Kidney transplantation is the preferred treatment for end-stage renal disease, and living donation is increasingly utilized to address organ shortages. Living donor kidney transplantation has several advantages over deceased donor transplantation, including opportunities for donor selection, preoperative preparation, and superior graft function outcomes. Additionally, the quality of the donated kidney can be evaluated, along with the risk of transmitting diseases to the recipient [1]. Absolute contraindications for organ donation include active blood-borne infectious diseases, uncontrolled sepsis, and metastatic or incurable malignancies. Apart from patients with systemic lupus erythematosus, individuals with autoimmune or platelet disorders are generally not prohibited from donation. Immune thrombocytopenia (ITP) is an autoimmune condition characterized by the autoantibody-mediated destruction of platelets. In the context of transplantation, donor lymphocytes from individuals with ITP may produce antiplatelet antibodies, potentially leading to transplant-mediated autoimmune thrombocytopenia (TMAT) [2]. TMAT has primarily been identified in cases of liver transplantation [3,4]. The UK Transplant Registry examined the outcomes of patients who received organs from deceased donors with ITP and found that none of the kidney recipients developed ITP or TMAT during the early posttransplantation period [5]. However, the literature includes no reports of live kidney donations from individuals with ITP, and detailed preventive strategies based on epidemiological studies are scarce.

The risks of disease transmission and TMAT in recipients of organs from donors with ITP are not well understood. Furthermore, no safety guidelines have yet been established for the use of organs from these donors [1,2,5]. Although the autoimmune disease activity and graft quality cannot be controlled with deceased donors, an opportunity exists to optimize platelet levels and manage ITP before living organ donation. We report the first documented case of living kidney transplantation from a donor with ITP. Immunoglobulin was administered prior to surgery, and perioperative platelet function was monitored for donor safety. Additionally, serial platelet counts of the recipient were measured after transplantation to exclude the possibility of TMAT. The graft outcome was satisfactory.

This case report was approved by the Research Ethics Committee at Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation (IRB no. CR112-13), and informed consent was obtained from the patient.

The recipient was a 55-year-old Asian man with hypertension and end-stage renal disease, who had been undergoing hemodialysis for 6 months. The donor, his wife, was a 55-year-old Asian woman. She had been diagnosed with ITP during pregnancy 23 years earlier, when her platelet count was 20×10⁹/L. Her condition responded poorly to corticosteroid therapy, and she ultimately delivered the child via cesarean birth with the support of platelet transfusion. Following delivery, she underwent no further treatment for ITP, and she experienced no serious bleeding episodes in the subsequent years. Her platelet count was similar, at 21×10⁹/L, when she was evaluated for kidney donation to her husband. The woman demonstrated high motivation to donate. The donor and recipient blood types were compatible, and human leukocyte antigen typing revealed a 1A2B2DR mismatch. In preparation for surgery, the donor received four doses of intravenous immunoglobulins at a dosage of 0.5 mg/kg/day. Consequently, her platelet count increased to 99×10⁹/L prior to the procedure.

A laparoscopic left donor nephrectomy and concurrent splenectomy were performed. Baseline rotational thromboelastometry (ROTEM) assays were conducted after anesthesia to ensure adequate platelet function before initiating surgery. Upon entering the peritoneal cavity, we observed that the spleen was of normal size, and we then explored the splenic artery through an anterior approach. Initially, this artery was clipped at the suprapancreatic level to optimize the platelet level. The blood platelet counts were 91×10⁹/L, 85×10⁹/L, and 82×10⁹/L at 15, 30, and 60 minutes after splenic artery ligation, respectively. Subsequently, the left kidney was harvested uneventfully and preserved in histidine–tryptophan–ketoglutarate (HTK) solution. No bleeding episode occurred, and intraoperative platelet transfusion was not necessary. Following splenectomy, the second and final ROTEM tests were performed 1 hour after ligation of the splenic artery and 72 hours after splenectomy to assess clot elasticity (Table 1). The donor recovered uneventfully and was discharged on postoperative day 2 without perioperative complications. Her platelet count had increased to 110×10⁹/L on the first postoperative day and rose further to 325×10⁹/L by day 13. These platelet counts remained within the normal range during the 9-month follow-up period.

