Proteinuria and the renal lesion in preeclampsia and abruptio placentae

The defect in glomerular permeability that leads to proteinuria can be assessed by determining the relative clearance of macromolecules of known but different dimensions, that is, glomerular selectivity. Such estimates can be made using naturally occurring plasma proteins and dextran or polyvinylpyrrolidone injected into the circulation. In preeclampsia, protein and dextran selectivities show good concordance. The proteinuria is intermediate in its selectivity. These findings confirm that proteinuria is glomerular in origin and that the glomerular abnormality is uniform throughout the majority of functioning glomeruli. In abruptio, protein selectivity is very low and dextran selectivity is high. This pattern is seen also in acute ischemic renal failure and suggests that the true glomerular functional defect is actually less severe than in preeclampsia and that much of the protein in the urine in abruptio is postglomerular in origin. The structural lesion in preeclampsia is "characteristic" only in the sense that a number of individual components of glomerular injury, which are themselves commonly seen in other glomerular disorders, occur in a particular balance, and not because of any single unique or specific feature. The important components--that is, endothelial swelling, mesangial cytoplasmic activity, subendothelial deposits, and occational thrombosis of the afferent arterioles--all occur, albeit to a lesser degree, in abruptio placentae, as well as in other glomerular disorders in which intravascular coagulation is a primary cause or plays a major role.