-microglobulin levels decreased substantially to 7 mg/L, consistent with enhanced middle-molecule clearance associated with the use of the Helixone® hydro dialysis membrane and the high convective volumes achieved during OL-HDF. Nevertheless, these favorable biochemical changes cannot be attributed exclusively to the dialysis membrane or treatment modality, as other factors may have contributed to the observed improvements.
This case illustrates the challenges of renal replacement therapy in a patient who underwent both peritoneal dialysis and extracorporeal hemodialysis-based treatments, with exposure to four different dialysis membranes, two of which were associated with severe, potentially life-threatening hypersensitivity reactions. The successful continuation of extracorporeal treatment following the selection of an alternative membrane and transition to OL HDF highlights the importance of individualized membrane selection and dialysis prescription in patients with suspected dialyzer-associated hypersensitivity.
The complete disappearance of reactions following transition to FX CorAL, together with discontinuation of corticosteroid, antihistamine, and bronchodilator premedication, represents the central therapeutic observation of this case. Rather than implicating a single membrane component, our findings emphasize the complex and patient specific nature of dialyzer-associated hypersensitivity and the importance of individualized dialyzer selection in patients with severe recurrent reactions. An additional clinically relevant benefit was the improvement in several hematological and biochemical parameters, including an increase in hemoglobin to levels consistent with recommended targets for patients receiving maintenance hemodialysis, a substantial reduction in β2-microglobulin concentrations, and improvements in serum phosphate, parathyroid hormone (PTH), and albumin levels. These findings suggest an overall improvement in the patient’s clinical and metabolic status following the modification of renal replacement therapy, particularly in comparison with the preceding treatment period.
Furthermore, the patient’s clinical stabilization was accompanied by a reduction in the overall medication burden, most notably a decreased requirement for antihypertensive therapy following improved blood pressure control. Collectively, these favorable clinical developments were associated with an apparent improvement in the patient’s quality of life and a reduction in treatment-related distress, both for the patient and the healthcare team. Importantly, these observations highlight not only the potential clinical benefits of an individualized dialysis strategy but also its broader implications for treatment tolerability, patient well-being, and the safe delivery of long-term renal replacement therapy.
Finally, the potential role of complement activation should be interpreted with caution, as its specific contribution to the observed hypersensitivity reaction cannot be definitively established.
The mildly reduced serum C3 concentration (0.76 g/L) and markedly decreased CH50 activity (18%) raised suspicion of complement system involvement in the observed hypersensitivity reaction. However, these findings are insufficient to identify the specific complement activation pathway or establish a causal relationship. Reduced C3 with preserved C4 may be compatible with alternative pathway activation, whereas decreased CH50 may reflect complement consumption, component deficiency, or preanalytical factors. Furthermore, extracorporeal circulation and blood–membrane interactions may induce complement activation even during uncomplicated hemodialysis. Accordingly, complement involvement should be considered a plausible contributing mechanism rather than a confirmed cause of the clinical reaction.
4. Conclusions
Severe dialyzer-associated hypersensitivity may involve multiple and overlapping immunological mechanisms. In this patient, decreased C3 and CH50 together with elevated IL-6 supported a complement-mediated inflammatory component but did not establish activation of a specific complement pathway. Although complement activation may have contributed to the observed reactions, the underlying immunological mechanisms remain incompletely understood.
The severity of the reaction was likely amplified by profoundly impaired cardiovascular reserve, with the acute hypersensitivity event acting as a trigger for profound hypoxemic and hemodynamic stress, ventricular tachycardia, and cardiac arrest.
Successful long-term HD with an FX CorAL Helixone® hydro dialyzer resulted in complete resolution of recurrent reactions without pharmacological premedication. This case highlights the importance of individualized membrane selection, careful clinical monitoring, and flexibility in dialysis prescription when managing severe dialyzer-associated hypersensitivity reactions.
Further research is warranted to clarify the underlying mechanisms, identify reliable predictors of susceptibility, and optimize preventive strategies.
Author Contributions
Conceptualization, D.K. and L.K.; methodology, D.K.; validation, D.K., L.K.; formal analysis, M.K.; investigation, D.K.; resources, D.K.; data curation, D.K.; writing—original draft preparation, D.K., L.K., M.K.; writing—review and editing, L.K., M.K.; visualization, M.K., L.K.; supervision, D.K.; project administration, D.K.; funding acquisition, D.K. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
The study was conducted in accordance with the Declaration of Helsinki, and approved by the Institutional Review Board of General Hospital Zadar (protocol code 01-8239-26-2/26).
Informed Consent Statement
Informed consent participation and publication was obtained from all subjects involved in the study.
Data Availability Statement
The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.
Conflicts of Interest
The authors declare no conflict of interest.
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