Glomerular ultrastructural lesions of idiopathic cutaneous and renal glomerular vasculopathy of greyhounds

Abstract

Idiopathic cutaneous and renal glomerular vasculopathy (CRGV) (Alabama rot) is a potentially fatal disease of unknown etiology that affects the skin and kidneys of racing- and training-age Greyhounds. Ultrastructural examinations were performed on two healthy control Greyhounds and 12 Greyhounds diagnosed with CRGV based on the presence of characteristic, well-demarcated cutaneous ulcers of the extremities (12/12), thrombocytopenia (< 200,000 platelets/dl) (12/12), and acute renal insufficiency (BUN > 40 mg/dl, serum creatinine > 2.0 mg/dl) (7/12). Early glomerular ultrastructural changes included endothelial swelling, detachment, and necrosis; membranous whorl formation; and platelet adhesion and aggregation. Some capillaries were occluded with aggregated platelets, cellular fragments, and fibrin. Later changes included narrowing of capillary lumina and thickening of glomerular capillary walls by subendothelial accumulation of flocculent, amorphous, variable electron-dense material and occasionally erythrocytes, cellular processes, and fibrin. Glomerular endothelial cells were increased in number and plump, with villouslike cytoplasmic projections. Mesangial cell cytoplasmic processes occasionally were interposed between the endothelium and the basement membrane. No etiologic agents or electron-dense deposits typical of immune complexes were observed. Although the specific etiology was not determined, the ultrastructural changes suggest that glomerular endothelial damage is an important early event in the pathogenesis of CRGV.