“…The cause and treatment of severe edema accompany ing the nephrotic syndrome (NS) have been subjects of controversy for many years [1][2][3][4], Although a certain serum albumin level is supposed to accompany or induce edema, no absolute correlation exists with serum albu min and clinical presentation, histology, glomerular fil tration rate (GFR, or its equivalent, serum creatinine) [5,6], serum electrolytes, or hematocrit -blood volume [4,7], In addition, there is no correlation between serum albu min and response to the administration of albumin and furosemide (Lasix®) [8], Even though the administration of 'salt poor' albumin does not aim to raise the serum albumin, this occurs transiently in many patients. The unpredictability of diuresis in response to the combined use of albumin and furosemide, and even more to albu min [ 1 ] or diuretics [1,6] given alone, further supports the notion that factors other than, or in addition to, hypoproteinemia are responsible for the sodium retention and edema of nephrotic patients [5,7,9,10], Recently it was postulated that the hyperlipidemia of these patients could be the result of an initial glomerular capillary wall damage leading to urinary loss of lipopro tein lipase activators, increase in serum lipids (low densi ty and very low density lipoproteins) which bind with glycosaminoglycans of the capillary basement mem brane and further increase its permeability [11], The per sistence of these findings in NS children after several years in remission [12], may lend support to the hypothe sis that an abnormal lipid metabolism is responsible for the initiation of NS and progression of glomerular and tubulo-interstitial disease [II], Similarly, excessive pro tein intake in the diet has been ascribed the main role in the progression of glomerular renal disease through chronic renal vasodilation [13], and food manipulation induced either remission or relapse in half of the NS children studied [14].…”