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| Year : 2009 | Volume
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| Issue : 4 | Page : 643-645 |
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| Is pulmonary histoplasmosis a risk factor for acute renal failure in renal transplant recipients? |
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Vahid Pourfarziani1, Saeed Taheri2
1 Dr. Taheri Medical Research Group and Baqiyatallah University of Medical Sciences, Tehran, Iran
2 Dr. Taheri Medical Research Group, Iran
Click here for correspondence address and email
| Date of Web Publication | 8-Jul-2009 |
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 Abstract | | |
Prolonged use of immunosuppressive medication is associated with an increased susceptibility to viral, bacterial and fungal infections. This paper reports a 42 year old kidney transplant recipient with 10 years of stable allograft function who developed pulmonary histoplasmosis and consequently lost his kidney. This report corroborates the previously proposed threat of infection with H. capsulatum for kidney allograft rejection.
How to cite this article:
Pourfarziani V, Taheri S. Is pulmonary histoplasmosis a risk factor for acute renal failure in renal transplant recipients?. Saudi J Kidney Dis Transpl 2009;20:643-5 |
How to cite this URL:
Pourfarziani V, Taheri S. Is pulmonary histoplasmosis a risk factor for acute renal failure in renal transplant recipients?. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2022 Jan 18];20:643-5. Available from: https://www.sjkdt.org/text.asp?2009/20/4/643/53256 |
| Introduction | |  |
Prolonged use of immunosuppressive medication is associated with an increased susceptibility to viral, bacterial and fungal infections, which are the second most important cause of death in long term follow up studies of renal transplant recipients. [1] Although, clinical cases of histoplasmosis have been reported from many parts of the world, most notably some parts of the United States and to a lesser extent from central and South America, [2] the infection is considered as an extremely rare problem in Iran. In fact so far there is just one case report of clinical histoplasmosis in Iran. [3]
We report a case of renal transplant recipient presented 10 years later with acute renal failure and a severe infection by Histoplasma capsulatum.
| Case Report | | |
In June 1993, a 32 year old man received a kidney transplant from a living unrelated donor at our Kidney Transplantation department. His end-stage renal disease (ESRD) was due to chronic pyelonephritis.
He was admitted with symptoms of coryza, arthralgia, prolonged fever and impaired allograft function in September 2003, 10 years after transplantation. At that time, his drug regimen was based on a triple immunosuppressive therapy with cyclosporine, prednisolone and azathioprine.
On physical examination, blood pressure was 125/75 mmHg, temperature 38.1°C and pulse rate 88 beats/min and rest of the examination was unremarkable. The renal allograft palpable in right lower quadrant of abdomen was neither enlarged nor tender.
His laboratory results included erythrocyte sedimentation rate: 46 mm/h, hemoglobin: 7.5 g/dL, white blood cells 4300/µL, platelets: 116000/mm 3 , and serum creatinine: 7.6 mg/dL. Liver function tests were normal.
After admission, azathioprine and cyclosporine were discontinued and broad spectrum antibiotics, ganciclovir and stress dose of glucocorticoid were initiated. Chest X-ray revealed mild haziness in the left lower lobe of his lung.
Stool examination was negative for cysts, ova and parasites; repeated cultures of blood and urine were negative as were serologic tests for Hepatitis B and C, Epstein-Barr (EBV) and HIV. Cytomegalovirus antigen and IgM-antibody were not detected, however CMV IgG was positive. Results of PPD test and smear of sputum for acid fast bacilli were negative On the third day of admission, anticoagulant therapy for suspected pulmonary embolism was initiated and a perfusion lung scan later was of low probability for pulmonary thromboembolism.
On 4 th day he was admitted to the intensive care unit and mechanical ventilation for respiratory support was started. Broad spectrum antibiotics were along with heparin and hemodialysis was initiated via temporary catheter.
Chest X ray on 7 th day now revealed a cavity in the left lung consolidation. A thoracic spiral CT scan also confirmed a cavitary lesion in the position.
