Refractory Thrombocytopenia Associated to Disseminated Histoplasmosis in a Living-Related Renal Transplant Recipient: A Case Report and Review of the Literature

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Austin J Clin Case Rep. 2021; 8(6): 1218.

Refractory Thrombocytopenia Associated to Disseminated Histoplasmosis in a Living-Related Renal Transplant Recipient: A Case Report and Review of the Literature

Rosario MD1, Alfredo G-G1, De Jesus AOA2 and Jorge AS1,2*

¹Department of Nephrology and Organ Transplant Unit, Specialties Hospital, National Western Medical Centre, Mexican Institute of Social Security, Mexico

²Department of Physiology, University Health Sciences Center, University of Guadalajara, Guadalajara, Jalisco, Mexico

*Corresponding author: Andrade Sierra Jorge, Department of Physiology, University Health Sciences Center, University of Guadalajara, Guadalajara, Jalisco, Mexico

Received: January 20, 2021; Accepted: June 01, 2021; Published: June 08, 2021


Opportunistic infections are frequent complications after renal transplantation because of the use of immunosuppressants. Disseminated Histoplasmosis (DH) is one such opportunistic infection, and its clinical presentation varies, which makes its diagnosis a challenge. There is no information regarding DH as a cause of refractory thrombocytopenia in renal transplant recipient (RTR); therefore, we consider this an atypical case, and, because of its clinical characteristics, we have classified it as an Immune Thrombocytopenic Purpura (ITP) induced by histoplasmosis. This is the first case reported in our milieu, and it opens up the possibility for use of intravenous immunoglobulin as a strategic therapy for thrombocytopenia induced by HP in immunosuppressed RTRs.

Keywords: Histoplasmosis; Thrombocytopenia; Renal transplant


Histoplasmosis (HP) is a systemic fungal infection, and the spectrum of the illness varies from asymptomatic primary infection to Disseminated Histoplasmosis (DH) in immunocompromised patients. Approximately 10% of infected patients can develop DH,and more so in states of sub-immunosuppression (organ transplant and/ or hematologic malignancies) [1]. Histoplasmosis after Solid Organ Transplantation (SOT) is not frequent, even in patients who live in endemic areas. The incidence of DH in SOT is less than 1% [2] and can compromise the Medulla Ossium (MO) in up to one third of cases, with anemia and leukopenia as the most common alterations [3]. Thrombocytopenia is also reported in DH [4,5]; however, refractory cases have only been documented in immunocompetent patients [6], and there is no existing information on the immunocompromised. Recuperation of the depletion of cell lines occurs in a few weeks and is associated with the response to antifungal treatment [7,8]. The persistence of thrombocytopenia despite medical treatment is not common, and little information exists in immunocompromised patients. We present the first case in Mexico of DH in a renal transplant recipient (RTR) with a case of refractory thrombocytopenia.

Past Medical History

This is the case of a single, 30year-old, male resident of Guadalajara, Jalisco, Mexico, with a history of chronic kidney disease of unknown etiology, treated with hemodialysis for two years, and a RTR from a living-related donor (08/11/2019); with blood group compatibility, a haplotype of HLA, and cross-matched negative by flow cytometry. The serologic status for Cytomegalovirus (CMV) was Donor IgG+/ Receptor IgG+. The patient refused transfusions of hemoderivatives pre- and post-transplant. Induction immunosuppression was based inbasiliximab 20 mgs (days 0 and 4 post-transplant), Tacrolimus (TAC) dose of 0.12 mg/kg/day, Mycophenolate Mofetil (MMF) with a dose of 2g, and methylprednisolone of 500mgs. Maintenance immunosuppression was with TAC: dose of 4mg/day, MMF: dose of 2g/day, and Prednisone (PDN): dose of 5mg/day. The antibacterial prophylaxis was comprised of trimethoprim/sulfamethoxazole 400/80 mg/day for 6 months, and antiviral prophylaxis was not used. Serum Creatinine (SCr) at post-transplant discharge was 1.3 mg/dL, without any clinical events of acute rejection; and, biopsies of the renal graft were not done in follow-up. The patient’s history of a CMV infection three months prior was treated with Valgancyclovir (VGC) 900 mg two times daily for 21 days followed by 450 mg every 12 hours without suspension; and a polymerase chain reaction (PCR)for CMV <150 copies/mL was performed at 2 months of treatment.

Diagnosis and Clinical Course of the Present Disease

History of fever for four weeks with no response to antipyretics, for which the patient required hospitalization by his treating physician. Upon hospitalization (18/05/2020), the patient presented with hyporexia, nausea, diarrhea, and a fever of 39.5°C. Physical examination showed an arterial pressure of130/80, normal oropharynx, no lymphadenopathies, no apparent respiratory and/or cardiovascular alterations, and no clinical presence of visceromegalies. Acute failure of the renal graft was documented with SCr 3.14 mg/dL and supra-optimal levels of TAC 17.6 ng/mL (Table 1). The patient received intensive hydration with crystalloid solutions and empirical antimicrobial management with levofloxacin, as well as modification of the immunosuppressionregimen (MMF 500 mg/day and TAC 2 mg/day).Throughout follow-up, the ultrasound of the renal graft did not show any structural alterations, and the resistance indices were normal. Transthoracic echocardiogram was without vegetations, and the Left Ventricle Ejection Fraction (LVEF) was 65%, without alterations in the segmental mobility. In the thoracic, abdominal, and pelvic tomography there were multiple inflamed lymph nodes of 12mm in the mediastinum and 6mm para-aortic and aortocaval nodes.