FACTORS ALTERING CONCENTRATION OF BLOOD LIPIDS 463 



j. The Blood Lipids in Diseases of the Kidney, (a) In Nephroses. 

 Marked lipemia occurs in nephrosis coincident with edema, when the 

 latter is of non-cardiac origin. 210,340,585,613,692,693 The concentration of 

 lipids is so high that the serum frequently exhibits a lactescence (milky 

 appearance). Serum cholesterol values as high as 1% have been noted. 

 Although Lichtenstein and Epstein 694 reported that the esters were present 

 in an unusually high proportion, most other workers have reported a 

 normal free cholesterol : total cholesterol ratio. 695 ~ 698 The lipid phosphorus 

 also increases, but to a lesser degree than does the cholesterol. Thomas 

 et al. m have reported that the increase in neutral fat is disproportionally 

 great in children with nephrotic lipemia. 



Although the most pronounced degree of hyperlipemia is usually found 

 in the patients with the lowest serum albumin and the greatest albu- 

 minuria (and hence the greatest degree of edema) , it has not been possible 

 to correlate the lipid concentration with the decrease in serum albu- 

 rn 694,696-700 However, Thomas et a/. 698 suggest that there is some evi- 

 dence of a correlation between lipid levels in the blood and those of al- 

 bumin and 7-globulin. 



In some cases, edema and lipemia exhibit an inverse relationship. 697 

 However, when the edema disappears, due either to a regression or to a 

 recovery from the disease, a concomitant decrease in hyperlipemia usu- 

 ally occurs. In some cases, hyperlipemia may continue for some time 

 after all evidence of edema has vanished. 701 In the terminal or uremic 

 phases of the nephrotic syndrome, the blood lipids drop to subnormal 

 levels. 696,697,702 ~ 704 These lower values may obtain during the terminal 

 stages of the disease, irrespective of whether or not the edema has sub- 

 sided. 696,697 The decrease in cholesterol following the initial maximal rise 

 is prevented by the oral administration of sodium cholate. 



In addition to the hyperlipemia associated with nephroses, Rosenman 



692 F. Erben, Z. klin. Med., 50, 441-463 (1903). 



693 F. Erben, Z. klin. Med., 57, 39-69 (1905). 



694 L. Lichtenstein and E. Z. Epstein, Arch. Internal Med., 47, 122-127 (1931 ). 



695 H. Gainsborough, Quart. J. Med., 23, 101-127 (1929). 



696 I. H. Page, E. Kirk, and D. D. Van Slyke, J. Clin. Invest, 15, 101-107 (1936). 



697 J. P. Peters and E. B. Man, /. Clin. Invest., 22, 721-726 (1943). 



698 E. M. Thomas, A. H. Rosenblum, H. B. Lander, and R. Fisher, Am. J. Diseases 

 Children, 81, 207-214 (1951). 



699 I. H. Page and L. E. Farr, /. Clin. Invest., 15, 181-191 (1936). 



700 J. Bing and U. Stamp, Acta Med. Scand., 86, 12-21 (1935). 



701 J. K. Calvin and A. H. Goldberg, Am. J. Diseases Children, 41, 1066-1080 (1931). 



702 B. I. Ashe and M. Bruger, Am. J. Med. Sci., 186, 670-678 (1933). 



703 A. A. Epstein and M. A. Rothschild, /. Biol. Chem., 29, iv-v (1917). 



704 J. Maxwell, Quart. J. Med., 3, 79-83 (1934). 



