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Saudi Journal of Kidney Diseases and Transplantation
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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 4  |  Page : 643-645
Is pulmonary histoplasmosis a risk factor for acute renal failure in renal transplant recipients?


1 Dr. Taheri Medical Research Group and Baqiyatallah University of Medical Sciences, Tehran, Iran
2 Dr. Taheri Medical Research Group, Iran

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Date of Web Publication8-Jul-2009
 

   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 2021 Apr 21];20:643-5. Available from: https://www.sjkdt.org/text.asp?2009/20/4/643/53256

   Introduction Top


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 Top


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 Top


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 Top


This article is supported by a grant from Dr. Taheri Medical Research Group.[Figure 1]

 
   References Top

1.Sweny P, Burroughs AK. Infections in solid organ transplantation. Curr Opin Infect Dis 1994;7:436-43.  Back to cited text no. 1    
2.Outbreak of histoplasmosis among cavers atten­ding the National speleological society Annual convention, Texas, Am Trop Med Hyg 1999; 899-903.  Back to cited text no. 2    
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.  Back to cited text no. 3    
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.  Back to cited text no. 4    
5.LaRocco MT, Burgert SJ. Fungal infections in the transplant recipient and laboratory methods for diagnosis. Rev Iberoam Micol 1997;14(4): 143-6.  Back to cited text no. 5    
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.  Back to cited text no. 6    
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.  Back to cited text no. 7    

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Correspondence Address:
Saeed Taheri
Dr. Taheri Medical Research Group, Baqiyatallah University of Medical Sciences, MullaSadra St., Tehran
Iran
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PMID: 19587508

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    Abstract
    Introduction
    Case Report
    Discussion
    Acknowledgement
    References
    Article Figures
 

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