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Abstract
A 9-month-old C57BL/6J mouse had progressive abdominal distension over a 1-week period, and a distended left renal capsule was discovered at postmortem examination. Incision of the capsule showed a tan, cloudy fluid that separated the renal capsule and the remnant left kidney. Microscopically, the capsule was significantly separated from the renal parenchyma by clear space and necrotic cellular debris. The majority of the lining of the renal capsule was composed of fibrous connective tissue and lacked an epithelial lining, consistent with a subcapsular perinephric pseudocyst. In addition, attached to intermittent portions of the renal capsule were thin rims of compressed cortical tissue lined by transitional epithelium. The finding of remnant cortical tissue lined by transitional epithelium is consistent with severe hydronephrosis and indicates that the hydronephrosis preceded the formation of the perinephric pseudocyst. To our knowledge, this is the first case report to characterize a perinephric pseudocyst secondary to severe hydronephrosis in a mouse.
Key words: C57BL/6J mice; hydronephrosis; perinephric pseudocyst; perirenal pseudocyst.
Perinephric pseudocysts are locally extensive accumulations of fluid in a fibrous sac surrounding one or both kidneys.8 The fluid accumulation may be extracapsular, but it is often subcapsular between the fibrous renal capsule and renal parenchyma.1 Whereas a cyst is defined as a fluid filled cavity lined by epithelium, the term pseudocyst is more appropriate for this lesion, as it lacks an epithelial lining.9 A review of the literature indicates multiple synonyms for this lesion, including capsulogenic renal cyst, capsular cyst, para-renal cyst, pararenal pseudocyst, capsular hydronephrosis, perirenal cyst, perirenal pseudocyst, and pseudohydronephrosis.6,8,9 Perinephric pseudocysts are uncommon lesions in cats and are rare in dogs, ferrets, pigs, and humans.4,7,1113 This manuscript characterizes a unilateral perinephric pseudocyst secondary to hydronephrosis in a C57BL/6J mouse.
A 9-month-old female C57BL/6J mouse, part of a control group of an impending research study, showed progressive abdominal distension over 1 week's time. The mouse was euthanatized with carbon dioxide, and an incision of the abdomen showed a distended left kidney. The entire body was placed in 10% neutral-buffered formalin and submitted to Iowa State University's Surgical Pathology Service for histopathologic diagnosis. On examination, the renal capsule was greatly distended (3.4 x 2.5 x 2.2 cm) (Fig. 1) and encased a tan, turbid fluid. Cytospin preparations were non-diagnostic due to formalin fixation. Near the hilus of the capsule was an aggregate of tissue compatible with the remnant kidney, and the adjacent proximal ureter had small, pale serosal nodules (
1 mm).
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In cats with perinephric pseudocyststhe domestic species with the most-documented incidence of perinephric pseudocyststhe most common presenting clinical complaint is progressive abdominal distention. Antemortem diagnosis of perinephric pseudocysts is readily achieved in small animals by abdominal ultrasound. Ultrasonographic evaluation showed an accumulation of free fluid within the perirenal space, and in cats, fluid accumulation is often subcapsular.1 Fluid analysis typically yields a transudate (e.g., uriniferous origin) or a modified transudate (e.g., hematoma). Urea nitrogen and creatinine concentrations are usually similar to those in serum for lymph and hematoma peri-nephric pseudocysts, but they are elevated compared to serum for those of uriniferous origin.1,3,8 Cytologic examination yields various findings, depending on the origin of the fluid. Unfortunately, fluid analysis and cytologic examination in this particular case were not possible because of the formalin contamination of the cyst fluid.
In this instance, severe hydronephrosis was the major differential diagnosis at gross examination. Hydronephrosis is an uncommon condition in mice due to some degree of urinary obstruction, and certain strains of mice (e.g., C57BL/KsJ, C57BL/6J) are prone to spontaneous and hereditary hydronephrosis.2,5,14,15 In severe cases of murine hydronephrosis, a minimal amount of grossly identifiable renal tissue remains, and the atrophied renal cortex may be replaced by thin bands of connective tissue that are consistently lined on one side by the renal capsule and on the other side by atrophied-to-hyperplastic transitional epithelium.14,15 In the mouse of this study, the intermittent foci of compressed cortical tissue with transitional epithelium on the renal capsule were indicative of previous hydronephrosis.15 However, the majority of the renal capsule lacked compressed cortical tissue and transitional epithelium. The large amount of remnant renal parenchyma remaining at the hilus is not consistent with severe hydronephrosis, but it is most compatible with perinephric pseudocyst formation secondary to hydronephrosis.10,14,15 Hydronephrosis with secondary perinephric pseudocyst formation has been described in humans and cats.9,13 The suggested pathogenesis involves some degree of urinary obstruction leading to hydronephrosis (Fig. 4). At some point during the development of the hydronephrosis, the integrity of the lining wall is compromised, causing the rupture/leakage of urine into the subcapsular space that, in turn, forms a fluid-filled cavity (perinephric pseudocyst) between the renal capsule and the remnant kidney.9,10,13 In the mouse of this study, the hydronephrosis had apparently progressed to a severe stage, as suggested by the thin rims of cortical tissue intermittently lining the renal capsule. We believe that, following the rupture/leakage into the subcapsular space, much of the injured renal parenchyma collapsed near the hilus, while small portions remained attached to the capsule. This is, to our knowledge, the first description of a peri-nephric pseudocyst secondary to hydronephrosis in the mouse and the first detailed veterinary description of the microscopic lesions associated with this dual condition.
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Acknowledgments
We thank Dr. Kathy Mullin, Dr. Charles Brockus, and Dr. Vanessa Preast for technical assistance and Dr. Ronald K. Myers for reviewing this manuscript.
References
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