Table 1. ROTEM assays (i.e., INTEM and FIBTEM) at various time periods

ROTEM assay	Time
	Baseline	1 hr	72 hr	Reference
INTEM
Clotting time (sec)	308	223	262	100–240
Alpha (°)	65	71	75	70–83
A5 (mm)	37	41	53	38–57
MCF (mm)	59	60	70	50–72
MCE	146	151	236	-
FIBTEM
A5 (mm)	11	14	28	4–17
MCF (mm)	14	20	29	9–25
MCE	16	24	40	-
Change in MCE	130	127	196	-

Clotting time, measured in seconds, is defined as the duration from the onset of the test until an amplitude of 2 mm is reached. This metric assesses the effectiveness of the coagulation cascade in the formation of fibrin. A(x) represents the amplitude of clot firmness at x minutes after initiation. Maximal clot firmness (MCF) indicates the strength and quality of the clot, primarily determined by the interaction between fibrinogen and platelets. INTEM assays were employed to assess the intrinsic coagulation pathways, while FIBTEM assays were used to eliminate platelet activity, thereby isolating the contribution of fibrinogen to clot formation. Maximal clot elasticity (MCE) is derived from MCF using the following equation: MCE = (100×MCF)/(100 − MCF). The change in MCE, denoted as change in MCE, is used to quantify the contribution of platelets to clot elasticity.

ROTEM, rotational thromboelastometry; INTEM, intrinsic thromboelastometry; FIBTEM, fibrin-based thromboelastometry.

The recipient received induction therapy with basiliximab. Prior to transplantation, the patient’s platelet count was 190×10⁹/L. The kidney graft was perfused with HTK solution until it was clear on the back table. Vascular anastomosis and ureteral reimplantation were performed smoothly, with immediate urine production observed. A triple immunosuppression regimen of tacrolimus, mycophenolate mofetil, and methylprednisolone was employed. Throughout the early postoperative period, the recipient’s platelet counts remained within the normal range, as shown in Fig. 1. His renal function recovered uneventfully without delayed graft function, perioperative bleeding complications, or TMAT. The patient was discharged on postoperative day 6 and continued to recover well through the 9-month follow-up.

Figure 1. Serial platelet counts of the recipient following kidney transplantation. The recipient’s serial platelet counts were monitored daily following transplantation to promptly identify any potential for transplant-mediated autoimmune thrombocytopenia. Throughout the early postoperative period, the platelet counts remained within the normal range. OP, operation; POD, postoperative day.

ITP occurs at a rate of 2.2–5.3 cases per 100,000 person-years among Asians [6]. Corticosteroids are the cornerstone of ITP therapy, with an approximate response rate of 75%; gamma-globulin provides a transient effect, while thrombopoietin receptor agonists often produce durable responses in cases that are refractory to steroids. Splenectomy is the definitive treatment for refractory ITP, demonstrating an efficacy of 50%–65% [2]. The variation in bleeding tendency and response to treatment suggests that the immunological mechanisms underlying ITP are heterogeneous [7]. It is plausible that ITP can lead to autoantibody-mediated platelet destruction of varying activity and severity. Previously reported cases of TMAT originated from ITP donors who died of intracranial hemorrhage, with most instances refractory to splenectomy, indicating a relatively severe bleeding phenotype. In contrast, our donor had asymptomatic ITP and demonstrated an adequate response to intensified treatment prior to donation. After consideration of the surgical risks, prophylactic splenectomy was scheduled to occur concurrently with laparoscopic surgery, with the aim of controlling thrombocytopenia and preventing future bleeding events.

