Mesangiolysis: an important glomerular lesion in thrombotic microangiopathy

Abstract

Six cases of malignancy-associated thrombotic microangiopathy and eight cases of idiopathic microangiopathy have been studied by renal biopsy. All patients of both groups had mild to severe renal impairment and microangiopathic hemolytic anemia. The renal lesions were histopathologically identical in the two groups. The most characteristic abnormalities were glomerular mesangiolysis and glomerular and arteriolar thrombosis. Subendothelial widening, presumably due to entrapment of blood components, and the formation of capillary and arteriolar thrombi may be attributed to endothelial damage. Glomerular fibrinogen was demonstrated by immunofluorescence in a majority of cases. Immunofluorescence also showed glomerular immunoglobulin M (IgM) and Clq in a majority of cases and C3 in slightly less than half. Mesangiolysis, present in every case, resulted in coalescence of capillary lumina, but mesangiolysis is a bland process, easily overlooked. The mesangial waists of the glomerular tufts seemed to unravel and come apart, with no inflammatory reaction or fibrin deposition on the luminal surface. The presence of capillary enlargement was confirmed morphometrically as an increased proportion of glomerular sectional area. In what appeared to be a late stage of mesangiolysis, the mesangium was thickened by pale fibrillary material, producing a lobulated glomerular tuft and eventual glomerular solidification. The early stages of mesangiolysis may be reflected only in glomerular capillary ectasia, whereas the late stages produce a distinctive form of glomerular sclerosis.