{"paper_id":"514b5133-98b5-49bf-81c7-0ab592430204","body_text":"TRANSPLANTATION CASE REPORTS  \n  \n \nAvailable online at www.sciencerepository.org  \n \nScience Repository \n \n \n \n \n \n*Correspondence to: Nizar Attallah, M.D., Department of Nephrology, Medical Subspecialties Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE;  Tel: \n9715019999; E-mail: attalln@clevelandclinicabudhabi.ae \n© 2020 Nizar Attallah. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, \ndistribution, and reproduction in any medium, provided the original author and source are credited.  Hosting by Science Repository. \nhttp://dx.doi.org/10.31487/j.TCR.2020.01.07 \nCase Report \nEndometriosis in a Renal Transplant Recipient  \nRakesh Madhyastha, Ammar Abdulbaki, Sudeendra Gupta and Nizar Attallah * \nDepartment of Nephrology, Medical Subspecialties Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, UAE \nA R T I C L E  I N F O \nArticle history: \nReceived: 23 April, 2020 \nAccepted: 6 May, 2020 \nPublished: 13 May, 2020 \nKeywords:  \nKidney transplantation \nendometriosis \nimmunosuppression \n \n A B S T R A C T \nHormonal abnormalities that are associated with advanced kidney failure normally reverses after kidney \ntransplantation. This usually helps to normalize menstrual cycles for female patients and helps improve \nfertility. Post-transplant gynaecological disorders are under -reported in general. We present a p atient who \ndeveloped endometriosis after second kidney transplant. She was treated with surgery followed by hormonal \ntherapy. We discuss the pathophysiology of endometriosis and possible relation to the immune system.  \n \n \n \n \n                                                                                  © 2020 Nizar Attallah. Hosting by Science Repository .  \nBackground \n \nOrgan transplantation is now a universally accepted treatment for organ \nfailure. Kidney Transplantation improves end -stage renal disease \npatients’ survival and quality of life in comparison with dialysis. \nHypothalamic pituitary axis  normalizes post-transplant. Some of the \nwell-known gynaecological complications post-transplant are prolonged \nand profuse menstruation and inter -menstrual bleeding or spotting. \nReports also suggest a higher rate of endometrial hyperplasia (without \natypia) in renal allograft reci pients [1 , 2 ]. After successful renal \ntransplantation, cyclical ovarian function and fertility are often restored. \n \nCase History \n \nWe present a case of a 33-year-old unmarried female who underwent a \nsecond living unrelated kidney transplant In September 201 7 with \nimmediate graft function and uneventful post -operative recovery. Her \nfirst transplant was a combined deceased donor kidney and heart \ntransplant that was done in December 2014 and complicated with loss of \nrenal allograft from antibody -mediated rejection leading to return to \ndialysis in May 2017 while the heart transplant continued to function \nwell. Her original heart disease was idiopathic Myocarditis while her \noriginal kidney disease was thought to be focal segmental \nglomerulosclerosis (FSGS) that got worse with worsening heart failure. \nShe was treated aggressively for the antibody -mediated rejection, but \ndespite that allograft dysfunction and proteinuria continued to progress. \nFollowing her second kidney transplant, she was placed on a triple \nimmunosuppressive regimen of Tacrolimus, Mycophenolate mofetil, \nand Prednisolone. Serum creatinine settled at 60 -80 micromole/L and \nproteinuria disappeared. \n \nIn February 2018 she presented to the clinic with right lower quadrant \npain started in December 2017, waxing, and waning in character and \ngradually worsening to the point where she was unable to sit, stand, or \nsleep without having pelvic fullness and pain as well as bloating. Her \nmenstrual cycles were regular till early January 2018 when she started \nto have bleeding twice a month. \n \nOn further questioning, she admitted to having always had painful \nperiods. No family members with known endometriosis. She denied any \nfamily history of ovarian, colorectal or breast malignancy. MRI scan was \ndone and revealed a right 13 cm complex, septated, hemorrhagic debris-\nfilled ovarian cyst (Figure s 1A & 1B). The patient was taken up for \nsurgical removal of the cyst and argon laser coagulation of endometrial \nimplants. Intra -operative findings revealed grade 3 endometriosis \ninvolving bilateral fallopian tubes and uterus had dense posterior \nadhesions to the re ctum and right pelvic sidewall and had anterior \nadhesions to bladder highly suggestive of endometriosis. The patient has \nnormal postoperative renal recovery with no evidence of acute kidney \n\nEndometriosis in a Renal Transplant Recipient                2 \n \nTransplant Case Rep  doi:10.31487/j.TCR.2020.01.07       Volume 1(1): 2-3 \nA \nB \ninjury. Post -surgery, the patient was maintained on Medoxy -\nprogesterone acetate