The patient underwent bronchoscopy. BronchoAlveolar Lavage (BAL) showed many mononuclear infiltrations, extra- and intra-cellular budding shape particles that were suggestive for histoplasma capsulatum infection. Amphotericin B was promptly initiated and his general condition improved over next several days. Cultures bronchial washings later grew H. capsulatum four weeks later.
Immediately after BAL evaluation, He was extubated successfully and transferred to transplant ward. His renal function never improved and required permanent hemodialysis.
| Discussion | | |
Histoplasmosis is an insidious disease, therefore, recognized clinical illness is far less common. Despite the occurrence of fungemia during the primary infection, acute pulmonary histoplasmosis is a mild, nonspecific, self-limited and rarely diagnosed infection and often needs no treatment. [4] In immuno compromised patients however, the infection can be fatal. It is speculated that in endemic areas, Histoplasma capsulatum is the most frequently encountered pathogen in organ recipients. [5] Iran is thought to be a non-endemic region for the fungi and apart from this paper, there is just one previous report of a clinical illness of H. capsulatum from Iran. [3] Our patient had never travelled to an endemic area for histoplasmosis and his only known predisposing factor was immuno suppression.
Immunological activation resulting in hypersensitivity or acute rejection by H. Capsulatum has been proposed. [6] ,[7] H. capsulatum was thought to be responsible for resurgence of a well controlled dermatomyositis in a 54 year-old man; [6] and in the other report, the infection was recognized as the cause of renal failure in a 49 year old kidney recipient after 6.5 years of stable allograft function. [7]
We did not perform renal allograft biopsy to confirm acute rejection and therefore the allograft loss in our case due to immunological mechanism is speculative. It is also important to notice that the H. Capsulatum infection was only present as consolidation initially when patient was relatively stable and had advanced renal dysfunction. We did not even document any noncompliance issues and repeated cultures were negative before the final diagnosis by BAL. In conclusion, H. Capsulatum infection may still be seen in non endemic areas and possibility of loss of stable allograft due to immunological mechanism needs further evaluation.
| Acknowledgement | | |
This article is supported by a grant from Dr. Taheri Medical Research Group.[Figure 1]
| References | | |
| 1. | Sweny P, Burroughs AK. Infections in solid organ transplantation. Curr Opin Infect Dis 1994;7:436-43.  |
| 2. | Outbreak of histoplasmosis among cavers attending the National speleological society Annual convention, Texas, Am Trop Med Hyg 1999; 899-903. |
| 3. | Aslani J, Jeyhounian M. First case of clinical histoplasmosis and successful treatment of it in Iran. Kowsar Med J 2001;6 (1):21-4. |
| 4. | Davies SF, Khan M, Sarosi GA. Disseminated histoplasmosis in immunologically suppressed patients. Occurrence in a nonendemic area. Am J Med 1978;64(1):94-100. |
| 5. | LaRocco MT, Burgert SJ. Fungal infections in the transplant recipient and laboratory methods for diagnosis. Rev Iberoam Micol 1997;14(4): 143-6. |
| 6. | Voloshin DK, Lacomis D, McMahon D. Disseminated histoplasmosis presenting as myositis and fasciitis in a patient with dermatomyositis. Muscle Nerve. 1995;18(5):531-5. |
| 7. | Sridhar NR, Tchervenkov JI, Weiss MA, Hijazi YM, First MR. Disseminated histoplasmosis in a renal transplant patient: a cause of renal failure several years following transplantation. Am J Kidney Dis 1991;17(6):719-21. |
Correspondence Address:
Saeed Taheri
Dr. Taheri Medical Research Group, Baqiyatallah University of Medical Sciences, MullaSadra St., Tehran
Iran
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PMID: 19587508 
[Figure 1] |
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| Wisanuyotin, S. and Jiravuttipong, A. and Siritunyaporn, S. | | Southeast Asian Journal of Tropical Medicine and Public Health. 2012; 43(4): 992-996 | | [Pubmed] | |
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