Sodium Excretion in the Nephrotic Syndrome

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Abstract
THE PATHOGENESIS of nephrotic edema is not known. Excess retention of sodium and water in this disease has been attributed to decreased glomerular filtration rate (GFR), increased tubular resorption, or combinations of these. Such alterations in glomerular or tubular function may occur as primary renal phenomena or as secondary responses to extrarenal factors.1-3 Hypoalbuminemia, through its effect upon colloid osmotic pressure, is considered a major factor in edema formation. Reduction of extracellular fluid resorption consequent to decreased colloid osmotic pressure4 is postulated to cause hypovolemia and circulatory inadequacy.1,2 The resultant reduction in renal blood flow could cause a decrease in GFR.1,2 An additional means by which hypoalbuminemia could influence sodium balance is suggested by the finding of elevated aldosterone levels in the nephrotic syndrome.5 It is proposed that the hypovolemia associated with hypoalbuminemia serves as a primary stimulus for augmented secretion of aldosterone.6,7 Increased