Uremia

INTRODUCTION: Calcium oxalate crystals (COC) have been reported on surgical or autopsy specimens or in association with hyphae or conidia in tissue and cytology specimens from patients with aspergillosis. We report here a case of Aspergillus niger (A. niger) infection in which the presence of crystals on transbronchial biopsy specimens was the only laboratory indication of aspergillosis before fungal cultures became positive.

CASE PRESENTATION: A 71 year-old woman presented with two month history of fevers, night sweats, hemoptysis and chest pain after one year of fatigue, decreased appetite and a 35 lb weight loss. Past medical history is significant for diabetes and pulmonary tuberculosis treated with four drug therapy nine months earlier. Physical examination disclosed crackles at the right lung base. Computed tomography showed lingular, right middle lobe and lower lobe thick walled cavities with intracavitary solid lesions and focal bronchiectasis (Figure 1). Bronchoscopy demonstrated inflammation and necrosis of the mucosa of the right middle and lower lobe bronchi. Bronchoscopic lung biopsies (Figure 2) revealed acute and chronic inflammation with the presence of oxalate crystals. Giemsa (GMS) and acid fast bacilli stains showed no fungal or acid -fast organisms. Fungal serology, blood culture, brushings and biopsy cultures were nondiagnostic but the bronchioloalveolar lavage (BAL) and sputum cultures eventually grew A. niger. Six weeks after initiating antifungal therapy with voriconazole the patient became asymptomatic.

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DISCUSSIONS: Oxalosis is the deposition of calcium oxalate in tissues. It results from a variety of causes including nephropathies and uremia, primary hyperoxaluria, ileal diseases and jejunoileal bypass, excessive intake of oxalate-rich food, ethylene glycol poisoning, methoxy-flurane anesthesia, glycerol and xylitol administration, vitamin C intoxication and pyridoxine and thiamine deficiency. It is usually systemic but may be localized with the renal tubules most commonly involved. In 1891 oxalic acid was demonstrated as a mycotoxin produced by A. niger. Starting in the 1960s, COC have been reported in association with pulmonary fungal infection, especially A. niger and were found to be more common in patients with diabetes. Oxalate, produced through the tricarboxilic acid cycle, combines with calcium ions to form calcium oxalate crystals (COC). Oxalic acid has been incriminated in blood vessel destruction, tissue damage and necrosis which seem to be more severe in immunosuppressed states. The presence of COC in pulmonary cytology specimens has been considered a reliable marker for the presence of Aspergillus infection, which may be detected before cultures are positive. Previous case reports, however, revealed the COC only in surgical or autopsy specimens or along with fungal elements (hyphae or conidia) in tissue or cytology specimens. In our patient, histology and cytology specimens failed to reveal any fungal elements. The bronchoscopic biopsy specimens showed crystals consistent with calcium oxalate. Sputum and BAL culture confirmed A. niger infection and patient responded well to voriconazole. Patient had no clinical or laboratory evidence of systemic oxalosis. We consider that previous tuberculosis infection and diabetes

Septimiu D. Murgn MD * Henri Colt MD UCI Medical Center, Orange, CA

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