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The possible role of fibrin deposition in the development of diabetic glomerulosclerosis has been investigated by light, immunofluorescence, and electron microscopy examination of renal tissue obtained by percutaneous biopsy from seven diabetic patients having minimal clinical evidence of renal involvement and at necropsy on nine diabetic patients. Although the biopsy specimens showed only early to moderate diffuse glomerulosclerosis without either nodular or exudative lesions, approximately 70% of glomeruli examined showed specific fluorescence for fibrinogen in a discontinuous linear pattern along the capillary basement membrane and diffusely in the mesangium. Moreover the immunofluorescence findings correlated well with the distribution patterns of material thought to be fibrin both in the light microscopy studies, by virtue of its staining properties, and by electron microscopy, because of periodicity, texture, and electron density. It is suggested that electron-dense granular deposits seen on electron microscopy may represent intermediate compounds in the fibrinogen to fibrin conversion, and that endothelial and mesangial trapping of fibrinogen or other macromolecules may initiate or accelerate mesangial enlargement, nodule formation, and irregularity of the basement membrane.

Twenty patients with idiopathic extracapillary glomerulonephritis and 16 patients with other forms of crescentic glomerulonephritis were examined by light and electron microscopy. Crescents were found to be composed of several types of cells which can be divided roughly into two groups: light and dark cells. Most of the crescent cells are apparently derived from the pariental epithelial cells of the Bowman's capsule, but at least in some cases podocytes participate in the cresent formation. Breaks in the glomerular capillary basement membrane were frequently seen (in 11 of 15 patients with idiopathic disease and in 4 of 15 other patients). Such breaks may significantly contribute to the leakage of fibrinogen and red blood cells into the Bowman's space and thus accelerate crescent formation. Proliferation of the epithelial cells appears to be related to precipitation of fibrin, though it is uncertain whether the actual stimulus is provided by the fibrin or by a coprecipitate of some normal or abnormal serum protein. Some of the proliferated cells acquire features of fibroblasts and are presumably responsible for laying down of collagen in the crescent, while other cells demonstrate phagocytic properties. These metaplastic changes of the epithelial cells are briefly discussed.

Localization of immunoglobulins (including IgE), complement and fibrinogen and the morphologic alterations in the kidneys of 10 patients with malignant nephrosclerosis were investigated. Thirteen kidneys with benign nephrosclerosis and 5 normal ones were also studied. In contrast to a previous series of patients with malignant nephrosclerosis, the number of necrotic arterioles and the deposition of IgG and complement in the renal arterioles, were reduced in a parallel fashion. These differences seem to reflect modern treatment and support the hypothesis that IgG and complement play a role in the pathogenesis of the arteriolar necrosis in the disease. IgE was deposited massively in many renal arterioles of 9 patients with malignant nephrosclerosis. The role of reaginic antibody in the pathogenesis of the disease is not clear since IgE was also focally present in some arterioles of 4 normal kidneys and of 8 kidneys with benign nephrosclerosis.

The case reported showed acute necrotic myelopathy and acute perivenous encephalomyelitis against a background of renal infection, malignant hypertension, and a history of injury. Death from renal disease and pneumonia halted the neurological pathology in the acute stage, thus allowing a more detailed histological examination than is possible in the later stages. The pathogenesis of acute necrotic myelopathy, together with the effects of oedema and vascular compression in the cord, are discussed briefly.