Nutritional Management of Nephrotic Syndrome

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Abstract

Nephrotic syndrome is caused by urinary loss of proteins of intermediate size. Albumin protein is lost in the greatest quantity, but important protein-bound nutrients—such as iron bound to transferrin, vitamin D bound to vitamin D—binding protein, copper bound to ceruloplasmin, and zinc bound mostly to albumin—are lost as well. The syndrome is characterized by hypoalbuminemia, edema formation, hyperlipidemia, and, less well appreciated, hypovitaminosis D, resulting in hypocalcemia and rarely in iron-deficiency edema. Muscle mass may also be depleted. Although hypovitaminosis D and iron deficiency can be treated by replacement, feeding high-protein diets does not correct depleted protein pools. Although albumin synthesis increases if high-protein diets are provided, urinary albumin excretion and albumin catabolism increase also, so that albumin pools are not repleted. High-protein diets may cause accelerated progression of renal disease. Dietary protein supplementation therefore is not advisable. In addition to increasing the risk of atherosclerosis, hyperlipidemia may also cause progression of renal disease and should be treated. Dietary fat should be restricted, and pharmacological means should be used if nutritional management is ineffective in reducing blood lipid levels. There is no compelling reason as yet for providing polyunsaturated fatty acid supplements to nephrotic patients. A diet low in total fat, low in cholesterol, and modestly restricted in protein (0.8 g/kg for adult patients) is recommended.

Original languageEnglish (US)
Pages (from-to)50-58
Number of pages9
JournalJournal of Renal Nutrition
Volume2
Issue number2
DOIs
StatePublished - 1992

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ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics
  • Nephrology

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