Plasma Lipid Interrelationships in Experimental Nephrosis1

Serum Lipid and Lipoprotein Alterations in Nephrosis

“…Serum triglyceride level was a good index of the quantity of very low density lipoproteins in the serum, and, in accord with the observations of Albrink, Man and Peters (26) (27), from studies on experimental nephrosis in rats, postulated that an accumulation of triglyceride due to a disturbance in the clearing mechanism is the primary lipid alteration in nephrosis, and that cholesterol and phospholipid accumulate passively as a result of trapping by the triglyceride. Lipoproteins were not studied.…”

Hepatic Metabolism of Cholesterol in Experimental Nephrosis in Rats *

“…Although a similar mechanism has not been demonstrated in the human disease, a comparable alteration of plasma-liver exchange of cholesterol has been noted in other experimental hypertriglyceridemic states in which associated excess plasma cholesterol is also transported in a nondiffusible form, namely in rats during the first 36 hours after injection of Triton® WR-1339 (13), and in rats continuously infused with triglycerides (21). The present findings are thus consistent with earlier demonstrations (19,22,23) of an intravascular partial block to the egress of cholesterol from nephrotic plasma, apparently occurring as a passive consequence of the excess triglycerides present in such plasma (18,21,24).…”

“…Earlier studies from this laboratory showed that the hepatic R. E. cell plays an important role in the disposition of dietary-derived (15) but not endogenously-derived (16) cholesterol in the rat. A possible role of altered Kupffer cell function in the genesis of nephrotic hypercholesteremia was considered because, although of endogenous origin (23), the lipid spectrum of nephrotic plasma resembles an exaggerated alimentary hyperlipemia, characterized as it is by a relatively greater excess of triglycerides (18) and chylomicronemia (24). However, no abnormality of Kupffer cell function, as presently assayed, was found in the nephrotic rats.…”

“…The data also indicate that the AKS-induced hypercholesteremia could not be ascribed to any prior or pari passu accumulation of cholesterol in the liver. The injection of potent AKS leads to a progressive rise of plasma triglycerides and cholesterol for some 72 to 96 hours after its administration (18). During this phase, the excess cholesterol in the plasma is largely present in a nondiffusible form (19).…”

Le Métabolisme Lipidique dans le Syndrome Néphrotique.

“…L'association obligatoire de l'hypoalbuminémie et de l'hyperlipémie, conduit à chercher lequel de ces deux phénomènes était la cause de l'autre (Heymann et Hackel, 1952 ;Rosenman, Friedman et Byers, 1956 ; Rosenman, Byers et Friedman, 1957 ; Heymann, Nash, Gilkey et Lewis, 1958). C'est pourquoi l'on s'est tout d'abord efforcé de déter miner lequel apparaissait en premier lieu.…”