every 3 months. She is currently asymptomatic with \nstable kidney function and no proteinuria. \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \n \nFigure 1: MRI pelvis with contrast in A) axial view and B) sagittal view \nshowing large midline pelvis mass reported to be arising from the right \novary containing multiple septations which does not enhance clearly. It \ncontains T2 dark and T1 bright non -enhancing debris. The mass is \ndiffusely T1 bright, contains dependent debris which is more T1 bright \nthan the remainder of the mass. \n \nDiscussion \n \nEndometriosis is an estrogen -dependent inflammatory disease, which \naffects 6%–10% of women of reproductive age [3 -5]. This disease is \ndefined as the presence of endometrial glandular and stromal tissues in \nsites outside the uterine cavity, primarily on ovaries and the pelvic \nperitoneum [6]. The Association of CKD with endometriosis is not well \nstudied. A few case reports of obstructive uropathy showed an \nassociation with endometriosis [7 -10]. A retrospective analysis on \n27,973 patients revealed endometriosis to be inversely proportional to \nCKD (crude HR 0.65, 95% CI 0.53–0.81, p < 0.001) [11]. However, in \nanother similar study designed to determine the prevalence o f organic \ncauses of abnormal uterine bleeding in this group of patients exposed to \nunopposed estrogen, only 2 of 8 patients (25%) with chronic renal failure \nhad endometrial lesions while 44 of 131 patients (33.6%) had either \nendometrial polyp, simple or at ypical endometrial hyperplasia or \nendometrial carcinoma (p > 0.05) [12]. \n \nPatients with secretory and atrophic endometrium were excluded from \nthis study. Uremia in CKD may have no role to play in endometrial \nresponsiveness to estrogen. Despite the substant ial effect that \nendometriosis has on women, their families and the economy, public and \nprofessional awareness of the disorder remains poor [13]. The true \nprevalence of endometriosis is uncertain, however, because the \ndefinitive diagnosis requires surgical visualization. The prevalence \nranges from 2 to 11% among asymptomatic women, 5 to 50% among \ninfertile women, and 5 to 21% among women hospitalized for pelvic \npain. \n \nEndometriotic cells and tissue elicit a localized immune and \ninflammatory response with the production of cytokines, chemokines, \nand prostaglandins. The dysfunction of the innate and adaptive immune \nsystem is evident but it is unclear whether immune dysfunction initiates \nendometriosis or is a pathophysiological hallmark of the disorder [14]. \nHowever, in general, it seems there is a local and sterile inflammation \nthat occurs in the peritoneal cavity and there is substantial evidence that \nimmunological factors and angiogenesis play a decisive role in the \npathogenesis of the disease. Peritoneal macrophages also play a pivotal \nrole in the intraabdominal environment [15]. Theoretically, \nimmunosuppressive therapy would halt those processes and that is why \nprobably it is uncommon to see patients with endometriosis after \ntransplantation. Other mechanisms contribute to the development of \nendometriosis. That is probably why it happened in this \nimmunocompromised patient. On the other hand, in our literature search, \nwe found only animal studies done on the effects of immunosuppression \non development and progression of endometriosis and this was done on \nbaboons and the result was largely inconclusive [16, 17]. \n \nConclusion \n \nIn this case report, we bring forward the importance of gynaecological \ncomplications following renal transplant which arises due to normalizing \nhormonal balance after transplant. Gynaecological complications \nfollowing transplant are under-reported. Our case report is unique in this \naspect as this is the first case of post-transplant endometriosis ever to be \nreported thus far. Theoretically, the  prevalence of endometriosis must \nhave been mitigated in a transplant patient however this case report \nshows that more studies need to be done in this front.  \n \nConsent \n \nInformed consent was obtained from the patient prior to writing this \nreport. \n \nConflicts of Interest \n \nNone. \n \nREFERENCES \n \n1. Kaminski P, Bobrowska K, Pietrzak B, Bablok L, Wielgos M (2008) \nGynecological issues after organ transplantation. Neuro Endocrinol \nLett 29: 852-856. [Crossref] \n2. Ruth Cochrane, Lesley Regan (1997) Undetected gynaecological \ndisorders in women with renal disease. Human Reproduction  12: 667-\n670. \n\nEndometriosis in a Renal Transplant Recipient                3 \n \nTransplant Case Rep  doi:10.31487/j.TCR.2020.01.07       Volume 1(1): 3-3 \n3. Lee WL, Chang WH, Wang KC, Guo CY, Chou YJ et al. 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(1995) The effects of immunosuppression on development and \nprogression of endometriosis in baboons (Papio anubis). Fertil Steril \n64: 172-178. [Crossref]","source_license":"CC0","license_restricted":false}