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Year : 2018  |  Volume : 61  |  Issue : 4  |  Page : 617-619
Bilateral renal fungal balls in an infant


1 Department of Pathology, Division of Cardiovascular and Thoracic, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India
2 Department of Pediatrics, Seth GS Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Date of Web Publication10-Oct-2018
 

How to cite this article:
Vaideeswar P, Karande S, Kadiyani L. Bilateral renal fungal balls in an infant. Indian J Pathol Microbiol 2018;61:617-9

How to cite this URL:
Vaideeswar P, Karande S, Kadiyani L. Bilateral renal fungal balls in an infant. Indian J Pathol Microbiol [serial online] 2018 [cited 2018 Dec 15];61:617-9. Available from: http://www.ijpmonline.org/text.asp?2018/61/4/617/242995




A 9-month-old male child presented with a 3-day history of nonfoul-smelling diarrhea, moderate-grade fever, and respiratory distress. On examination, the child was stunted, undernourished, and febrile. There were tachycardia (heart rate of 180 beats/min), tachypnea (respiratory rate of 80 breaths/min), severe hypotension, and coarse crepitations all over the chest. In view of low hemoglobin (8.7 g/dL), neutrophilia (15,100/mm3), hypotension, hypokalemia (2 mEq/L), metabolic acidosis, and intermittent bronchospasm, the child was transferred to the Pediatric Intensive Care Unit (PICU) and mechanically ventilated. The urine examination revealed pH of 4.8, anion gap of 22 mEq/L, and calcium/creatinine ratio of 0.2; microscopy showed 4–5 epithelial cells and 5–6 pus cells per high-power field. He was given packed red cells, broad-spectrum antibiotics, normal saline boluses, potassium supplements, sodium bicarbonate boluses, and dopamine/aminophylline infusions. The patient then developed oliguria and progressive azotemia (mean BUN of 42.7 mg/dL and mean creatinine of 2.3 mg/dL) with no response to peritoneal dialysis. Blood cultures had no growths. In the last few days, he developed persistent bradycardia (heart rate ranging from 60 to 52 beats/min), which did not respond to maximal inotropic support.

A complete autopsy was performed. The respiratory distress was due to extensive diffuse alveolar damage with focal areas of interstitial pneumonitis, probably viral etiology [Figure 1]; viral inclusions were not seen. Despite the loose motions, the gastrointestinal tract did not show any changes. The cause for the acute renal failure (ARF) was distinctly unusual. Both the kidneys were of normal size and shape [Figure 2]a. On the cut surface, the pelvicalyceal systems were occluded by multiple, pale red, rubbery masses [Figure 2]b. A squash preparation of these masses revealed acute inflammatory exudate with yeasts and pseudohyphae [suggestive of Candida species, [Figure 2]c, while histopathology of the same also revealed irregular-to-circular eosinophilic material [Figure 2]d. Subsequent histopathology of the pelvicalyceal system and adjoining medulla revealed necrotizing pyelitis and papillitis; necrotic bits of the papilla were present in the exudates [Figure 3]a and [Figure 3]b. Most of the tubules were filled with eosinophilic granular casts with or without neutrophils [Figure 3]c.
Figure 1: (a) Hilar aspect of the left lung showing focal pleural opacification and fibrinous exudates; (b) the lung was firm and revealed a diffuse congested and hemorrhagic cut surface; (c and d) thickened and inflamed alveolar septa lined by very thick hyaline membranes. Spaces also contain red cells (H and E, ×400)

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Figure 2: (a) External surface of the kidney is smooth and pale yellow; (b) the cut surface reveals the pelvicalyceal system to be filled with irregular, congested, and rubbery tissue; (c) squash preparation of the rubbery material revealed yeast and pseudohyphae amidst inflammatory cells (Giemsa, ×400); (d) apart from inflammation and fungal elements, the material also showed fragmented irregular to circular pink material (H and E, ×400)

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Figure 3: (a) Ulceration of the urothelial lining of the pelvis (H and E, ×400); (b) pseudohyphae rimming tip of the necrotic papilla (H and E, ×400); (c) many tubules were filled with inflammatory cell casts (H and E, ×400)

