Sticky Platelet Syndrome: An Underrecognized Cause of Graft Dysfunction and Thromboembolic Complications in Renal Transplant Recipients

Abstract

Sticky platelet syndrome (SPS) leads to hyperaggregabilty of platelets in response to physiologic stimuli. In this report we describe three patients with clinical symptoms of SPS after renal transplantation. The first patient developed an infarction of her transplant kidney with additional, subsequent renal microinfarctions. The second patient suffered multiple strokes and deep vein thrombosis with episodes of pulmonary embolism and ischemic bowel disease due to colonic microinfarctions. The third patient experienced a long episode of unexplained respiratory and graft dysfunction immediately after transplantation until therapy for SPS was initiated, at which point symptoms resolved quickly.Kidney transplant recipients with SPS may be at increased risk of developing thrombosis, given that most immunosuppressive drugs are known to induce either endothelial cell damage or augment platelet aggregation. All patients awaiting renal transplantation should be screened for a history of thrombosis and, if appropriate, tested for SPS. Affected patients should receive dose-adjusted acetylsalicylic acid.

Sticky Platelet Syndrome: A Manageable Risk Factor for Posttransplant Thromboembolic Events

“…We read with great interest the article by Mühlfeld et al (1) in which the authors report three patients with clinical symptoms of sticky platelet syndrome (SPS) following kidney transplantation, resulting in graft loss in one case and life-threatening thromboembolic and respiratory complications in the other two cases, respectively. SPS is a disorder of platelet hyperresponsiveness first described at our institution (2).…”

Sticky platelet syndrome as a possible cause for free flap failure—A case report

“…In type I, increased platelet aggregation can be induced by ADP and epinephrine, in type II (which is the most common type) by epinephrine alone and in type III only by ADP. 4 Although the overall clinical picture of 4,5,10,11 It is suspected that patients with SPS have a predisposition for vascular thromboses, but do not necessarily experience the possible consequences of aggregational disorders. Furthermore, it is hypothesized that adrenalin release in vivo may induce platelet aggregation.…”

“…Although these disorders are well-described, disorders of platelet function leading to a predisposition for thrombosis are less well understood. [4][5][6] In our report, we describe the case of a previously asymptomatic patient who suffered from thrombosis after repeated microsurgical free flap transfer. Thromboses were a probable consequence of the sticky platelet syndrome (SPS), a thrombocyte hyperreactivity with accelerated maximum aggregation.…”

Evaluation of Heparin Anticoagulation Protocols in Post–Renal Transplant Recipients (EHAP-PoRT Study)

“…Perioperative stress can induce platelet aggregation, and the use of calcineurin inhibitors (e.g., cyclosporine A or tacrolimus) for immunosuppression may enhance agonistinduced platelet aggregation through modulation of protein phosphorylation. 5 Furthermore, postoperative hypertensive episodes and additional insults to the vascular epithelium by cyclosporine A contribute to thromboembolism and have been hypothesized to trigger thrombosis in patients with previously asymptomatic sticky platelet syndrome. 5 After renal transplant, the incidence of venous thromboembolism (VTE) is 6.2%-18.1% and that of pulmonary embolism is 2%-14%, with renal artery or vein thrombosis contributing to 45% of early renal graft losses.…”

“…5 Furthermore, postoperative hypertensive episodes and additional insults to the vascular epithelium by cyclosporine A contribute to thromboembolism and have been hypothesized to trigger thrombosis in patients with previously asymptomatic sticky platelet syndrome. 5 After renal transplant, the incidence of venous thromboembolism (VTE) is 6.2%-18.1% and that of pulmonary embolism is 2%-14%, with renal artery or vein thrombosis contributing to 45% of early renal graft losses. 6,7 Moreover, the rate of recurrence after a first episode of VTE is much higher among renal transplant recipients than among matched patients without a history of renal disease (50% versus 10%).…”