Spontaneous Glomerulonephritis in Mice. ∗

Abstract

Although the clinical signs and symptoms, morphologic pathology, and the chemical alterations of the blood and body fluids are known in glomerulonephritis, investigations on etiology and pathogenesis have been retarded because experimental material has not been available. Spontaneous glomerulonephritis in animals has not been described; the disease has been induced in rats according to several investigators. 1 , 2 , 3

When mice of the Strong NH strain developed anasarca, ascites, and hydrothorax spontaneously, and became dysponeic, the condition was considered worthy of detailed study. Eight edematous animals of this strain were investigated from the morphologic standpoint. The kidneys were pale, but of approximately normal size and weight. On histologic section they revealed glomeruli with alterations strikingly similar to those seen in human chronic glomerulonephritis⁴-hyalinized glomeruli, and glomerular closure due to endothelial proliferation. These features were elucidated by staining with azo-carmine. In some cases not all the glomeruli were involved, whereas in others the process was general enough so that the term “diffuse glomerulonephritis” was applicable. Albuminuria was evidenced by casts in the tubules, but only a small degree of tubular degenerative change was present. Contracted kidneys have not been observed.

Preliminary chemical study has confirmed the morphologic diagnosis. Albuminuria, decreased total plasma proteins (5.0 g as compared with a normal for the mouse of 6.2-6.5 g %), and hyperlipemia have been demonstrated for one typical case.

The age of clinical appearance of the disease, when associated with edema, has ranged from 5 to 18 months; death ensued within 2 to 3 weeks in most cases after the development of massive edema. Glomerular pathology has been noted in animals which did not exhibit the nephrotic tendency. The incidence of the disease in untreated strain NH mice of the Minnesota stock has not been determined.† Further studies on the pathology of the disease in mice are being pursued; investigations on the genetic, chemical, bacteriologic, and nutritional aspects of the problem are being planned.