Joseph W. Berkow

Studies on Diabetic Retinopathy: II. Retinopathy and Nephropathy in Spontaneous Canine Diabetes

Retinal and renal observations on dogs with spontaneous diabetes mellitus are presented. Retinal vessels were prepared by the trypsin digestion, flat retinal technic and examined by light microscopy. Kidneys were examined by light and electron microscopy. Nondiabetic dogs of comparable ages served as controls. Retinal vessels in some diabetic subjects showed mural pericyte degeneration with “ghost” formation and zones of focal acellularity surrounded by aneurysms or hypercellular capillary shunts. These changes were indistinguishable from those observed in human diabetic retinas prepared by the same technic. Kidneys of the diabetic dogs showed a significantly greater incidence and severity of diffuse glomerulosclerosis and thickening of the basement membrane of the peripheral glomerular capillary loops than was found in the controls. Nodular glomerular lesions of Kimmelstiel and Wilson were not observed. Cataracts were noted in all diabetic animals with diabetes known to be six months in duration or longer but were rare in the controls. The pancreas was either described grossly by the contributing veterinarian or submitted for histologic examination in eight of the diabetic dogs. Five of these suggested possible pancreatitis and their diabetes may be secondary to pancreatic disease. The remaining three dogs with no evidence of pancreatitis are considered as primary (possibly hereditary) diabetes mellitus. Retinopathy and prominent diffuse glomerulosclerosis occurred in diabetic dogs with and without evidence of pancreatitis.

Dominant slowly progressive macular dystrophy.

Twenty-three members of one white family were studied for a new form of dominant slowly progressive macular dystrophy in which visual acuity remained good until the seventh decade. Ten patients had positive signs of this entity. Eight patients had possible early forms. Five had no signs. Several patients had visual acuity fluctuations, documented by their ophthalmologists who saw associated pigment epithelial alterations in some cases. Obvious macular changes included perifoveal pigment epithelial atrophy, posterior pole flecks, and fundus lesions resembling an atrophic form of senile macular degeneration. We suggest a possible hereditary predisposition to senile macular degeneration in our patients.