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In the present case, invasive renal candidiasis had manifested as multiple fungal balls, leading to obstruction of the pelvicalyceal systems and subsequent recalcitrant ARF. Important causes of ARF in children are hemolytic–uremic syndrome, acute glomerulonephritis, and sepsis.[1] In the current era of advanced patient care, there is an increase in the incidence of health-care-associated fungal sepsis. In this context, the Candida species are important agents. Children are predisposed to invasive candidal infection as a result of central venous or urinary bladder catheterization, prolonged antibiotic therapy, established neutropenia, immunocompromised states, immunosuppressive therapy, total parenteral nutrition, low birth weight, and malnutrition.[2] Our patient was malnourished and had been admitted in the PICU for 11 days with venous catheterization and broad-spectrum antibiotic therapy.

Candida species are commensals that inhabit the gastrointestinal and lower urogenital tracts, the skin, and the oropharynx. Increased colonization at these sites depends on the host immune status and the environmental setting, while invasion is aided by breach in the mucosal barriers. Candidal renal infections produce acute pyelonephritis or renal abscesses, through either hematogenous dissemination or more commonly as retrograde/ascending infections from the lower urinary tract.[3] An uncommon manifestation is the formation of candidal fungal ball, mycetoma, or bezoar.[4] This begins as a superficial layer of fungal growth over the urothelium. Infiltration of the renal parenchyma, aided by the urea metabolism by the Candida species, leads to inflammation and necroses of the tips of the renal papillae.[5] Herein, the mycetomas were seen as rubbery dark-red material that completely filled bilateral pelvicalyceal systems, leading to obstruction to the urine flow.

The diagnosis of renal fungal ball is also often delayed or missed due to lack of specific clinical features. The fungal balls may result in unexplained fever, hematuria, palpable flank masses, or nonspecific laboratory features (like consistent fall in platelet count on antibiotic therapy), but unfortunately, ARF may be the first and only manifestation.[4] In such instances, the single most important investigation to be performed is ultrasonography, which is useful in assessing the size, number, and location of the fungal balls.[6] This is important to formulate therapeutic regimen in the affected children as timely intervention is a key to successful management of renal fungal balls. The treatment ranges from local or systemic antifungal agents, percutaneous drainage or irrigation, percutaneous streptokinase injection, or endoscopic/open surgical removal.[4] It should be noted that surgical management may be the only definitive treatment for renal fungal balls. Renal fungal ball is not commonly thought of in the differential diagnosis of ARF in children. Our experience should prove useful while evaluating such cases, so that this rare occurrence is kept in mind.

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.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
   References Top

1.
Basu RK, Wheeler DS. Approaches to the management of acute kidney injury in children. Recent Pat Biomark 2011;1:49-59.  Back to cited text no. 1
    
2.
Dornbusch HJ, Manzoni P, Roilides E, Walsh TJ, Groll AH. Invasive fungal infections in children. Pediatr Infect Dis J 2009;28:734-7.  Back to cited text no. 2
    
3.
Kauffman CA. Diagnosis and management of fungal urinary tract infection. Infect Dis Clin North Am 2014;28:61-74.  Back to cited text no. 3
    
4.
Bisht V, Voort JV. Clinical practice: Obstructive renal candidiasis in infancy. Eur J Pediatr 2011;170:1227-35.  Back to cited text no. 4
    
5.
de Wall LL, van den Heijkant MM, Bökenkamp A, Kuijper CF, van der Horst HJ, de Jong TP, et al. Therapeutic approach to Candida bezoar in children. J Pediatr Urol 2015;11:81.e1-7.  Back to cited text no. 5
    
6.
Sadegi BJ, Patel BK, Wilbur AC, Khosla A, Shamim E. Primary renal candidiasis: Importance of imaging and clinical history in diagnosis and management. J Ultrasound Med 2009;28:507-14.  Back to cited text no. 6
    

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Correspondence Address:
Pradeep Vaideeswar
Department of Pathology, Division of Cardiovascular and Thoracic, Seth GS Medical College and KEM Hospital, Parel, Mumbai - 400 012, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/IJPM.IJPM_57_18

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  [Figure 1], [Figure 2], [Figure 3]



 

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