Antithymocyte globulin-induced refractory hypotension in renal transplantation recipient

Shamim, Rafat; Sahu, Sandeep; Siddiqui, Tasneem; Sanjay, Agarwal

doi:10.4103/joacp.joacp_128_16

Cited by 4 publications

(5 citation statements)

References 5 publications

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“…162 ATG can cause some adverse events, such as cytokine release syndrome (fever, chills, and nausea/vomiting) and thrombocytopenia. 21,163,164 Anti-CD20 mAb (Rituximab, Genentech, South San Francisco, CA) Rituximab is a mAb, which targets CD20, a protein expressed on the surface of B cells. It acts by depleting CD20 + B cells mainly through 3 different mechanisms (antibody-dependent cell-mediated cytotoxicity, complement-dependent cytotoxicity, and apoptosis).…”

Section: Appendix: Mechanisms Of Action and Potential Side Effects Of...mentioning

confidence: 99%

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What Therapeutic Regimen Will Be Optimal for Initial Clinical Trials of Pig Organ Transplantation?

et al. 2021

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We discuss what therapeutic regimen might be acceptable/successful in the first clinical trial of genetically engineered pig kidney or heart transplantation. As regimens based on a calcineurin inhibitor or CTLA4-Ig have proved unsuccessful, the regimen we administer to baboons is based on induction therapy with antithymocyte globulin, an anti-CD20 mAb (Rituximab), and cobra venom factor, with maintenance therapy based on blockade of the CD40/CD154 costimulation pathway (with an anti-CD40 mAb), with rapamycin, and a corticosteroid. An anti-inflammatory agent (etanercept) is administered for the first 2 wk, and adjuvant therapy includes prophylaxis against thrombotic complications, anemia, cytomegalovirus, and pneumocystis. Using this regimen, although antibody-mediated rejection certainly can occur, we have documented no definite evidence of an adaptive immune response to the pig xenograft. This regimen could also form the basis for the first clinical trial, except that cobra venom factor will be replaced by a clinically approved agent, for example, a C1-esterase inhibitor. However, none of the agents that block the CD40/CD154 pathway are yet approved for clinical use, and so this hurdle remains to be overcome. The role of anti-inflammatory agents remains unproven. The major difference between this suggested regimen and those used in allotransplantation is the replacement of a calcineurin inhibitor with a costimulation blockade agent, but this does not appear to increase the complications of the regimen.

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Section: Appendix: Mechanisms Of Action and Potential Side Effects Of...mentioning

confidence: 99%

“…162 ATG can cause some adverse events, such as cytokine release syndrome (fever, chills, and nausea/vomiting) and thrombocytopenia. 21,163,164…”

Section: Induction Therapymentioning

confidence: 99%

What Therapeutic Regimen Will Be Optimal for Initial Clinical Trials of Pig Organ Transplantation?

et al. 2021

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“…However, neither infusion reaction nor serum sickness‐related hypotension could explain our finding of persistent hypotension at 6 months. Lymphocyte depletion may be a surrogate marker for overall immune sensitization in this small population, who also had more mismatches, and persistent hypotension was related to tissue ischemia and the resultant nitric oxide release due to immune‐mediated damage 15 . However, the lack of long‐term negative graft effects contradicts this theory.…”

Section: Discussionmentioning

confidence: 97%

“…Lymphocyte depletion may be a surrogate marker for overall immune sensitization in this small population, who also had more mismatches, and persistent hypotension was related to tis-sue ischemia and the resultant nitric oxide release due to immunemediated damage. 15 However, the lack of long-term negative graft effects contradicts this theory. Overall, our data do not suggest a causative effect of lymphocyte depletion, and further investigation in larger cohorts is needed to elucidate the etiology of this association.…”

Section: Discussionmentioning

confidence: 99%

Risk factors and outcomes of persistent post‐transplant hypotension among simultaneous pancreas and kidney transplant recipients

Aziz,

Mandelbrot,

Jorgenson

et al. 2023

Clinical Transplantation

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BackgroundThe risk factors and outcomes associated with post‐ transplant hypotension after simultaneous pancreas and kidney (SPK) Transplantation are poorly defined.MethodsSPK recipients at our center between 2010 and 2021 with functioning pancreas and kidney grafts for >6 months were included. Recipients were then divided into three groups based on active medications for the treatment of hypo‐or hypertension at 6‐months post‐transplant: those with normal blood pressure (NBP) not requiring medication (NBP group), those on antihypertensive medications (HTN group), and those on medications for hypotension (fludrocortisone and/or midodrine) (Hypotensive group).ResultsA total of 306 recipients were included in the study: 54 (18%) in the NBP group, 215 (70%) in the HTN group, and 37 (12%) in the Hypotensive group. On multivariate analysis, the use of T‐depleting induction (aHR = 9.64, p = .0001, 95% Cl = 3.12–29.75), pre‐transplant use of hypotensive medications (aHR = 4.53, p = .0003, 95% Cl = 1.98–10.38), and longer duration of dialysis (aHR = 1.02, p = .01, 95% Cl = 1.00–1.04) were associated with an increased risk of post‐transplant hypotension. Post‐transplant hypotension was not associated with an increased risk of death‐censored kidney or pancreatic allograft failure, or patient death.ConclusionHypotension was common even 6 months post‐SPK transplantation. With appropriate management, hypotension was not associated with detrimental graft or patient outcomes.

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“…Given the known cause and effect in these situations, CRS is relatively well-understood; why some patients demonstrate such a dramatic effect compared with others remains a mystery. A few case reports have described severe reactions after receiving antithymocyte globulin with varying survival outcomes following resuscitation [3,4]. However, as far as we are aware, there have been no documented cases of such severe multi-organ failure related to CRS following anti-thymocyte globulin for renal transplant that have resulted in a good patient outcome.…”

Section: Discussionmentioning

confidence: 99%

Severe anti‐thymocyte globulin‐induced cytokine release syndrome in a renal transplant patient

Huh¹,

Baines

Talbot

2021

Anaesthesia Reports

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Cytokine release syndrome is a systemic inflammatory response that can be triggered by a variety of factors such as infection or exposure to certain drugs, particularly novel T cell-engaging immunotherapies. Severe cytokine release syndrome as a complication following treatment with anti-thymocyte globulin, although recognised, is not well-reported in the literature. We report the case of a 64-year-old man who developed catastrophic cytokine release syndrome after receiving anti-thymocyte globulin during kidney transplantation. We highlight the importance of prompt recognition of severe cytokine release syndrome with strategies to aid survival in life-threatening cases.

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Antithymocyte globulin-induced refractory hypotension in renal transplantation recipient

Cited by 4 publications

References 5 publications

What Therapeutic Regimen Will Be Optimal for Initial Clinical Trials of Pig Organ Transplantation?

What Therapeutic Regimen Will Be Optimal for Initial Clinical Trials of Pig Organ Transplantation?

Risk factors and outcomes of persistent post‐transplant hypotension among simultaneous pancreas and kidney transplant recipients

Severe anti‐thymocyte globulin‐induced cytokine release syndrome in a renal transplant patient

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