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Research Article Free access | 10.1172/JCI105639
Department of Medicine, Universidad del Valle, Calli, Colombia
Washington University School of Medicine, St. Louis, Missouri
‡† Present address: Dr. Oscar Bolanos, Department of Medicine, Tulane University School of Medicine, New Orleans, La.
Address requests for reprints to Dr. Saulo Klahr, Renal Division, Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid, St. Louis, Mo. 63110.
*Submitted for publication 18 April 1967; accepted 9 June 1967.
This investigation was supported in part by N.I.H. grant No. 9R07-TW00103-05 (ICMRT Award).
Presented in part at the III International Congress of Nephrology, Washington, D. C., September 1966. An abstract has been published in the Proceedings of the III International Congress of Nephrology. 1966. 2: 222.
Find articles by Klahr, S. in: JCI | PubMed | Google Scholar
Department of Medicine, Universidad del Valle, Calli, Colombia
Washington University School of Medicine, St. Louis, Missouri
‡† Present address: Dr. Oscar Bolanos, Department of Medicine, Tulane University School of Medicine, New Orleans, La.
Address requests for reprints to Dr. Saulo Klahr, Renal Division, Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid, St. Louis, Mo. 63110.
*Submitted for publication 18 April 1967; accepted 9 June 1967.
This investigation was supported in part by N.I.H. grant No. 9R07-TW00103-05 (ICMRT Award).
Presented in part at the III International Congress of Nephrology, Washington, D. C., September 1966. An abstract has been published in the Proceedings of the III International Congress of Nephrology. 1966. 2: 222.
Find articles by Tripathy, K. in: JCI | PubMed | Google Scholar
Department of Medicine, Universidad del Valle, Calli, Colombia
Washington University School of Medicine, St. Louis, Missouri
‡† Present address: Dr. Oscar Bolanos, Department of Medicine, Tulane University School of Medicine, New Orleans, La.
Address requests for reprints to Dr. Saulo Klahr, Renal Division, Department of Internal Medicine, Washington University School of Medicine, 660 South Euclid, St. Louis, Mo. 63110.
*Submitted for publication 18 April 1967; accepted 9 June 1967.
This investigation was supported in part by N.I.H. grant No. 9R07-TW00103-05 (ICMRT Award).
Presented in part at the III International Congress of Nephrology, Washington, D. C., September 1966. An abstract has been published in the Proceedings of the III International Congress of Nephrology. 1966. 2: 222.
Find articles by Bolanos, O. in: JCI | PubMed | Google Scholar
Published September 1, 1967 - More info
A qualitative and quantitative analysis of urinary lipids in the nephrotic syndrome is presented. The following lipids were identified in the urine of patients with the nephrotic syndrome: free cholesterol, cholesterol esters, triglycerides, free fatty acids, and phospholipids. Glass paper chromatography identified the cholesterol esters as palmitate, oleate, linoleate, and arachidonate, and identified the phospholipids as phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine.
Urinary lipid excretion was much greater in patients with the nephrotic syndrome than in patients with chronic renal disease and minimal proteinuria, or in patients with hyperlipidemia from other causes.
Urinary lipid excretion varied widely among the 13 patients with the nephrotic syndrome studied, and no quantitative correlation with serum lipid levels was observed. However, qualitatively at least, the proportion of cholesterol esters excreted in the urine was similar to the proportion of these esters in plasma. A good correlation was found between lipid excretion and glomerular permeability. Furthermore, during steroid therapy urinary lipid excretion decreased concomitant with a decrease in proteinuria. All these observations support the idea that lipiduria in the nephrotic syndrome is related to protein loss and that most of the lipid in the urine enters the glomerular filtrate in the form of lipoproteins.