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Year : 2020  |  Volume : 14  |  Issue : 2  |  Page : 170-171

Knee swelling in a renal transplant recipient

1 Department of Nephrology, PGIMER, Chandigarh, India
2 Department of Cytology and Gynecological Pathology, PGIMER, Chandigarh, India
3 Department of Radiodiagnosis, PGIMER, Chandigarh, India

Date of Submission11-Mar-2020
Date of Acceptance07-May-2020
Date of Web Publication06-Jul-2020

Correspondence Address:
Dr. Jasmine Sethi
Department of Nephrology, PGIMER, Chandigarh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijot.ijot_19_20

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Histoplasma knee infection in a renal transplant recipient has not been reported in the literature. The present case illustrates an interesting case of unilateral Histoplasma monoarthritis in a patient 3 years after renal transplantation who presented with pain and swelling of the right knee. The diagnosis was established by tissue aspiration from a focal lesion in lateral femur condyle. The patient was successfully managed with amphotericin followed by itraconazole with complete resolution of the symptoms. It is important to consider such rare differentials in an immunocompromised patient to avoid delays in treatment.

Keywords: Histoplasmosis, intracellular yeasts, renal transplantation

How to cite this article:
Sethi J, Divyaveer SS, Gupta N, Prakash M, Kohli HS. Knee swelling in a renal transplant recipient. Indian J Transplant 2020;14:170-1

How to cite this URL:
Sethi J, Divyaveer SS, Gupta N, Prakash M, Kohli HS. Knee swelling in a renal transplant recipient. Indian J Transplant [serial online] 2020 [cited 2021 Jun 21];14:170-1. Available from: https://www.ijtonline.in/text.asp?2020/14/2/170/289036

  Introduction Top

Invasive fungal infections including progressive disseminated histoplasmosis (PDH), are uncommon in renal transplant recipients. We report an unusual initial presentation of PDH presenting as acute monoarticular arthritis in a renal transplant recipient. This report highlights the point that H. Capsulatum may present as focal lesions and a high level of suspicion is needed to make the diagnosis, especially in posttransplant recipients.

  Case Report Top

A 40-year-old male was admitted with severe pain of the right knee for the past 1 week. Examination revealed marked tenderness over the right knee joint with redness and swelling. He underwent renal transplant 3 years back with wife as a donor and basic disease being autosomal dominant polycystic kidney disease. The immunosuppression consisted of cyclosporine 75 mg twice daily, mycophenolate mofetil 1000 mg twice daily, and prednisolone 5 mg daily, without induction therapy. The patient had acute rejection 2 years posttransplant that was treated with intravenous pulses of steroid and his baseline creatinine before admission was 2 mg/dl. Present admission, laboratory examinations showed normal total leukocyte count, hemoglobin of 7 g/dl, uric acid 7.8 mg/dl, and serum creatinine 6 mg/dl. Cyclosporine trough level was 69 ng/ml, graft Doppler was normal, urine culture, and blood cultures were sterile. Serum cytomegalovirus was negative by a polymerase chain reaction and the tuberculin skin test was negative. Echocardiography was unremarkable, computed tomography (CT) of the chest revealed centrilobular nodules and ground-glass opacities in the right upper lung. The right knee arthrocentesis revealed clear fluid with 40 cells (75% lymphocytes) and no crystals were seen. Gram stain, fungal, and tubercular cultures failed to reveal any infectious organism. Magnetic resonance imaging of the right knee showed a focal lesion in the metaphysis of the lateral condyle of the femur along with effusion [Figure 1]a and [Figure 1]b. Fine-needle aspiration cytology from the lesion showed foamy macrophages containing periodic acid Schiff positive intracellular organisms suggestive of Histoplasmosis and culture grew Histoplasma capsulatum [Figure 2]. A diagnosis of disseminated Histoplasmosis involving lungs and right knee joint was considered and the patient was started on Liposomal amphotericin (250 mg/day) and mycophenolate mofetil was stopped indefinitely. Prednisolone dose was increased to 7.5 mg daily and cyclosporine dose was unchanged. Clinically, pain and swelling subsided and serum creatinine decreased to 3.5 mg/dl. The patient did not give consent for renal biopsy. After 2 weeks, amphotericin was switched to oral itraconazole (200 mg twice daily). The plan is to continue lifelong suppressive therapy with itraconazole with dual immunosuppression (cyclosporine and prednisolone) and repeat knee MR imaging after 3 months.
Figure 1: Magnetic resonance imaging of the knee. T2-weighted coronal (a) and axial (b) images showing a well defined focal lesion in the metaphysis of lateral condyle of the femur with focal cortical breach and inflammation of adjacent soft tissue

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Figure 2: Microphotograph showing foamy macrophages having intracellular organisms which show periodic acid Schiff positivity (PASs stain, ×40)

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  Discussion Top

Incidence of clinical histoplasmosis in solid organ transplant recipients is <0.5%.[1] We report the first case of knee Histoplasmosis likely secondary to pulmonary infection in a transplant recipient. Once the diagnosis of Histoplasmosis in any site has been established, the disseminated disease should be ruled out by doing a CT of the chest and abdomen. PDH is a disease where Histoplasma capsulatum affects multiple organs due to the inability of host cellular immunity to control the infection. It may present as a rapidly progressing illness, characterized by a high persistent fever, hepatosplenomegaly, pancytopenia, and interstitial pneumonia or may follow a subacute/chronic course, being associated with destructive focal lesions, with milder constitutional symptoms.[2]

The diagnosis of PDH can be made based on the culture of blood, bone marrow, or any other infected tissue. However, it is limited by the slow growth of the fungus, requiring more than 3 weeks to grow. Histopathology results from a tissue biopsy of the bone marrow, liver, skin, synovial and mucocutaneous lesions are useful.[3] The diagnosis of Histoplasmosis can be made by the presence of distinctive 2–4 μm, oval, narrow-based budding yeast. Histoplasmosis antigen assays in the serum and urine are sensitive assays for the diagnosis for disseminated disease and allow a rapid diagnosis.[4] For the treatment of mild-to-moderate disease, oral itraconazole 200 mg twice a day is recommended. For severe disease, treatment with amphotericin B (deoxycholate formulation 0.7–1.0 mg/kg daily; lipid formulation 3.0–5.0 mg/kg/daily) for 2 weeks followed by oral itraconazole 200 mg twice a day is recommended. The standard duration for treatment is at least 12 months. (2) However, lifelong suppressive therapy can be considered in transplant recipients to prevent relapse. This case illustrates the importance of considering infections with unusual organisms in immunocompromised hosts.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Cuellar-Rodriguez J, Avery RK, Lard M, Budev M, Gordon SM, Shrestha NK, et al. Histoplasmosis in solid organ transplant recipients: 10 years of experience at a large transplant center in an endemic area. Clin Infect Dis 2009;49:710-6.  Back to cited text no. 1
Wheat LJ, Freifeld AG, Kleiman MB, Baddley JW, McKinsey DS, Loyd JE, et al. Clinical practice guidelines for the management of patients with histoplasmosis: 2007 update by the Infectious Diseases Society of America. Clin Infect Dis 2007;45:807-25.  Back to cited text no. 2
Kauffman CA. Histoplasmosis: A clinical and laboratory update. Clin Microbiol Rev 2007;20:115-32.  Back to cited text no. 3
Wheat LJ. Current diagnosis of histoplasmosis. Trends Microbiol 2003;11:488-94.  Back to cited text no. 4


  [Figure 1], [Figure 2]


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