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Lipids of the blood serum were studied in 29 patients with untreated nephrotic syndrome (NS) and in 28 patients treated with corticosteroids or nonsteroid drugs. None of the patients had evidence of renal failure, either acute or chronic. The patients with untreated NS showed massive proteinuria, marked hypoproteinemia, considerable hypertriglyceridemia and hypercholesterolemia. Serum high-density lipoprotein cholesterol (HDL cholesterol) concentrations were lower in these patients than in the control group, including 35 normal subjects, and correlated with the total serum protein (r = 0.46, p < 0.05) and serum albumin (r = 0.46, p < 0.05). An inverse correlation was observed between HDL cholesterol and serum triglyceride levels (r = -0.58, p < 0.01). In the treated patients the laboratory indices of NS were less pronounced. HDL cholesterol levels were within normal limits in 14 patients with NS treated mostly with nonsteroid drugs, while in the patients receiving the corticosteroids (14 subjects) they were significantly higher than in the control group.

Vitamin E was quantified in renal cell carcinomas (RCC) and in ‘intact’ renal cortex, obtained from 31 patients subjected either to unilateral nephrectomy or to partial resection of the only kidney. Histologically, 14 tumors consisted predominantly of clear cells (group 1) and 17 of other cell types (group 2). In both groups, a significant increase in vitamin E concentration, as compared to the ‘intact’ cortex, was observed: 167.8 ± 27.9 and 68.2 ± 15.2 μg/g wet tissue weight (mean ± SEM) for groups 1 and 2, respectively, versus 10.1 ± 0.53 μg/ g wet tissue weight for the cortex. Although the total lipid content was also increased in tumors (especially in group 1), the vitamin E concentration in tumor tissue, calculated per milligram of total lipids, proved to be much higher in both groups than in ‘intact’ cortex. A significant positive correlation was observed between vitamin E and total lipid content in group 1 and 2 carcinomas. It was also found that vitamin E accumulation in RCC is unlikely to be attributed to an enhanced lipid deposit in the tumor cells. Thus, in 8 tumors of group 2 the vitamin E levels were markedly enhanced although these tumors did not differ from the cortex in total lipid concentrations. Vitamin A content determined in 17 carcinomas, when calculated per milligram of total lipids, was the same as in ‘intact’ cortex.

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