Alterations of ultrastructure and anionic molecular organization in the basement membranes of chronic uremic myocardium.

Ultrastructural and cytochemical studies on the basement membranes of chronic uremic myocardium which was obtained in vivo in 6 uremic patients with severe-grade pericarditis were carried out with special reference to the investigation of anionic molecular organization in the basement membranes of myocardial cells and capillaries. Irregular thickening of the basement membranes of myocardial cells and capillaries was consistently observed in chronic uremic heart. The central electron-lucent surface coat of the sarcolemmal complex and the inner lamina lucida of the capillary basement membrane were often absent with only a thick, dense zone comprising the membranes. In addition, focal splitting of myocardial basement membranes into two layers separated by clear spaces was occasionally demonstrated. The anionic binding sites characterized by cationic polyethyleneimine (PEI) were irregularly and loosely distributed in the basement membranes of chronic uremic myocardium, particularly in the abnormal basement membranes. Apparent increase of PEI deposition in the surface coat of myocardial basement membranes was present in chronic uremia in comparison to that in the controls. Furthermore, the PEI particles were not infrequently observed to be distributed in the intercalated discs and even in the interior of myocardial cells. From the aforementioned results we disclosed the ultrastructural alterations of the basement membranes associated with disorganization of anionic binding sites in the membranes in chronic uremic myocardium. Thus, the present study provides the ultrastructural and molecular basis for the explanation of many clinical manifestations and pathologic findings in the chronic uremic heart. It is suggested that altered membrane permeability of myocardial cells and capillaries resulting from their basement membrane changes in the chronic uremic state appears to play a relevant role in the pathogenesis of uremic cardiomyopathy.