Glomerulonephritis and Cardiovascular Disease in the Pygmy Marmoset (Callithrix pygmaea)
American Association of Zoo Veterinarians Conference 2000

Luis R. Padilla1, DVM; James R. Raymond1, DVM; Richard J. Montali1, DVM; Sharda G. Sabnis2, MD

1Department of Pathology, Smithsonian National Zoological Park, Washington, DC, USA; 2Division of Nephropathology, Armed Forces Institute of Pathology, Washington, DC, USA


Renal disease has been a common pathologic finding among the Callitrichidae. This study characterizes a specific type of glomerulonephritis in the pygmy marmoset (Callithrix pygmaea), which can progress to a hypertensive syndrome. A retrospective study of adult pygmy marmosets (n=25) necropsied at the Smithsonian National Zoological Park, Washington, DC revealed a 56% prevalence of glomerulonephritis in this captive population. The disease was determined to be the primary cause of death in 36% of the cases. It was most commonly seen in young adult animals (36–60 months), with no sex predilection. Histologically, glomeruli had a prominent lobular pattern, with varying degrees of mesangial cell proliferation and matrix hyperplasia. Electron microscopy of some affected animals showed minimal increase in basement membrane thickness, but marked increases in mesangial matrix and cells, mixed with some deposits. Immunohistochemistry studies performed on kidney sections of selected animals showed focal mesangial staining to IgG and IgM, but not to IgA. Staining for immunoglobulins was not observed in kidney sections of an age-matched control that died due to traumatic injuries.

Histopathology, electron microscopy and immunohistochemistry were consistent with an immune-mediated membranoproliferative glomerulonephritis (MPGN). Renal vessels in animals with advanced renal disease were often thickened with hyaline arteriosclerosis. Affected animals in the end stages of the disease often showed evidence of hypertension with cardiovascular disease, including left-sided heart failure, chronic passive pulmonary congestion and cavitary effusions. These findings suggest a clinically significant, progressive immune mediated process leading to chronic renal deposition of IgG and IgM in the affected animals and subsequent cardiovascular disease. Although specific antigenic causes initiating glomerulonephritis were not determined in these pygmy marmosets, MPGN in humans can be triggered by chronic infections or parasitism.


Speaker Information
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Luis R. Padilla, DVM
Department of Pathology
Smithsonian National Zoological Park
Washington, DC, USA

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