With ITP, the primary concerns associated with splenectomy and subsequent procedures are perioperative hemorrhage and achieving effective hemostasis, rather than enlarged spleen. Hematologic intensification of treatment is warranted to increase the platelet count above 50×10⁹/L; if this threshold is not reached, preoperative or intraoperative platelet transfusion becomes necessary. Additionally, early ligation of the splenic artery by the surgeon is crucial to halt platelet destruction within the spleen [8]. In this context, we monitored serial platelet counts and performed ROTEM assays to assess and ensure proper clot function during the procedure and in the immediate postoperative period. ROTEM is a viscoelastic test for hemostasis that graphically depicts the kinetic changes in a whole blood sample, from the onset of clot activation and polymerization to clot firmness and lysis. Clotting time represents the efficiency of the coagulation cascade in the formation of fibrin. Maximal clot firmness (MCF) is used to measure the strength and quality of the clot through the interaction of fibrinogen and platelets. Maximal clot elasticity (MCE) is a parameter derived from MCF, and change in MCE indicates the contribution of platelets to clot elasticity [9]. In the present case, serial MCE results for the donor revealed that the immediate impact of platelets on clot strength remained stable following splenic artery ligation and considerably improved after 72 hours. The platelet count was then normalized. Despite these promising results, long-term follow-up is necessary to verify the benefits of concurrent splenectomy.

Donor-derived thrombocytopenia following solid organ transplantation from donors with ITP has been previously reported. Diaz et al. [2] described a severe case of TMAT after liver and kidney transplantation, which ultimately resulted in allograft failure due to a massive subcapsular hematoma. The recipient, who was resistant to medical therapy and splenectomy, ultimately survived thrombocytopenia following emergent liver retransplantation. In a retrospective analysis of the UK Transplant Registry, none of the 31 recipients of kidneys from donors with ITP developed ITP or TMAT in the early posttransplantation period. However, within the same cohort, one liver transplant recipient experienced TMAT and died of pulmonary hemorrhage. The transmission of lymphocytes specifically within the liver graft may explain the absence of TMAT after kidney or heart transplantation [10]. Clinically significant TMAT is uncommon but potentially fatal, and both its natural history and optimal treatment remain poorly understood. TMAT is expected to resolve with the elimination of donor leukocytes; until then, however, recipients face a substantial bleeding risk. Friend et al. [11] suggested that the liver represents a primary source of retained lymphocytes and a site of platelet destruction in patients with postsplenectomy ITP. Consequently, using allografts for liver transplantation from this donor group, particularly in cases refractory to splenectomy, is contraindicated [11]. Utilizing donors with ITP who have a normal platelet count at the time of donation—whether due to medical or surgical treatment and regardless of being living or deceased—may pose minimal risk, as shown by Takatsuki et al. [4]. However, a normalized platelet count does not guarantee the absence of autoreactive lymphocytes or autoantibodies. Therefore, careful selection of donors with ITP is advised, and the early detection and management of TMAT can lead to favorable outcomes for recipients [12].

No evidence suggests that using the kidneys, pancreas, or heart of a deceased donor with ITP is unsafe; thus, discarding these organs is unwarranted. However, in the context of living donor transplantation, the safety of the donor and the benefits to the recipient are paramount. To our knowledge, this report describes the first case of a living kidney donor with ITP. Prior to transplantation, we prepared for potential complications and explained them to the patients. The surgical outcomes were satisfactory. However, the primary limitation of our study is the absence of long-term follow-up data. We propose that kidney transplantation from a donor with ITP who has responded well to medical or surgical treatment is safe and should not be considered a contraindication for donation.

Conflict of Interest

No potential conflict of interest relevant to this article was reported.

Author Contributions

Conceptualization: CCH, YCC. Data curation: HHY. Formal analysis: HHY, CLL, YFW. Writing–original draft: HHY, YCC. Writing–review & editing: all authors. All authors read and approved the final manuscript.

Acknowledgments

The authors would like to thank our organ transplant coordinators, Mrs. Ming-Hui Shih and Kuei-Chun Chou, for their nursing profession, love and patience in caring the transplant patients.