A challenging case: A German shepherd with a decreasing appetite and azotemia - Veterinary Medicine
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A challenging case: A German shepherd with a decreasing appetite and azotemia
Obtaining samples by using ultrasound guidance and re-reviewing results helped these clinicians identify a rare and easily overlooked disease.


Figure 1. A longitudinal sonogram of the left kidney. Note the increased cortical and medullary echogenicity. The renal pelvis is moderately dilated and contains a moderate amount of echogenic material (arrow).
Thoracic and abdominal radiographs were obtained to assess the extent of the possible fungal disease, but no abnormalities were noted. Abdominal ultrasonography was performed to further evaluate the kidneys. Both kidneys were irregularly shaped and exhibited increased echogenicity and a nearly absent corticomedullary distinction. The left renal pelvis was moderately dilated and contained amorphous, poorly echogenic material extending into the mildly dilated proximal left ureter (Figure 1). Similar but less severe changes were noted in the right kidney. Bladder contents and wall thickness were normal.

Differential diagnoses and further tests

The history, physical examination results, and laboratory findings were consistent with chronic renal disease. The ultrasonographic findings suggested chronic nephritis (interstitial, glomerular, or tubular nephritis) or pyelonephritis. However, the amorphous echogenic material seen in the collecting system was considered unusual in the absence of macroscopic hematuria. Our differential diagnoses for this finding were a blood clot, cellular debris, or, less likely, neoplastic or proliferative changes associated with the lining of the collecting system. In the absence of macroscopic hematuria, a blood clot was also considered less likely. And because there was no shadowing, the echogenic material was not considered to be a calculus. The echogenic material appeared amorphous and moved slightly during the examination, so cellular debris was considered most likely.

To establish a definitive diagnosis, the dog was anesthetized two days later, and an ultrasound-guided renal biopsy and pyelocentesis (for bacterial and fungal cultures) were performed. Pyelectasis and proximal hydroureter were present bilaterally and appeared to have mildly progressed since the previous ultrasonographic examination. Microscopic examination of the urine sample obtained by pyelocentesis revealed moderate neutrophilic inflammation and mats of branching, septate fungal hyphae. The morphologic features of the fungus were initially considered to be most consistent with Aspergillus species. A blood sample was obtained to test for Aspergillus species antibodies.

Diagnosis and outcome

We presumptively diagnosed renal aspergillosis. Because of the uncertain prognosis and the need for long-term therapy, the owners elected euthanasia. A postmortem examination was not performed.

The results of the aerobic and anaerobic bacterial cultures of the urine sample collected by pyelocentesis were negative. The Aspergillus species antibody titer (agar gel immunodiffusion test) results were also negative.

Figure 2. A photomicrograph of a renal core biopsy sample. The tubules are displaced by interstitial inflammation (arrows) that varies from lymphocytic to necrosuppurative (hematoxylin-eosin stain; 100X; bar = 50 μm).
Histologic examination of the renal biopsy sample revealed multiple focal, nodular areas of pyogranulomatous and lymphohistiocytic interstitial inflammation. Additionally, severe membranoproliferative glomerulonephritis and multifocal, pyogranulomatous nephritis (possibly of fungal origin) were present (Figure 2). The results of periodic acid-Schiff staining were negative. Grocott-Gomori methenamine-silver nitrate stain revealed that the areas of pyogranulomatous inflammation contained widely scattered, branching, septate fungal hyphae (roughly parallel walls, 3 to 5 μm diameter, occasional branching, and an absence of conidia) considered to be most consistent with Aspergillus fumigatus (Figure 3).1


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